An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
An essential amino acid that is physiologically active in the L-form.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Chemicals that are used to cause the disturbance, disease, or death of humans during WARFARE.
Tactical warfare using incendiary mixtures, smokes, or irritant, burning, or asphyxiating gases.
Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed).
An organophosphorus ester compound that produces potent and irreversible inhibition of cholinesterase. It is toxic to the nervous system and is a chemical warfare agent.
Warfare involving the use of living organisms or their products as disease etiologic agents against people, animals, or plants.
An organophosphorus compound that inhibits cholinesterase. It causes seizures and has been used as a chemical warfare agent.
Events that overwhelm the resources of local HOSPITALS and health care providers. They are likely to impose a sustained demand for HEALTH SERVICES rather than the short, intense peak customary with smaller scale disasters.

Synergistic protective effects of antioxidant and nitric oxide synthase inhibitor in transient focal ischemia. (1/1201)

Both nitric oxide synthase (NOS) inhibitors and free radical scavengers have been shown to protect brain tissue in ischemia-reperfusion injury. Nitric oxide and superoxide anion act via distinct mechanisms and react together to form the highly deleterious peroxynitrite. Therefore the authors examined the effects and the interaction between the NOS inhibitor, NG nitro-L-arginine (LNA) and the antioxidant/superoxide scavenger, di-tert-butyl-hydroxybenzoic acid (DtBHB) in the rat submitted to 2 hours of middle cerebral artery occlusion. Posttreatment was initiated 4 hours after the onset of ischemia and infarct volume was measured at 48 hours. The dose-related effect of LNA resulted in a bell-shaped curve: 15, 56, 65, and 33% reduction of total infarct for 0.03, 0.1, 0.3, and 1 mg/kg (intravenously [IV]) respectively and 11% increase in infarct volume for 3 mg/kg (IV). Whereas DtBHB (20 mg/kg; intraperitoneally [IP]) was ineffective, the dose of 60 mg/kg produced 65% protection in infarct volume. The combination of a subthreshold dose of LNA (0.03 mg/kg; IV) and DtBHB (20 mg/kg; IP) resulted in significant reduction (49%) in infarct volume. These results show that LNA and DtBHB act synergistically to provide a consistent neuroprotection against ischemic injury when administered 4 hours after ischemia. This suggests that nitric oxide and free radicals are involved and interact in synergy in ischemia-reperfusion injury.  (+info)

Neurogenic vasodilatation of canine isolated small labial arteries. (2/1201)

Mechanisms underlying vasodilatation to nerve stimulation by electrical pulses and nicotine were analyzed in isolated canine small labial arteries. Transmural electrical stimulation (5 and 20 Hz) produced a contraction followed by a relaxation in labial arterial strips denuded of the endothelium, partially contracted with prostaglandin F2alpha. The contraction was abolished by prazosin or combined treatment with alpha, beta-methylene ATP. In the treated strips, neurogenic relaxation was abolished by NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor, and restored by L-arginine. The D-enantiomers were without effect. Nicotine (10(-4) M) also relaxed the arteries, in which the contractile response was abolished by prazosin and alpha, beta-methylene ATP. The relaxant response was attenuated but not abolished by L-NA; the inhibition was reversed by L-arginine. The remaining relaxation by nicotine was abolished by calcitonin gene-related peptide (CGRP)-[8 to 37], a CGRP1 receptor antagonist. Relaxations elicited by a lower concentration of nicotine (2 x 10(-5) M) sufficient to produce similar magnitudes of response to those induced by 5-Hz electrical nerve stimulation were also inhibited partially by L-NA. Histochemical study with the NADPH-diaphorase method demonstrated positively stained nerve fibers and bundles in the arterial wall, suggesting the presence of neuronal NO synthase. It is concluded that the relaxation induced by electrical nerve stimulation of small labial arteries is mediated exclusively by NO synthesized from L-arginine in nerve terminals, whereas nicotine in the concentrations used evokes relaxations by a mediation of nerve-derived NO and also CGRP, possibly from sensory nerves. The reason why nicotine but not electrical pulses stimulates sensory nerves and elicits vasorelaxation remains unsolved.  (+info)

Effects of tumour necrosis factor-alpha on left ventricular function in the rat isolated perfused heart: possible mechanisms for a decline in cardiac function. (3/1201)

1. The cardiac depressant actions of TNF were investigated in the isolated perfused rat heart under constant flow (10 ml min(-1)) and constant pressure (70 mmHg) conditions, using a recirculating (50 ml) mode of perfusion. 2. Under constant flow conditions TNF (20 ng ml(-1)) caused an early (< 25 min) decrease in left ventricular developed pressure (LVDP), which was maintained for 90 min (LVDP after 90 min: control vs TNF; 110 +/- 4 vs 82 +/- 10 mmHg, P < 0.01). 3. The depression in cardiac function seen with TNF under constant flow conditions, was blocked by the ceramidase inhibitor N-oleoylethanolamine (NOE), 1 microM, (LVDP after 90 min: TNF vs TNF with NOE; 82 +/- 10 vs 11 +/- 5 mmHg, P < 0.05). 4. In hearts perfused at constant pressure, TNF caused a decrease in coronary flow rate (change in flow 20 min after TNF: control vs TNF; -3.0 +/- 0.9 vs -8.7 +/- 1.2 ml min(-1), P < 0.01). This was paralleled by a negative inotropic effect (change in LVDP 20 min after TNF: control vs TNF; -17 +/- 7 vs -46 +/- 6 mmHg, P < 0.01). The decline in function was more rapid and more severe than that seen under conditions of constant flow. 5. These data indicate that cardiac function can be disrupted by TNF on two levels, firstly via a direct, ceramidase dependant negative inotropic effect, and secondly via an indirect coronary vasoconstriction.  (+info)

