A coronary vasodilator agent.

Cloricromene, a coumarine derivative, protects against collagen-induced arthritis in Lewis rats. (1/14)

1. The aim of the present study was to investigate the effects of cloricromene, a coumarine derivative, in rats subjected to collagen-induced arthritis. 2. Collagen-induced arthritis (CIA) was induced in Lewis rats by an intradermal injection of 100 microl of the emulsion (containing 100 microg of bovine type II collagen) (CII) and complete Freund's adjuvant (CFA) at the base of the tail. On day 21, a second injection of CII in CFA was administered. 3. Lewis rats developed an erosive hind paw arthritis when immunized with CII in CFA. Macroscopic clinical evidence of CIA first appeared as peri-articular erythema and oedema in the hind paws. The incidence of CIA was 100% by day 27 in the CII challenged rats and the severity of CIA progressed over a 35-day period with radiographic evaluation revealing focal resorption of bone together with osteophyte formation in the tibiotarsal joint and soft tissue swelling. 4. The histopathology of CIA included erosion of the cartilage at the joint margins. Treatment of rats with cloricromene (10 mg kg(-1) i.p. daily) starting at the onset of arthritis (day 23), delayed the development of the clinical signs at days 24 - 35 and improved histological status in the knee and paw. 5. Immunohistochemical analysis for iNOS, COX-2, nitrotyrosine and for poly (ADP-ribose) synthetase (PARS) revealed a positive staining in inflamed joints from collagen-treated rats. The degree of staining for iNOS, COX-2, nitrotyrosine and PARS were markedly reduced in tissue sections obtained from collagen-treated rats, which had received cloricromene. 6. Radiographic signs of protection against bone resorption and osteophyte formation were present in the joints of cloricromene-treated rat. 7. This study provides the first evidence that cloricromene, a coumarine derivative, attenuates the degree of chronic inflammation and tissue damage associated with collagen-induced arthritis in the rat.  (+info)

Effect of estrogen replacement therapy on distribution of myocardial blood flow in female anesthetized rabbits. (2/14)

Estrogen replacement therapy reduces risk of cardiovascular events by altering coronary vasoregulation and distribution of blood flow. Vessel reactivity and blood flow distribution were assessed in anesthetized female rabbits in the following groups: 1) sham, 2) ovariectomy, 3) ovariectomy + 17beta-estradiol, and 4) ovariectomy + dehydroepiandrosterone. After a 2-wk treatment, cardiac hemodynamics, vascular reserve, and blood flow were evaluated during the following infusions: 1) NaCl, or vehicle (0.5 ml/min), 2) acetylcholine (2 mg/kg), 3) isoproterenol (2 mg. kg(-1). min(-1)), and 4) chromonar (8 mg/kg). In hearts from ovariectomized rabbits, autoregulatory blood flow was preserved despite lower diastolic perfusion pressures (55 +/- 8 vs. 64 +/- 8 mmHg in sham) and rate-pressure product (14.4 +/- 0.8 vs. 19.3 +/- 0.8 beats/min. mmHg x 10(-3)). Estrogen replacement therapy restored coronary pressure and reserve, and all drugs increased vascular conductance. In conclusion, in hearts from ovariectomized rabbits, vascular reserve declined because coronary pressure was lower; however, blood flow was preserved at a higher level than expected for oxygen demand. Estrogen replacement therapy restores myocardial oxygen supply-demand indices and returns coronary pressure-flow data to levels observed in animals with intact ovaries.  (+info)

Effects of cloricromene, a coumarin derivative, on endotoxin-induced uveitis in Lewis rats. (3/14)

PURPOSE: To investigate the effects of cloricromene, a coumarin derivative, in rats subjected to endotoxin-induced uveitis (EIU). METHODS: Endotoxin uveitis was induced in male Lewis rats by a single footpad injection of 200 microg lipopolysaccharide (LPS). Cloricromene was topically applied to the rat eye twice at 1 hour before and 7 hours after injection of LPS. A separate group of animals was treated with vehicle. Rats were killed 16 hours after injection and the eyes enucleated for histologic examination and immunohistochemical analysis. The effect of treatment was also evaluated by slit lamp examination, by the number of intraocular inflammatory cells on histologic sections, and by measuring the protein and TNFalpha levels in the aqueous humor. Nitrite and nitrate production was also measured in the aqueous humor. RESULTS: The histopathology of the iris-ciliary body included inflammatory cell infiltration and nuclear modification of vessel endothelial cells. Cloricromene treatment reduced the inflammatory cell infiltration and improved histologic status of the ocular tissue. Immunohistochemical analysis for P-selectin, intracellular adhesion molecule (ICAM)-1, nitrotyrosine, and poly(ADP-ribose) synthetase (PARS) revealed a positive staining in inflammatory cell infiltration from LPS-treated rats. The degree of staining for P-selectin, ICAM-1, nitrotyrosine, and PARS was markedly reduced in tissue sections obtained from LPS-recipient rats that had received cloricromene. Cloricromene strongly inhibited cell infiltration, protein exudation, TNFalpha production, and nitrite-nitrate formation. CONCLUSIONS: This study provides the first evidence that cloricromene, a coumarin derivative, attenuates the degree of inflammation and tissue damage associated with EIU in rats.  (+info)

