Pulmonary Alveoli
Lung
Orthopedics
Orthopedic Procedures
Shock, Septic
Risk Factors
Pulmonary capillary perfusion: intra-alveolar fractal patterns and interalveolar independence. (1/4148)
Pulmonary capillary perfusion was analyzed from videomicroscopic recordings to determine flow switching characteristics among capillary segments in isolated, blood-perfused canine lungs. Within each alveolus, the rapid switching pattern was repetitive and was, therefore, nonrandom (fractal dimensions near 1.0). This self-similarity over time was unexpected in a network widely considered to be passive. Among adjacent alveoli, the relationship among the switching patterns was even more surprising, for there was virtually no relationship between the perfusion patterns (coefficients of determination approaching zero). These findings demonstrated that the perfusion patterns in individual alveolar walls were independent of their next-door neighbors. The lack of dependence among neighboring networks suggests an interesting characteristic: the failure of one alveolar-capillary bed would leave its neighbors relatively unaffected, a feature of a robust design. (+info)Acinar flow irreversibility caused by perturbations in reversible alveolar wall motion. (2/4148)
Mixing associated with "stretch-and-fold" convective flow patterns has recently been demonstrated to play a potentially important role in aerosol transport and deposition deep in the lung (J. P. Butler and A. Tsuda. J. Appl. Physiol. 83: 800-809, 1997), but the origin of this potent mechanism is not well characterized. In this study we hypothesized that even a small degree of asynchrony in otherwise reversible alveolar wall motion is sufficient to cause flow irreversibility and stretch-and-fold convective mixing. We tested this hypothesis using a large-scale acinar model consisting of a T-shaped junction of three short, straight, square ducts. The model was filled with silicone oil, and alveolar wall motion was simulated by pistons in two of the ducts. The pistons were driven to generate a low-Reynolds-number cyclic flow with a small amount of asynchrony in boundary motion adjusted to match the degree of geometric (as distinguished from pressure-volume) hysteresis found in rabbit lungs (H. Miki, J. P. Butler, R. A. Rogers, and J. Lehr. J. Appl. Physiol. 75: 1630-1636, 1993). Tracer dye was introduced into the system, and its motion was monitored. The results showed that even a slight asynchrony in boundary motion leads to flow irreversibility with complicated swirling tracer patterns. Importantly, the kinematic irreversibility resulted in stretching of the tracer with narrowing of the separation between adjacent tracer lines, and when the cycle-by-cycle narrowing of lateral distance reached the slowly growing diffusion distance of the tracer, mixing abruptly took place. This coupling of evolving convective flow patterns with diffusion is the essence of the stretch-and-fold mechanism. We conclude that even a small degree of boundary asynchrony can give rise to stretch-and-fold convective mixing, thereby leading to transport and deposition of fine and ultrafine aerosol particles deep in the lung. (+info)Regulation of an amiloride-sensitive Na+-permeable channel by a beta2-adrenergic agonist, cytosolic Ca2+ and Cl- in fetal rat alveolar epithelium. (3/4148)
1. In cell-attached patches formed on the apical membrane of fetal alveolar epithelium, terbutaline (a specific beta2-adrenergic agonist) increased the open probability (Po) of an amiloride-sensitive Na+-permeable non-selective cation (NSC) channel (control, 0.03 +/- 0.04; terbutaline, 0.62 +/- 0.18; n = 8, P < 0. 00001) by increasing the mean open time 100-fold without any significant change in the mean closed time and without any change in the single channel conductance (control, 27.8 +/- 2.3 pS; terbutaline, 28.2 +/- 2.1 pS; n = 8). 2. The Po of the unstimulated channel increased when the apical membrane was depolarized due to a decrease in the closing rate and an increase in the opening rate, while the Po of the terbutaline-stimulated channel did not depend on the membrane potential. 3. Increased cytosolic [Ca2+] also increased the Po of the channel in a manner consistent with one Ca2+-binding site on the cytosolic surface of the channel. Terbutaline increased the sensitivity of the channel to cytosolic Ca2+ by shifting the concentration of cytosolic Ca2+ ([Ca2+]c) required for half-maximal activation to a lower [Ca2+]c value, leading to an increase in Po. 4. An increase in the cytosolic Cl- concentration ([Cl-]c) decreased the Po of the channel consistent with two Cl--binding sites by increasing the closing rate without any significant change in the opening rate. Terbutaline increased Po by reducing the effect of cytosolic Cl- to promote channel closing. 5. Taken together, these observations indicate that terbutaline activates a Ca2+-activated, Cl--inhibitable, amiloride-sensitive, Na+-permeable NSC channel in fetal rat alveolar epithelium in two ways: first, through an increase in Ca2+ sensitivity, and second, through a reduction in the effect of cytosolic Cl- to promote channel closing. (+info)Opportunistic Pneumocystis carinii infection in red-bellied tamarins (Saguinus labiatus). (4/4148)