Acetylcholine-induced relaxation in blood vessels from endothelial nitric oxide synthase knockout mice. (4/1201)

1. Isometric tension was recorded in isolated rings of aorta, carotid, coronary and mesenteric arteries taken from endothelial nitric oxide synthase knockout mice (eNOS(-/-) mice) and the corresponding wild-type strain (eNOS(+/+) mice). The membrane potential of smooth muscle cells was measured in coronary arteries with intracellular microelectrodes. 2. In the isolated aorta, carotid and coronary arteries from the eNOS(+/+) mice, acetylcholine induced an endothelium-dependent relaxation which was inhibited by N(omega)-L-nitro-arginine. In contrast, in the mesenteric arteries, the inhibition of the cholinergic relaxation required the combination of N(omega)-L-nitro-arginine and indomethacin. 3. The isolated aorta, carotid and coronary arteries from the eNOS(-/-) mice did not relax in response to acetylcholine. However, acetylcholine produced an indomethacin-sensitive relaxation in the mesenteric artery from eNOS(-/-) mice. 4. The resting membrane potential of smooth muscle cells from isolated coronary arteries was significantly less negative in the eNOS(-/-) mice (-64.8 +/- 1.8 mV, n = 20 and -58.4 +/- 1.9 mV, n = 17, for eNOS(+/+) and eNOS(-/-) mice, respectively). In both strains, acetylcholine, bradykinin and substance P did not induce endothelium-dependent hyperpolarizations whereas cromakalim consistently produced hyperpolarizations (- 7.9 +/- 1.1 mV, n = 8 and -13.8 +/- 2.6 mV, n = 4, for eNOS(+/+) and eNOS(-/-) mice, respectively). 5. These findings demonstrate that in the blood vessels studied: (1) in the eNOS(+/+) mice, the endothelium-dependent relaxations to acetylcholine involve either NO or the combination of NO plus a product of cyclo-oxygenase but not EDHF; (2) in the eNOS(-/-) mice, NO-dependent responses and EDHF-like responses were not observed. In the mesenteric arteries acetylcholine releases a cyclo-oxygenase derivative.  (+info)

In vitro simultaneous measurements of relaxation and nitric oxide concentration in rat superior mesenteric artery. (5/1201)

1. The relationship between nitric oxide (NO) concentration measured with an NO-specific microelectrode and endothelium-dependent relaxation was investigated in isolated rat superior mesenteric artery contracted with 1 microM noradrenaline. 2. Acetylcholine (10 microM) induced endothelium-dependent simultaneous increases in luminal NO concentration of 21 +/- 6 nM, and relaxations with pD2 values and maximum of 6.95 +/- 0.32 and 97.5 +/- 0.7 % (n = 7), respectively. An inhibitor of NO synthase, N G-nitro-L-arginine (L-NOARG, 100 microM) inhibited the relaxations and increases in NO concentration induced by acetylcholine. 3. Oxyhaemoglobin (10 microM) reversed the relaxations and increases in NO concentrations induced by acetylcholine, S-nitroso-N-acetylpenicillamine (SNAP) and S-morpholino-sydnonimine (SIN-1), but not the relaxations induced with forskolin. Oxyhaemoglobin also decreased the NO concentration below baseline level. 4. In the presence of L-NOARG (100 microM), a small relaxation to acetylcholine (10 microM) of noradrenaline-contracted segments was still seen; oxyhaemogobin inhibited this relaxation and decreased the NO concentration by 14 +/- 4 nM (n = 4). 5. The NO concentration-relaxation relationship for acetylcholine resembled that for SNAP and SIN-1 more than for authentic NO. Thus while 7-17 nM NO induced half-maximal relaxations in response to SNAP or SIN-1, 378 +/- 129 nM NO (n = 4) was needed for half-maximal relaxation to authentic NO. 6. The present study provides direct evidence that the relaxation of the rat superior mesenteric artery with the endothelium-dependent vasodilator acetylcholine is correlated to the endogeneous release of NO. The study also suggests that NO mediates the L-NOARG-resistant relaxations in this artery, and that there is a basal NO release.  (+info)

Angiotensin II-induced constrictions are masked by bovine retinal vessels. (6/1201)