Preparation and characterization of eudragit retard nanosuspensions for the ocular delivery of cloricromene. (4/14)

The purpose of this study was to improve the stability of cloricromene (AD6) in ophthalmic formulations and its drug availability at the ocular level. To this end, AD6-loaded polymeric nanoparticle suspensions were made using inert polymer resins (Eudragit RS100 and RL100). We modified the quasi-emulsion solvent diffusion technique by varying some formulation parameters (the drug-to-polymer ratio, the total drug and polymer amount, and the stirring speed). The chemical stability of AD6 in the nanosuspensions was assessed by preparing some formulations using (unbuffered) isotonic saline or a pH 7 phosphate buffer solution as the dispersing medium. The formulations were stored at 4 degrees C, and the rate of degradation of AD6 was followed by high performance liquid chromatography (HPLC). The obtained nanosuspensions showed mean sizes and a positive surface charge (zeta-potential) that make them suitable for an ophthalmic application; these properties were maintained upon storage at 4 degrees C for several months. In vitro dissolution tests confirmed a modified release of the drug from the polymer matrixes. Nanosuspensions prepared with saline solution and no or lower amounts of surfactant (Tween 80) showed an enhanced stability of the ester drug for several months, with respect to an AD6 aqueous solution. Based on the technological results, AD6-loaded Eudragit Retard nanoparticle suspensions appear to offer promise as a means to improving the shelf life and bioavailability of this drug after ophthalmic application.  (+info)

Protective effects of a coumarin derivative in diabetic rats. (5/14)

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Synthesis and vasorelaxant and platelet antiaggregatory activities of a new series of 6-halo-3-phenylcoumarins. (6/14)

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Decreased coronary vascular reserve in Watanabe heritable hyperlipidemic rabbits. (7/14)

Watanabe heritable hyperlipidemic (WHHL) rabbits have severe hypercholesterolemia due to a genetic defect in their low density lipoprotein receptors. Therefore, they develop severe premature atherosclerosis of the large arteries including the coronary arteries. In the present study, we measured the coronary vascular reserve of these rabbits to evaluate the total cross-sectional coronary surface area. This method allowed us to quantify the functional consequences of the coronary atherosclerotic lesions. To evaluate coronary vascular reserve, we measured coronary blood flow with the radioactive microsphere technique before and after induction of maximal coronary vasodilation by an intravenous dose of 9 mg/kg of carbocromen. A group of pure-bred WHHL rabbits was compared to a group of normal Burgundy rabbits at ages of 100 and 300 days. At 100 days, there was no difference in coronary vascular reserve between the two groups. However, at 300 days, the coronary vascular reserve in WHHL rabbits was 48% smaller than in the normal Burgundy rabbits (p less than 0.001). In addition, by making corrosion casts and morphological studies, we were able to show that at 300 days nearly all the WHHL rabbits had severe coronary atherosclerotic lesions located mainly at the origin of the large coronary arteries. We conclude that WHHL rabbits at 300 days have a severe impairment of their coronary vascular reserve due to proximal atherosclerotic lesions in the coronary arteries.  (+info)

Thyroxine-induced hypertrophy of the rabbit heart. Effect on regional oxygen extraction, flow, and oxygen consumption. (8/14)

The effects of the administration of 0.5 or 1 mg/kg of 1-thyroxine for 3 or 16 days were studied in 55 New Zealand white rabbits. Heart size was 29% above control after 16 days of 1-thyroxine, despite lower body weights. In an anesthetized open-chest animal, regional microspectro-photometric observations of small arteries and veins to determine oxygen extraction were combined with regional blood flow measurements using radioactive microspheres to determine regional oxygen consumption by the Fick principle. Vascular flow reserves were studied through measurement of blood flow after the administration of chromonar HCl, 10 mg/kg. Myocardial oxygen consumption was, respectively, 2.4 and 3.8 times control after 3 and 16 days of 1-thyroxine. This was accompanied by significant increases in both coronary blood flow and oxygen extraction. In control, oxygen extraction and consumption were higher in the subendocardial region compared to the subepicardial area. No significant regional differences were found in flow, oxygen extraction, or consumption after 1-thyroxine administration. Chromonar increased coronary blood flow 2.8 times in the control animals, but did not significantly increase flow or decrease vascular resistance in the rabbits given 1-thyroxine. Adenosine increased coronary blood flow 3.5 times in the control animals but only 2.2 times in animals given 1-thyroxine for 3 days. Animals given 1-thyroxine had hypertrophied hearts with increased oxygen consumption, markedly increased flow, and increased oxygen extraction but without regional left ventricular differences.  (+info)

I'm sorry for any confusion, but "Chromonar" does not appear to be a recognized medical term or substance. It is possible that you may have misspelled the word or it could be a term specific to a particular context within the medical field. If you have more information about where this term came from or its intended meaning, I'd be happy to help you try and clarify it further. However, without additional context, it is difficult for me to provide an accurate definition or explanation related to "Chromonar."