P. carinii infection in red-bellied tamarins (Saguinus labiatus), born and maintained in a laboratory breeding colony, was examined by histopathologic examination postmortem. P. carinii cysts were detected in 6 of 10 red-bellied tamarins examined, by using Grocott's, toluidine blue O and immunostaining with avidin-biotin complex using antisera for rat-, simian-, and human-P. carinii. The results obtained from the present studies imply that P. carinii may be an important pathogen in this species. (+info)Acute saline infusion reduces alveolar-capillary membrane conductance and increases airflow obstruction in patients with left ventricular dysfunction. (5/4148)
BACKGROUND: Impaired alveolar-capillary membrane conductance is the major cause for the reduction in pulmonary diffusing capacity for carbon monoxide (DLCO) in heart failure. Whether this reduction is fixed, reflecting pulmonary microvascular damage, or is variable is unknown. The aim of this study was to assess whether DLCO and its subdivisions, alveolar-capillary membrane conductance (DM) and pulmonary capillary blood volume (Vc), were sensitive to changes in intravascular volume. In addition, we examined the effects of volume loading on airflow rates. METHODS AND RESULTS: Ten patients with left ventricular dysfunction (LVD) and 8 healthy volunteers were studied. DM and Vc were determined by the Roughton and Forster method. The forced expiratory volume in 1 second (FEV1), vital capacity, and peak expiratory flow rates (PEFR) were also recorded. In patients with LVD, infusion of 10 mL. kg-1 body wt of 0.9% saline acutely reduced DM (12.0+/-3.3 versus 10.4+/-3.5 mmol. min-1. kPa-1, P<0.005), FEV1 (2.3+/-0.4 versus 2.1+/-0.4 L, P<0.0005), and PEFR (446+/-55 versus 414+/-56 L. min-1, P<0.005). All pulmonary function tests had returned to baseline values 24 hours later. In normal subjects, saline infusion had no measurable effect on lung function. CONCLUSIONS: Acute intravascular volume expansion impairs alveolar-capillary membrane function and increases airflow obstruction in patients with LVD but not in normal subjects. Thus, the abnormalities of pulmonary diffusion in heart failure, which were believed to be fixed, also have a variable component that could be amenable to therapeutic intervention. (+info)TNF-alpha increases ceramide without inducing apoptosis in alveolar type II epithelial cells. (6/4148)
Ceramide is a bioactive lipid mediator that has been observed to induce apoptosis in vitro. The purpose of this study was to determine whether endogenous ceramide, generated in response to in vivo administration of tumor necrosis factor-alpha (TNF-alpha), increases apoptosis in primary rat alveolar type II epithelial cells. Intratracheal instillation of TNF-alpha (5 microgram) produced a decrease in sphingomyelin and activation of a neutral sphingomyelinase. These changes were associated with a significant increase in lung ceramide content. TNF-alpha concomitantly activated the p42/44 extracellular signal-related kinases and induced nuclear factor-kappaB activation in the lung. Hypodiploid nuclei studies revealed that intratracheal TNF-alpha did not increase type II cell apoptosis compared with that in control cells after isolation. A novel observation from separate in vitro studies demonstrated that type II cells undergo a gradual increase in apoptosis after time in culture, a process that was accelerated by exposure of cells to ultraviolet light. However, culture of cells with a cell-permeable ceramide, TNF-alpha, or a related ligand, anti-CD95, did not increase apoptosis above the control level. The results suggest that ceramide resulting from TNF-alpha activation of sphingomyelin hydrolysis might activate the mitogen-activated protein kinase and nuclear factor-kappaB pathways without increasing programmed cell death in type II cells. (+info)Pattern of total and regional lung function in subjects with bronchoconstriction induced by 15-me PGF2 alpha. (7/4148)