PURPOSE: To unmask the vasoconstricting effect of angiotensin II (Ang II) on retinal smooth muscle by studying its interaction with endothelium-derived paracrine substances. This study focused specifically on determining the changes in vascular diameter and the release of endothelial-derived vasodilators, nitric oxide (NO) and prostaglandin (PG) I2, from isolated retinal microvessels. METHODS: Bovine retinal central artery and vein were cannulated, and arterioles and venules were perfused with oxygenated/heparinized physiological salt solution at 37 degrees C. This ex vivo perfused retinal microcirculation model was used to observe the contractile effects of Ang II on arterioles and venules of different diameters. The NO and PGI2 synthase inhibitors, 1-NOARG and flurbiprofen, respectively, were used to unmask Ang II vasoconstriction; the changes in vascular diameters were then measured. Enzyme immunoassays were used to measure the release of cGMP (an index of NO release) and 6-keto-PG-F1alpha (a stable metabolite of PGI2) from isolated bovine retinal vessels. RESULTS: Topically applied Ang II (10(-10) M to 10(-4) M) caused significant (P < 0.05) arteriolar and venular constrictions in a dose-dependent manner, with the smallest retinal arterioles (7+/-0.2 microm luminal diameter) and venules (12+/-2 microm luminal diameter) significantly more sensitive than larger vessels. After the inhibition of endogenous NO and PGI2 synthesis by 1-NOARG and flurbiprofen, respectively, the vasoconstriction effects of Ang II became more pronounced. Again, the smallest vessels tested were significantly more sensitive, and synthesis of endothelial-derived relaxing factor (EDRF), therefore, may be most important in these vessels. Vasoactive doses of Ang II (10(-10) M to 10(-4) M) caused a dose-dependent increase in the release of NO and PGI2 from isolated bovine retinal vessels, indicating that the increase in EDRF may nullify direct Ang II-induced vasoconstriction. Interestingly, intraluminal administration of Ang II caused only vasodilation. CONCLUSIONS: This study demonstrates that the retinal vascular endothelium acts as a buffer against the vasoconstricting agent Ang II via release of vasodilators NO and PGI2, and the vasoconstriction effects due to Ang II are most prominent in the smallest diameter vessels.  (+info)

Inhibition of NO synthesis or endothelium removal reveals a vasoconstrictor effect of insulin on isolated arterioles. (7/1201)

In this study we tested the hypothesis that insulin may differentially affect isolated arterioles from red (RGM) and white gastrocnemius muscles (WGM) because of their differences in function and metabolic profile. We also determined whether the responses of these arterioles are endothelium dependent and mediated by either prostaglandins or nitric oxide (NO). Arterioles were isolated, pressurized to 85 mmHg, equilibrated in Krebs bicarbonate-buffered solution (pH 7.4) gassed with 10% O2 (5% CO2-85% N2), and studied in a no-flow state. Control diameters for first-order arterioles from RGM averaged 77 +/- 8 micrometers and from WGM averaged 77 +/- 5 micrometers. Cumulative dose-response curves to insulin (10 microU/ml, 100 microU/ml, 1 mU/ml, and 10 mU/ml) were obtained in arterioles before and after endothelium removal or administration of either indomethacin (Indo, 10(-5) M) or NG-nitro-L-arginine (L-NNA, 10(-4) M). Insulin evoked concentration-dependent increases in control diameter of intact RGM and WGM arterioles of 6-26% and 9-28%, respectively. Indo was without any effect on insulin-induced dilation in RGM and WGM arterioles. Insulin-evoked dilation in both RGM and WGM arterioles was completely inhibited and converted to vasoconstriction by endothelium removal and administration of L-NNA. These results indicate that in endothelium-intact arterioles from RGM and WGM, insulin evokes an endothelium-dependent dilation that is equivalent and mediated by NO. In contrast, in the absence of a functional endothelium, insulin evokes arteriolar constriction. The finding that insulin can constrict arterioles, at physiological concentrations, suggests that insulin may play a more significant role in the regulation of vascular tone and total peripheral resistance than previously appreciated.  (+info)

Genetic control of renal thiazide receptor response to dietary NaCl and hypertension. (8/1201)

Excess NaCl increases blood pressure in some strains of animals but not others. An 8% NaCl diet did not change renal thiazide receptor (TZR) density in two salt-resistant normotensive rat strains (Wistar-Kyoto and Sprague-Dawley) [Fanestil, D. D., D. A. Vaughn, and P. Blakely. Am. J. Physiol. 273 (Regulatory Integrative Comp. Physiol. 42): R1241-R1245, 1997]. However, the renal response to salt differs in normal and hypertensive kidneys [Rettig, R., N. Bandelow, O. Patschan, B. Kuttler, B. Frey, and A. Uber. J. Hum. Hypertens. 10: 641-644, 1996]. Therefore, we examined two strains with salt-aggravated hypertension. Renal TZR did not change when Dahl-S (salt sensitive) animals became hypertensive with 8% dietary NaCl. In contrast, renal TZR decreased 34%, whereas blood pressure increased further, in SHR with 8% dietary NaCl. Blood pressure increased after NG-nitro-L-arginine in SHR, but renal TZR did not change, indicating the salt-induced decrease in TZR in SHR cannot be attributed nonspecifically to elevated arterial pressure. We conclude that the renal response to NaCl-induced increases in blood pressure can be genetically modulated independently of the genes that mediate either the primary hypertension or the salt sensitivity of the hypertension. This finding may be of use in future studies directed at identifying genotypes associated with salt-dependent hypertension.  (+info)

Nitro-L-arginine or Nitroarginine is not a medical term per se, but it is a chemical compound that is sometimes used in medical research and experiments. It is a salt of nitric acid and L-arginine, an amino acid that is important for the functioning of the body.