... chromonar MeSH D03.438.150.446.350 - coumestrol MeSH D03.438.150.446.400 - esculin MeSH D03.438.150.446.520 - 4- ... chromonar MeSH D03.830.219.446.350 - coumestrol MeSH D03.830.219.446.400 - esculin MeSH D03.830.219.446.520 - 4- ...
... chromonar MeSH D03.438.150.446.350 - coumestrol MeSH D03.438.150.446.400 - esculin MeSH D03.438.150.446.520 - 4- ... chromonar MeSH D03.830.219.446.350 - coumestrol MeSH D03.830.219.446.400 - esculin MeSH D03.830.219.446.520 - 4- ...
Chromonar D3.830.219.446.280 D3.383.663.283.446.280 Chromones D3.830.219.266 D3.383.663.283.266 Chromosome Pairing G4.299. ...
Chromonar D3.830.219.446.280 D3.383.663.283.446.280 Chromones D3.830.219.266 D3.383.663.283.266 Chromosome Pairing G4.299. ...
Chromonar D3.830.219.446.280 D3.383.663.283.446.280 Chromones D3.830.219.266 D3.383.663.283.266 Chromosome Pairing G4.299. ...
Chromonar D3.830.219.446.280 D3.383.663.283.446.280 Chromones D3.830.219.266 D3.383.663.283.266 Chromosome Pairing G4.299. ...
Chromonar D3.438.150.446.280 D3.633.100.150.446.280 Chromones D3.438.150.266 D3.633.100.150.266 Chromosomal Position Effects ...
Chromonar D3.438.150.446.280 D3.633.100.150.446.280 Chromones D3.438.150.266 D3.633.100.150.266 Chromosomal Position Effects ...
Chromonar. Nysted Reagent. Oxymethurea. Cadmium Telluride. Eleutherobin. Isethionic Acid. Mercurous Acetate. Amiprilose. HCS. ...
Chromonar D3.438.150.446.280 D3.633.100.150.446.280 Chromones D3.438.150.266 D3.633.100.150.266 Chromosomal Position Effects ...
Chromonar Hydrochloride Narrower Concept UI. M0330662. Registry Number. 52C937V399. Terms. Chromonar Hydrochloride Preferred ... Chromonar Preferred Concept UI. M0004398. Registry Number. R0C9NIE5JJ. Related Numbers. 52C937V399. 655-35-6. 804-10-4. Scope ... Chromonar Preferred Term Term UI T008327. Date01/01/1999. LexicalTag NON. ThesaurusID ... Chromonar Hydrochloride Intensain Intercordin Pharm Action. Vasodilator Agents. Registry Number. R0C9NIE5JJ. Related Numbers. ...
Chromonar Hydrochloride Narrower Concept UI. M0330662. Registry Number. 52C937V399. Terms. Chromonar Hydrochloride Preferred ... Chromonar Preferred Concept UI. M0004398. Registry Number. R0C9NIE5JJ. Related Numbers. 52C937V399. 655-35-6. 804-10-4. Scope ... Chromonar Preferred Term Term UI T008327. Date01/01/1999. LexicalTag NON. ThesaurusID ... Chromonar Hydrochloride Intensain Intercordin Pharm Action. Vasodilator Agents. Registry Number. R0C9NIE5JJ. Related Numbers. ...
Chromonar Hydrochloride. Hydrochloride, Chromonar. Intensain. Intercordin. Tree number(s):. D03.383.663.283.446.280. D03.633. ...
C28931 8LV49809UC CHROMIUM TRIOXIDE C45886 FY38S0790W CHROMOCARB C78116 DVW027E7NL CHROMOMYCIN A3 C895 R0C9NIE5JJ CHROMONAR ...
Chromonar D3.830.219.446.280 D3.383.663.283.446.280 Chromones D3.830.219.266 D3.383.663.283.266 Chromosome Pairing G4.299. ...
Chromonar D3.830.219.446.280 D3.383.663.283.446.280 Chromones D3.830.219.266 D3.383.663.283.266 Chromosome Pairing G4.299. ...
Chromonar D3.438.150.446.280 D3.633.100.150.446.280 Chromones D3.438.150.266 D3.633.100.150.266 Chromosomal Position Effects ...

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