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Effect of L‐NAME on hemodynamic parameters and thoracic aorta tension in rats of severe sepsis
Author(s) -
Xia Manli,
Huang Yueyan,
Qian Lingbo,
Xia Qiang
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.812.17
Subject(s) - hemodynamics , medicine , vasoconstriction , sepsis , blood pressure , anesthesia , thoracic aorta , aortic pressure , cardiac output , ventricular pressure , cardiology , aorta , vasodilation , nitric oxide , vascular resistance
The objective of the present study was to explore the effect of N ω ‐nitro‐L‐arginine methyl ester hydrochloride (L‐NAME) on hemodynamic parameters and thoracic aorta tension in rats of severe sepsis. We used cecal ligation and puncture (CLP) method to establish severe septic rats, and L‐NAME (5 mg/kg body weight, i.p. ), the nitric oxide synthase inhibitor, was injected after CLP for 4 h. In the phase of severe sepsis (20 h after CLP), the carotid artery was cannulated and connected to a pressure transducer to determine mean arterial blood pressure (MABP); Ventricular dynamic parameters were determined following intraventricular cannulation via the carotid artery, including heart rate (HR), left ventricular developed pressure (LVDP), and maximal rise/fall velocity of ventricular pressure (±dP/dt max ); Isolated thoracic aortic rings were mounted on the organ bath and the tension of the vessel was recorded. We found that MABP and ventricular‐dynamic parameters, including HR, LVDP and ±dP/dt max , were decreased in severe septic rats, which were markedly recovered by treatment with L‐NAME. Vasoconstriction to PE, KCl, and Ca 2+ was also markedly increased by L‐NAME in both endothelium‐intact and ‐denuded aorta of severe septic rats. The results indicate that overproduction of nitric oxide (NO) may involve the change of hemodynamic parameters and the vascular hyporeactivity in severe septic rats induced by CLP, and the mechanism of L‐NAME improving hemodynamic parameters and vasoconstriction responsiveness in rats of severe sepsis is mediated by inhibiting the overproduction of NO.