Nitroarginine is known to inhibit the production of nitric oxide, a molecule that plays a role in various physiological processes such as blood flow regulation, immune response, and neurotransmission. As a result, nitroarginine has been used in research to study the effects of reduced nitric oxide levels on different systems in the body.

It's worth noting that nitroarginine is not approved for use as a medication in humans, and its use is generally limited to laboratory settings.

Nitric Oxide Synthase (NOS) is a group of enzymes that catalyze the production of nitric oxide (NO) from L-arginine. There are three distinct isoforms of NOS, each with different expression patterns and functions:

1. Neuronal Nitric Oxide Synthase (nNOS or NOS1): This isoform is primarily expressed in the nervous system and plays a role in neurotransmission, synaptic plasticity, and learning and memory processes.
2. Inducible Nitric Oxide Synthase (iNOS or NOS2): This isoform is induced by various stimuli such as cytokines, lipopolysaccharides, and hypoxia in a variety of cells including immune cells, endothelial cells, and smooth muscle cells. iNOS produces large amounts of NO, which functions as a potent effector molecule in the immune response, particularly in the defense against microbial pathogens.
3. Endothelial Nitric Oxide Synthase (eNOS or NOS3): This isoform is constitutively expressed in endothelial cells and produces low levels of NO that play a crucial role in maintaining vascular homeostasis by regulating vasodilation, inhibiting platelet aggregation, and preventing smooth muscle cell proliferation.

Overall, NOS plays an essential role in various physiological processes, including neurotransmission, immune response, cardiovascular function, and respiratory regulation. Dysregulation of NOS activity has been implicated in several pathological conditions such as hypertension, atherosclerosis, neurodegenerative diseases, and inflammatory disorders.

Nitric oxide (NO) is a molecule made up of one nitrogen atom and one oxygen atom. In the body, it is a crucial signaling molecule involved in various physiological processes such as vasodilation, immune response, neurotransmission, and inhibition of platelet aggregation. It is produced naturally by the enzyme nitric oxide synthase (NOS) from the amino acid L-arginine. Inhaled nitric oxide is used medically to treat pulmonary hypertension in newborns and adults, as it helps to relax and widen blood vessels, improving oxygenation and blood flow.

NG-Nitroarginine Methyl Ester (L-NAME) is not a medication, but rather a research chemical used in scientific studies. It is an inhibitor of nitric oxide synthase, an enzyme that synthesizes nitric oxide, a molecule involved in the relaxation of blood vessels.

Therefore, L-NAME is often used in experiments to investigate the role of nitric oxide in various physiological and pathophysiological processes. It is important to note that the use of L-NAME in humans is not approved for therapeutic purposes due to its potential side effects, which can include hypertension, decreased renal function, and decreased cerebral blood flow.

Arginine is an α-amino acid that is classified as a semi-essential or conditionally essential amino acid, depending on the developmental stage and health status of the individual. The adult human body can normally synthesize sufficient amounts of arginine to meet its needs, but there are certain circumstances, such as periods of rapid growth or injury, where the dietary intake of arginine may become necessary.

The chemical formula for arginine is C6H14N4O2. It has a molecular weight of 174.20 g/mol and a pKa value of 12.48. Arginine is a basic amino acid, which means that it contains a side chain with a positive charge at physiological pH levels. The side chain of arginine is composed of a guanidino group, which is a functional group consisting of a nitrogen atom bonded to three methyl groups.

In the body, arginine plays several important roles. It is a precursor for the synthesis of nitric oxide, a molecule that helps regulate blood flow and immune function. Arginine is also involved in the detoxification of ammonia, a waste product produced by the breakdown of proteins. Additionally, arginine can be converted into other amino acids, such as ornithine and citrulline, which are involved in various metabolic processes.

Foods that are good sources of arginine include meat, poultry, fish, dairy products, nuts, seeds, and legumes. Arginine supplements are available and may be used for a variety of purposes, such as improving exercise performance, enhancing wound healing, and boosting immune function. However, it is important to consult with a healthcare provider before taking arginine supplements, as they can interact with certain medications and have potential side effects.

Enzyme inhibitors are substances that bind to an enzyme and decrease its activity, preventing it from catalyzing a chemical reaction in the body. They can work by several mechanisms, including blocking the active site where the substrate binds, or binding to another site on the enzyme to change its shape and prevent substrate binding. Enzyme inhibitors are often used as drugs to treat various medical conditions, such as high blood pressure, abnormal heart rhythms, and bacterial infections. They can also be found naturally in some foods and plants, and can be used in research to understand enzyme function and regulation.