Closing volume (single breath nitrogen test), regional ventilation and perfusion (using intravenous xenon-133), and total lung function (TLC, VC, and FEV) were measured before and after intramuscular administration of 250 mug 15-methyl prostaglandin F2alpha (15-me PGF2alpha) in 10 healthy women. The cardiac output was measured with the Minnesota impedance cardiograph model 304A and the transthoracic impedance was used as an expression of the thoracic fluid volume. The slope of the alveolar plateau on the closing volume tracing showed a 271% increase 20 minutes after the prostaglandin administration, at which time the closing volume per cent (CV%) had decreased (P less than 0-01) and the closing capacity (CC%) had increased (P less than 0-05). Vital capacity (VC) decreased (P less than 0-01), residual volume (RV) increased (P less than 0-01), and the total lung capacity (TLC) remained unchanged. The maximal decrease (9%) in FEV1 was seen after 20 minutes. All these measurements except the slope of the alveolar plateau returned to control levels after 60 minutes. The redistribution of regional ventilation was more pronounced than that of the regional pulmonary blood flow. No change was observed in cardiac output and transthoracic impedance. None of the patients experienced any dyspnoea. Our results are consistent with a more pronounced effect of prostaglandin F2alpha on the small airways (the alveolar plateau) than on the larger airways (FEV1). In cases where an increase in the slope of the alveolar plateau is observed, the closing volume per cent should not be used as a measurement of the lung disease. It is concluded that the single breath nitrogen test (N2 closing volume) is more sensitive than the conventional tests. (+info)Apoptosis is a pathway responsible for the resolution of endotoxin-induced alveolar type II cell hyperplasia in the rat. (8/4148)
Previous studies showed that intratracheal instillation of endotoxin induces transient type II cell hyperplasia in the rat lung and described some of the mechanisms involved in the proliferative response of type II cells. The purpose of the present study was to investigate how long the type II cell hyperplasia persists and how it is resolved. The portion of epithelial cells in hyperplastic lesions of the rat lung expressing cyclin D1, an indicator for cells in the G1 phase of the cell cycle, was greatest at 3 d post instillation and decreased after 4 and 6 d. The fate of the proliferating epithelial cells was traced by injecting the rats with 5-bromo-2' deoxy uridine (BrdU) 2 d post instillation, the peak time point for maximum incorporation of BrdU. Exfoliated BrdU-positive epithelial cells were detected in the alveolar spaces in tissue sections from rats 4, 5, and 6 d post instillation. BrdU-positive epithelial cells showed flattened nuclei at 6 and 10 d post instillation. Expression of the 116 kD poly(ADP-ribose) polymerase (PARP) was low in type II cells from control rats, and was increased at 3, 4, and 6 d post instillation. In cells obtained by lavage, only a 35 kD cleavage product of PARP was detected, which is an indicator of necrotic cell death. In isolated type II cells from rats 3, 4, and 6 d post endotoxin instillation, progressive cleavage of the PARP to its 89 kD residual fragment was detected, which is a direct evidence for the activation of caspases. Furthermore, apoptotic epithelial cells with condensed nuclei were identified by electron microscopy in rats 4 d post instillation. These results indicate that apoptosis is an additional mechanism for the resolution of endotoxin-induced lung epithelial hyperplasias. (+info)Pulmonary alveoli, also known as air sacs, are tiny clusters of air-filled pouches located at the end of the bronchioles in the lungs. They play a crucial role in the process of gas exchange during respiration. The thin walls of the alveoli, called alveolar membranes, allow oxygen from inhaled air to pass into the bloodstream and carbon dioxide from the bloodstream to pass into the alveoli to be exhaled out of the body. This vital function enables the lungs to supply oxygen-rich blood to the rest of the body and remove waste products like carbon dioxide.
A lung is a pair of spongy, elastic organs in the chest that work together to enable breathing. They are responsible for taking in oxygen and expelling carbon dioxide through the process of respiration. The left lung has two lobes, while the right lung has three lobes. The lungs are protected by the ribcage and are covered by a double-layered membrane called the pleura. The trachea divides into two bronchi, which further divide into smaller bronchioles, leading to millions of tiny air sacs called alveoli, where the exchange of gases occurs.
Multiple trauma, also known as polytrauma, is a medical term used to describe severe injuries to the body that are sustained in more than one place or region. It often involves damage to multiple organ systems and can be caused by various incidents such as traffic accidents, falls from significant heights, high-energy collisions, or violent acts.
