Altered microvascular responses of the small intestine to sepsis during renovascular hypertension

• Published in: Shock (Augusta, Ga.) Ga.), 1994-02, Vol.1 (2), p.108-114
• Main Authors: Lübbe, A S, Cryer, H G, Harris, P D, Garrison, R N
• Format: Article
• Language: English
• Subjects: Acetylcholine - pharmacology; Animals; Arterioles; Cardiac Output, Low - etiology; Cardiac Output, Low - physiopathology; Escherichia coli Infections - complications; Escherichia coli Infections - physiopathology; Hypertension, Renovascular - complications; Hypertension, Renovascular - physiopathology; Intestine, Small - blood supply; Male; Microcirculation; Rats; Rats, Sprague-Dawley; Sepsis - complications; Sepsis - physiopathology; Venules
• ISSN: 1073-2322
• DOI: 10.1097/00024382-199402000-00005

Renovascular hypertension alters endothelial-dependent mechanisms to affect the response of small arterioles in skeletal muscle to sepsis. Small arteriole responses to sepsis differ between skeletal muscle and small intestine in normotensives. Our study now shows that renovascular (1K1C) hypertension alters small arteriole responses in the small intestine to Escherichia coli sepsis. Large arterioles (A1, A2) constricted by 10-20% in the small intestine of both normotensive and hypertensive rats during both high and low cardiac output sepsis. Small arterioles (premucosal A3 and preserosal A4) constricted during high cardiac output sepsis in normotensive but not hypertensive rats. Small A3 and A4 arterioles dilated (20-40%) during low cardiac output sepsis in hypertensives; but only A3 and not A4 arterioles dilated in normotensives during low cardiac output sepsis. Acetylcholine, which releases endothelial-derived relaxing factor in skeletal muscle, dilated both premucosal A3 and preserosal A4 in both normotensive and hypertensive rats. Thus, hypertension alters small arteriole responses to sepsis in both skeletal muscle and small intestine, but apparently by different mechanisms.