Acetylcholine is a neurotransmitter, a type of chemical messenger that transmits signals across a chemical synapse from one neuron (nerve cell) to another "target" neuron, muscle cell, or gland cell. It is involved in both peripheral and central nervous system functions.

In the peripheral nervous system, acetylcholine acts as a neurotransmitter at the neuromuscular junction, where it transmits signals from motor neurons to activate muscles. Acetylcholine also acts as a neurotransmitter in the autonomic nervous system, where it is involved in both the sympathetic and parasympathetic systems.

In the central nervous system, acetylcholine plays a role in learning, memory, attention, and arousal. Disruptions in cholinergic neurotransmission have been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, and myasthenia gravis.

Acetylcholine is synthesized from choline and acetyl-CoA by the enzyme choline acetyltransferase and is stored in vesicles at the presynaptic terminal of the neuron. When a nerve impulse arrives, the vesicles fuse with the presynaptic membrane, releasing acetylcholine into the synapse. The acetylcholine then binds to receptors on the postsynaptic membrane, triggering a response in the target cell. Acetylcholine is subsequently degraded by the enzyme acetylcholinesterase, which terminates its action and allows for signal transduction to be repeated.

Vasodilation is the widening or increase in diameter of blood vessels, particularly the involuntary relaxation of the smooth muscle in the tunica media (middle layer) of the arteriole walls. This results in an increase in blood flow and a decrease in vascular resistance. Vasodilation can occur due to various physiological and pathophysiological stimuli, such as local metabolic demands, neural signals, or pharmacological agents. It plays a crucial role in regulating blood pressure, tissue perfusion, and thermoregulation.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Chemical warfare agents are defined as chemical substances that are intended or have the capability to cause death, injury, temporary incapacitation, or sensory irritation through their toxic properties when deployed in a military theater. These agents can be in gaseous, liquid, or solid form and are typically categorized based on their physiological effects. Common categories include nerve agents (e.g., sarin, VX), blister agents (e.g., mustard gas), choking agents (e.g., phosgene), blood agents (e.g., cyanide), and incapacitating agents (e.g., BZ). The use of chemical warfare agents is prohibited by international law under the Chemical Weapons Convention.

Chemical warfare is the use of chemicals in military conflict to incapacitate, injure, or kill enemy personnel or destroy equipment and resources. It involves the employment of toxic gases, liquids, or solids that have harmful effects on humans, animals, or plants. Chemical weapons can cause a wide range of symptoms, from temporary discomfort to permanent disability or death, depending on the type and amount of chemical used, as well as the duration and route of exposure.

Chemical warfare agents are classified into several categories based on their primary effects:

1. Nerve agents: These chemicals inhibit the enzyme acetylcholinesterase, which is essential for the proper functioning of the nervous system. Examples include sarin, tabun, soman, and VX. Exposure to nerve agents can cause symptoms such as muscle twitching, convulsions, respiratory failure, and death.
2. Blister agents: Also known as vesicants, these chemicals cause severe blistering and burns to the skin, eyes, and mucous membranes. Mustard gas is a well-known example of a blister agent. Exposure can lead to temporary or permanent blindness, respiratory problems, and scarring.
3. Choking agents: These chemicals cause damage to the lungs and respiratory system by irritating and inflaming the airways. Phosgene and chlorine are examples of choking agents. Symptoms of exposure include coughing, wheezing, shortness of breath, and potentially fatal lung edema.
4. Blood agents: These chemicals interfere with the body's ability to transport oxygen in the blood, leading to asphyxiation. Cyanide is a common example of a blood agent. Exposure can cause rapid heart rate, dizziness, headache, seizures, and death due to lack of oxygen.
5. Incapacitating agents: These chemicals are designed to temporarily disable or disorient enemy personnel without causing serious harm or death. Examples include riot control agents such as tear gas (CS) and pepper spray (OC). Exposure can cause symptoms such as coughing, sneezing, tears, and temporary blindness.

The use of chemical weapons in warfare is prohibited by several international treaties, including the Geneva Protocol and the Chemical Weapons Convention. Despite these bans, there have been numerous instances of their use throughout history, most notably during World War I and more recently in Syria's ongoing civil war.

Mustard gas, also known as sulfur mustard or HS, is a chemical warfare agent that has been used in military conflicts. It is a viscous, oily liquid at room temperature with a garlic-like odor. Its chemical formula is (ClCH2CH2)2S.

Mustard gas can cause severe burns and blistering of the skin, eyes, and respiratory tract upon contact or inhalation. It can also damage the immune system and lead to serious, potentially fatal, systemic effects. The onset of symptoms may be delayed for several hours after exposure, making it difficult to recognize and treat the injury promptly.

Mustard gas is classified as a vesicant, which means it causes blistering or tissue damage upon contact with the skin or mucous membranes. It can also have long-term effects, including an increased risk of cancer and other health problems. The use of mustard gas in warfare is banned by international law under the Chemical Weapons Convention.

