title: Effect of Candida albicans septicemia on the cardiovascular function of rabbits.
abstract: Candida albicans is an opportunistic pathogen that causes life-threatening systemic infection in immunocompromised host. However, little is known about the effects of yeast on the cardiovascular functions. This study examined the effects of C. albicans septicemia on the heart and vessel functions and nitric oxide (NO) production in infected rabbits. Anaesthetized animals were challenged with intravenous C. albicans (6 x 10(8)/kg) or saline and the blood pressure of rabbits were measured over 5 h. After that response of the isolated thoracic aorta, right atrium and left papillary muscle were recorded. Blood pressure significantly decreased in the infected rabbits during the septicemia but in the control animals it was stable. The blood nitrite levels and NO-synthases (eNOS, iNOS) expression and tissue nitrite levels in the heart and aorta were similar in the both groups. In the aorta isolated from C. albicans-infected rabbits, acetylcholine-induced endothelium-dependent relaxation was decreased, but contractions induced by phenylephrine were potentiated. The NOS inhibitor, L-N(G)-nitro-arginine methyl ester (L-NAME)-induced contraction increase in the right atrium was depressed by the yeast-infection. In the heart and aorta, microscopic examination revealed no tissue invasion of C. albicans. These results indicate the ability of C. albicans-induced septicemia to destroy NO-related responses of the heart and aorta and may have important implications for functional damage to endothelium and the regulation of cardiovascular functions. In addition, NOS induction and NO over-production are not stimulated by systemic C. albicans infection, which would alter the host immune reaction and homeostasis.
authors.affiliation: Department of Pharmacology/Clinical Pharmacology, Ankara University, School of Medicine, Sihhiye, Ankara 06100, Turkey.
authors.forename: M
authors.initials: M
authors.lastname: Buluc
authors.forename: H
authors.initials: H
authors.lastname: Ataoğlu
authors.forename: D
authors.initials: D
authors.lastname: Doğan
authors.forename: H
authors.initials: H
authors.lastname: Ergün
authors.forename: H
authors.initials: H
authors.lastname: Gürdal
authors.forename: E
authors.initials: E
authors.lastname: Erdemli
authors.forename: E
authors.initials: E
authors.lastname: Demirel-Yilmaz
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology; D002177:Candidiasis / Q000473:pathology / Q000503:physiopathology*; D002320:Cardiovascular Physiological Phenomena; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D016469:Fungemia / Q000473:pathology / Q000503:physiopathology*; D006325:Heart Atria / Q000187:drug effects / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000473:pathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000096:biosynthesis; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D010210:Papillary Muscles / Q000187:drug effects / Q000503:physiopathology; D011817:Rabbits
chemical_list: D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D019331:NG-Nitroarginine Methyl Ester