Role of renin-angiotensin system in cardiopulmonary bypass hypertension

• Published in: Canadian Anaesthetists' Society journal Vol. 31; no. 2; pp. 160 - 165
• Main Authors: TOWNSEND, G. E, WYNANDS, J. E, WHALLEY, D. G, WONG, P, BEVAN, D. R
• Format: Journal Article
• Language: English
• Published: Toronto, ON Canadian Anaesthetists' Society 01.03.1984
• Subjects: Anesthesia; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Angiotensin II - antagonists & inhibitors; Biological and medical sciences; Cardiopulmonary Bypass - adverse effects; Female; General anesthesia. Technics. Complications. Neuromuscular blocking. Premedication. Surgical preparation. Sedation; Humans; Hypertension - drug therapy; Hypertension - etiology; Male; Medical sciences; Middle Aged; Renin - blood; Renin-Angiotensin System; Saralasin - therapeutic use; Vascular Resistance; Cardiopulmonary bypass; Human; Hypertension; Renin angiotensin system; Surgery; Coronary artery; Anesthesia
• DOI: 10.1007/BF03015254
• ISSN: 0008-2856

The role of the renin-angiotensin system in the aetiology of perioperative hypertension was studied in 15 previously normotensive patients undergoing coronary artery surgery and anaesthetized with fentanyl. Measurements of plasma renin activity were made at intervals before and during cardiopulmonary bypass (CPB). In addition, angiotensin II blockade with saralasin was used in an attempt to treat hypertension during CPB. Nine of the patients became hypertensive (increase in systemic pressure of more than 20 per cent) before CPB and although the mean plasma renin activity was higher in this group than in the normotensive patients it was within normal limits for each group. Hypertension during CPB (mean blood pressure greater than 100 mmHg at 1.8 l X m-2 flow), occurred in seven patients but was not associated with increased renin activity and did not respond to saralasin in doses up to 20 micrograms X kg-1 X min-1. It is concluded that cardiopulmonary bypass associated hypertension is not mediated by activation of the renin-angiotensin system.