Sarin is a potent and deadly nerve agent, a type of organic compound called a phosphoro-organic fluid. It is a colorless, odorless, and tasteless liquid, which is also known as GB. Sarin is a human-made chemical warfare agent that is considered a weapon of mass destruction and is banned under the Chemical Weapons Convention of 1993.

Sarin works by inhibiting the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the body. This leads to an overaccumulation of acetylcholine at the neuromuscular junctions and synapses, causing uncontrolled muscle contractions, paralysis, respiratory failure, and ultimately death if not treated promptly.

Exposure to Sarin can occur through inhalation, skin contact, or ingestion. Symptoms of exposure include runny nose, tightness in the chest, difficulty breathing, nausea, vomiting, diarrhea, blurred vision, and confusion. Immediate medical attention is required for anyone exposed to Sarin, as antidotes such as atropine and pralidoxime can be administered to counteract its effects.

Biological warfare, also known as germ warfare, is the use of biological agents or toxins with the intent to cause disease or death in humans, animals, or plants. These agents can be spread through the air, water, or food and can include bacteria, viruses, fungi, or toxic substances produced by living organisms. The purpose of using these agents is typically to cause widespread illness, fear, and disruption. Biological warfare is considered a weapon of mass destruction and is illegal under international law.

Soman is a chemical compound with the formula (CH3)2(C=O)N(CH2)4SH. It is a potent nerve agent, a type of organic compound that can cause death by interfering with the nervous system's ability to regulate muscle movement. Soman is an odorless, colorless liquid that evaporates slowly at room temperature and is therefore classified as a "v-type" or "volatile" nerve agent. It is considered to be one of the most toxic substances known. Exposure to soman can occur through inhalation, skin contact, or ingestion, and it can cause a range of symptoms including nausea, seizures, respiratory failure, and death.

A Mass Casualty Incident (MCI) is a situation in which the number of injured or deceased individuals exceeds the local resources available to respond and manage the incident. It typically involves multiple victims, often resulting from natural disasters, transportation accidents, terrorist attacks, or industrial incidents. The severity and scale of injuries require additional resources, coordination, and response from regional, national, or international emergency management and healthcare systems.