The injuries sustained in multiple trauma may include fractures, head injuries, internal bleeding, chest and abdominal injuries, and soft tissue injuries. These injuries can lead to a complex medical situation requiring immediate and ongoing care from a multidisciplinary team of healthcare professionals, including emergency physicians, trauma surgeons, critical care specialists, nurses, rehabilitation therapists, and mental health providers.
Multiple trauma is a serious condition that can result in long-term disability or even death if not treated promptly and effectively.
Orthopedics is a branch of medicine that deals with the prevention, diagnosis, and treatment of disorders of the musculoskeletal system, which includes the bones, joints, muscles, ligaments, tendons, and nerves. The goal of orthopedic care is to help patients maintain or restore their mobility, function, and quality of life through a variety of treatments, including medication, physical therapy, bracing, and surgery. Orthopedic surgeons are medical doctors who have completed additional training in the diagnosis and treatment of musculoskeletal conditions, and they may specialize in specific areas such as sports medicine, spine care, joint replacement, or pediatric orthopedics.
Orthopedic procedures are surgical or nonsurgical methods used to treat musculoskeletal conditions, including injuries, deformities, or diseases of the bones, joints, muscles, ligaments, and tendons. These procedures can range from simple splinting or casting to complex surgeries such as joint replacements, spinal fusions, or osteotomies (cutting and repositioning bones). The primary goal of orthopedic procedures is to restore function, reduce pain, and improve the quality of life for patients.
Septic shock is a serious condition that occurs as a complication of an infection that has spread throughout the body. It's characterized by a severe drop in blood pressure and abnormalities in cellular metabolism, which can lead to organ failure and death if not promptly treated.
In septic shock, the immune system overreacts to an infection, releasing an overwhelming amount of inflammatory chemicals into the bloodstream. This leads to widespread inflammation, blood vessel dilation, and leaky blood vessels, which can cause fluid to leak out of the blood vessels and into surrounding tissues. As a result, the heart may not be able to pump enough blood to vital organs, leading to organ failure.
Septic shock is often caused by bacterial infections, but it can also be caused by fungal or viral infections. It's most commonly seen in people with weakened immune systems, such as those who have recently undergone surgery, have chronic medical conditions, or are taking medications that suppress the immune system.
Prompt diagnosis and treatment of septic shock is critical to prevent long-term complications and improve outcomes. Treatment typically involves aggressive antibiotic therapy, intravenous fluids, vasopressors to maintain blood pressure, and supportive care in an intensive care unit (ICU).
In medical terms, shock is a life-threatening condition that occurs when the body is not getting enough blood flow or when the circulatory system is not functioning properly to distribute oxygen and nutrients to the tissues and organs. This results in a state of hypoxia (lack of oxygen) and cellular dysfunction, which can lead to multiple organ failure and death if left untreated.
Shock can be caused by various factors such as severe blood loss, infection, trauma, heart failure, allergic reactions, and severe burns. The symptoms of shock include low blood pressure, rapid pulse, cool and clammy skin, rapid and shallow breathing, confusion, weakness, and a bluish color to the lips and nails. Immediate medical attention is required for proper diagnosis and treatment of shock.
Medical Definition:
"Risk factors" are any attribute, characteristic or exposure of an individual that increases the likelihood of developing a disease or injury. They can be divided into modifiable and non-modifiable risk factors. Modifiable risk factors are those that can be changed through lifestyle choices or medical treatment, while non-modifiable risk factors are inherent traits such as age, gender, or genetic predisposition. Examples of modifiable risk factors include smoking, alcohol consumption, physical inactivity, and unhealthy diet, while non-modifiable risk factors include age, sex, and family history. It is important to note that having a risk factor does not guarantee that a person will develop the disease, but rather indicates an increased susceptibility.
Health surveys are research studies that collect data from a sample population to describe the current health status, health behaviors, and healthcare utilization of a particular group or community. These surveys may include questions about various aspects of health such as physical health, mental health, chronic conditions, lifestyle habits, access to healthcare services, and demographic information. The data collected from health surveys can be used to monitor trends in health over time, identify disparities in health outcomes, develop and evaluate public health programs and policies, and inform resource allocation decisions. Examples of national health surveys include the National Health Interview Survey (NHIS) and the Behavioral Risk Factor Surveillance System (BRFSS).