saralasin and Shock--Septic

Endotoxin decreases arteriolar sensitivity to norepinephrine and sympathetic neural activity, but vasopressin sensitivity is increased. Vascular responses to the renin-angiotensin system may also be altered by endotoxin (ENDT). Reactivity of cremaster muscle microvessels of pentobarbital anesthetized Wistar rats was studied using videomicroscopy. Escherichia coli endotoxin (6 mg/kg) was infused i.v. over a 1 hr period. Femoral arterial pressure (Pm) and arteriolar diameter changes, to i.a. bolus injections (60 ng) of angiotensin II (AII) were obtained in Group A at control and at 30 and 90 min post-ENDT, and in Group B at control, 30 min after continuous infusion of saralasin (10 micrograms/min/kg) began, and at 30 and 90 min post-endotoxin. In Group A, the control Pm was 106 +/- 4 mm Hg, and at 30 and 90 min post-ENDT was 96 +/- 4 and 89 +/- 7 mm Hg. All increased Pm 29 +/- 4% before ENDT but the increase was significantly less (P less than .05) at 7 +/- 1% and 6 +/- 1% 30 and 90 min post-ENDT. In Group B, the control Pm was 116 +/- 6 mm Hg, 103 +/- 5 after saralasin, 85 +/- 2 after ENDT infusion, and 83 +/- 4 and 63 +/- 8 mm Hg at 30 and 90 min post-ENDT. All increased Pm 34 +/- 7% before saralasin but only 5 +/- 2% (P less than .05) during saralasin infusion. In Group A, the A1 and A2 arterioles were constricted significantly more post-endotoxin by AII than during control. A3 arterioles post-endotoxin were constricted similar to control amounts by AII.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Angiotensin II; Animals; Arterioles; Blood Pressure; Endotoxins; Male; Muscles; Rats; Rats, Inbred Strains; Renin; Saralasin; Shock, Septic; Vasoconstriction; Venules