... , or Nω-nitro-l-arginine, also known as L-NOARG, is a nitro derivative of the amino acid arginine. It is an ... Moore, P. K.; Al‐Swayeh, O. A.; Chong, N. W. S.; Evans, R. A.; Gibson, A. (1990). "l-NG-nitro arginine (l-NOARG), a novel, l- ... Nitroarginine has been used in research studying coronary constriction, and it was found that, in the presence of midazolam ... vasodilatation was unaffected by nitroarginine. Due to the presence of all three isoforms of nitric oxide synthase in striatal ...
... prevented from developing angiotensin II-induced and N-Nitroarginine methyl ester-induced hypertension along with associated ...
... ng-nitroarginine methyl ester MeSH D12.125.068.050.587 - nitroarginine MeSH D12.125.068.050.650 - omega-n-methylarginine MeSH ... ng-nitroarginine methyl ester MeSH D12.125.095.104.587 - nitroarginine MeSH D12.125.095.104.650 - omega-n-methylarginine MeSH ...
Nitroarginine, or Nω-nitro-l-arginine, also known as L-NOARG, is a nitro derivative of the amino acid arginine. It is an ... Moore, P. K.; Al‐Swayeh, O. A.; Chong, N. W. S.; Evans, R. A.; Gibson, A. (1990). "l-NG-nitro arginine (l-NOARG), a novel, l- ... Nitroarginine has been used in research studying coronary constriction, and it was found that, in the presence of midazolam ... vasodilatation was unaffected by nitroarginine. Due to the presence of all three isoforms of nitric oxide synthase in striatal ...
Amino Acids, Diamino - NG-Nitroarginine Methyl Ester PubMed MeSh Term *Overview. Overview. subject area of * Aging compounds ...
NG-Nitroarginine Methyl Ester / pharmacology * Perfusion / methods* * Permeability * Rabbits * Serotonin / pharmacology* * Time ...
The structure of Bovine Enos N368D Single Mutant with L-N(Omega)-Nitroarginine-(4R)- Amino-L-Proline Amide Bound also contains ... Nitroarginine-(4R)- Amino-L-Proline Amide Bound within 5.0Å range: probe atom residue distance (Å) B Occ ... Nitroarginine-(4R)- Amino-L-Proline Amide Bound within 5.0Å range: probe atom residue distance (Å) B Occ ... Iron in PDB 1zzs: Bovine Enos N368D Single Mutant with L-N(Omega)-Nitroarginine-(4R)- Amino-L-Proline Amide Bound. Enzymatic ...
NG-Nitroarginine Methyl Ester / pharmacology * Nitric Oxide / biosynthesis* * Nitric Oxide / metabolism * Optic Nerve / drug ...
5. l-Nitroarginine methyl ester (10−4 mol/l, n = 6) completely inhibited the effect of mixed amino acids on [14C]inulin ... l-Nitroarginine methyl ester also inhibited the increase in fractional sodium reabsorption produced by the mixed amino acids. ... and l-nitroarginine methyl ester (an inhibitor of nitric oxide synthesis). ...
... nitroarginine methyl ester). ...
... such as L-NG-nitro-arginine methyl ester (L-NAME). ...
IL-8 increase was not inhibited by polymyxin B or l-nitroarginine methyl ester, indicating lack of involvement of ...
Male wild-type and αCGRP knockout mice received L-nitro-arginine methyl ester (150 mg/kg in drinking water) to induce a ... Male wild-type and αCGRP knockout mice received L-nitro-arginine methyl ester (150 mg/kg in drinking water) to induce a ... Male wild-type and αCGRP knockout mice received L-nitro-arginine methyl ester (150 mg/kg in drinking water) to induce a ... Male wild-type and αCGRP knockout mice received L-nitro-arginine methyl ester (150 mg/kg in drinking water) to induce a ...
hypoxia, nitric oxide synthase inhibitors, ng-nitroarginine methyl ester, nitroarginine, 3-nitrotyrosine ... M L-nitroarginine methyl ester (L-NAME), and 10-54 [micro sign]M L-nitroarginine (L-NOarg). For 7-NI, no protection against ... M L-nitroarginine methyl ester (L-NAME) pretreatment (solid circles), 27 [micro sign]M L-nitroarginine (L-NOarg) pretreatment ( ... M L-nitroarginine methyl ester (L-NAME) pretreatment (solid circles), 27 [micro sign]M L-nitroarginine (L-NOarg) pretreatment ( ...
... coronary arteries with normal endothelium was characterised before and after inhibition of NO synthesis with L-nitroarginine ...
To determine the role of NO in the second window of preconditioning we administered the NO-synthase inhibitor L-omega-nitro-arginine ...
N(G)-Nitroarginine Methyl Ester N(omega)-Nitro-L-arginine Methyl Ester NG-Nitro-L-Arginine Methyl Ester NG-Nitroarginine Methyl ... use NG-NITROARGININE METHYL ESTER (NM) to search N(G)-NITROARGININE METHYL ESTER 1990-96. History Note. 97; was N(G)- ... NG-Nitroarginine Methyl Ester, D-Orn-Isomer Preferred Term Term UI T359385. Date09/13/1999. LexicalTag NON. ThesaurusID NLM ( ... NG-Nitroarginine Methyl Ester, L-Orn-Isomer, Monohydrochloride Preferred Term Term UI T359386. Date09/13/1999. LexicalTag NON. ...
NG-Nitroarginine Methyl Ester 22% * Mitochondrial Membrane Potential 20% * Brain Injuries 19% ...
... under control conditions and in the presence of L-nitroarginine methyl ester (L-NAME 1 mM), D-NAME (1 mM), or superoxide ...
l-nitroarginine methyl ester (l-NAME), PGH2, 1S[1α, 2B(5Z),3b,4α]-7-[3-[2(phenylamino) carbonyl] hydrazino methyl [-7- ... l-nitroarginine methyl ester, or sepiapterin not only reversed the effects of high glucose on both angiotensin II-induced ...
NG-Nitroarginine Methyl Ester. A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce ... WalkerNG-Nitroarginine Methyl EsterMuscle, SkeletalTissue AdhesionsEthylene GlycolNitric Oxide SynthaseAvoidance Learning ... Nitric OxideAndrosteroneCorticosteroneCatalaseInsulinSuperoxide DismutaseAspartate AminotransferasesNG-Nitroarginine Methyl ...
NG-Nitroarginine Methyl Ester * NITROPRUSSIDE * Phenylephrine * Random Allocation * Soft Tissue Injuries * Vasoconstrictor ...
Dive into the research topics of Sex differences in vascular endothelial cell function reveal a gender specific role for nitroxyl. Together they form a unique fingerprint. ...
Dive into the research topics of Nitric oxide production and its contribution to hepatocyte proliferation in normal juvenile rats. Together they form a unique fingerprint. ...
NG-Nitroarginine Methyl Ester 27% * Proteins 26% * High-Temperature Requirement A Serine Peptidase 2 22% ...
Dive into the research topics of ROS and endothelial nitric oxide synthase (eNOS)-dependent trafficking of angiotensin II type 2 receptor begets neuronal NOS in cardiac myocytes. Together they form a unique fingerprint. ...
Bai, Y., Osinubi, M. O. V., Osikowicz, L., McKee, C., Vora, N. M., Rizzo, M. R., Recuenco, S., Davis, L., Niezgoda, M., Ehimiyein, A. M., Kia, G. S. N., Oyemakinde, A., Adeniyi, O. S., Gbadegesin, Y. H., Saliman, O. A., Ogunniyi, A., Ogunkoya, A. B., Kosoy, M. Y., Kuzmin, I. V., Blau, D., y 15 otrosEllison, J., Greenberg, L., Person, M., Wallace, R., Satheshkumar, P. S., Aman-Oloniyo, A., Adedire, E. B., Soleye, M. O., Okara, G. C., Yennan, S., Abdurrahman, M., Sani, M. A., Audu, S. W., Lawal, M. & Mshelbwala, P. P., 1 dic. 2018, En: Emerging Infectious Diseases. p. 2317-2323 7 p.. Producción científica: Contribución a una revista › Artículo › revisión exhaustiva ...
NG-Nitroarginine Methyl Ester / pharmacology; Nitric Oxide Synthase / antagonists & inhibitors; Prospective Studies; Swine; ...
Dive into the research topics of Cerebral blood flow in primates is increased by isoflurane over time and is decreased by nitric oxide synthase inhibition. Together they form a unique fingerprint. ...
L-NG-Nitro arginine methyl ester (L-NAME); Low density lipoprotein (LDL); Mammalian target of rapamycin (mTOR); Mas-related G ...
  • 1. The response of the isolated rat kidney to a mixed amino acid solution was examined in the presence of three renal autacoid inhibitors, indomethacin (a cyclo-oxygenase inhibitor), sulpiride (a dopamine antagonist) and l -nitroarginine methyl ester (an inhibitor of nitric oxide synthesis). (portlandpress.com)
  • 5. l -Nitroarginine methyl ester (10 −4 mol/l, n = 6) completely inhibited the effect of mixed amino acids on [ 14 C]inulin clearance, but did not inhibit the increase in renal perfusate flow, even though the basal vascular resistance was markedly enhanced. (portlandpress.com)
  • l -Nitroarginine methyl ester also inhibited the increase in fractional sodium reabsorption produced by the mixed amino acids. (portlandpress.com)
  • IL-8 increase was not inhibited by polymyxin B or l-nitroarginine methyl ester, indicating lack of involvement of lipopolysaccharide and nitric oxide in the induction. (cdc.gov)
  • Slices were not treated or were pretreated with 27 microM L-nitroarginine methyl ester (L-NAME), 27 microM 7-nitroindozole (7-NI), or 27 microM L-nitroarginine. (asahq.org)
  • Objective: The effect of the nitric oxide donor, SIN-1, in proximal and distal coronary arteries with normal endothelium was characterised before and after inhibition of NO synthesis with L-nitroarginine methyl ester (L-NAME). (eurekamag.com)
  • Concurrent administration of polyethylene-glycolated superoxide dismutase (SOD), l -nitroarginine methyl ester, or sepiapterin not only reversed the effects of high glucose on both angiotensin II-induced relaxation and PGI 2 release but also abolished high-glucose-enhanced PGIS nitration, as well as its association with eNOS. (diabetesjournals.org)
  • We then demonstrate that endothelium-derived bioactive NO primarily mediates its effects through TG2, using TG2 -/- mice chronically treated with the NOS inhibitor l-N G -nitroarginine methyl ester (L-NAME). (johnshopkins.edu)
  • Khedara A, Kawai Y Kayashita J Kato N. Feeding rats the nitric oxide synthase inhibitor, L-N(omega) nitroarginine, elevates serum triglycerides and cholesterol and lowers hepatic fatty acid oxidation. (argi9.net)
  • A small percentage of these deaths occurredRelaxation was inhibited by the NO-synthase inhibitor in both the human and rabbit tissues, and in the rabbit strips by the guanylate cyclase inhibitor methylene blue, L-n-nitroarginine confirming that the NO/cGMP pathway is involved in the relaxation. (fotballdeaf.no)
  • We find that ODQ and the nitric oxide synthase inhibitor, nitroarginine, reduce hippocampal long-term potentiation in an equal and mutually exclusive manner, suggesting that the actions of nitric oxide in this phenomenon are entirely mediated through cyclic GMP. (shengsci.com)
  • sildenafil 50mg Relaxation was inhibited by the NO-synthase inhibitor in both the human and rabbit tissues, and in the rabbit strips by the guanylate cyclase inhibitor methylene blue, L-n-nitroarginine confirming that the NO/cGMP pathway is involved in the relaxation. (btownerrant.com)
  • Nitroarginine, or Nω-nitro-l-arginine, also known as L-NOARG, is a nitro derivative of the amino acid arginine. (wikipedia.org)
  • Nitroarginine has been used in research studying coronary constriction, and it was found that, in the presence of midazolam vasodilatation was unaffected by nitroarginine. (wikipedia.org)
  • or = 3, 65 +/- 6, and 25 +/- 4% of control in slices that were untreated or treated with L-nitroarginine, L-NAME, and 7-NI, respectively. (asahq.org)
  • After 120 min of hyperoxic recovery, adenosine triphosphate levels returned to control values in slices pretreated with L-NAME and 7-NI, but to only 30% of control in untreated or L-nitroarginine-treated slices. (asahq.org)
  • Therefore, a single-residue difference is responsible for more than two orders of magnitude selectivity in inhibition of nNOS over eNOS by L-N(omega)-nitroarginine-containing dipeptide inhibitors. (rcsb.org)
  • Pharmacokinetics and steady-state tissue distribution of L- and D-isomers of nitroarginine in rats. (aspetjournals.org)