Blood Pressure Control during Anesthesia

Abstract
Newborn rats were treated with guanethidine sulfate for the first 3 wk of life in order to produce a partial permanent peripheral sympathectomy. The rats were allowed to grow to 250-300 g on a normal Na diet. Using diethyl ether anesthesia, arterial and venous cannulas were placed and the animals allowed to awaken in restraining cages. The rats were divided into 4 groups: awake (n [no.] = 6); halothane 1.3 vol % (n = 8); enflurane 2.2 vol % (n = 8); and ketamine 125 mg/kg, i.p. (n = 8). The protocol consisted of a 1-h control awake period, 1 h of stable anesthesia (1 group received no anesthesia), and 1/2 h i.v. infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity was measured at the end of each time period. Thirty untreated normal rats were similarly divided into 4 groups and served as the control. The degree of peripheral sympathectomy was assessed through cardiac norepinephrine concentrations, plasma catecholamines and response to 50% hemorrhage. Guanethidine treatment resulted in a 78% decrease in cardiac norepinephrine from 189 .+-. 15 ng/g in the untreated animals compared with 42.4 .+-. 5 ng/g in the treated animals. The 5-fold increase seen in plasma norepinephrine to acute decapitation was completely absent in the treated animals. Hemorrhage of 50% of blood volume resulted in a 75% mortality rate in the treated animals, while there were no deaths 30 min after hemorrhage in the normal animals. Blood pressure for the 30 treated animals during the awake period was 114 .+-. 2 mmHg, which was significantly less than 124 .+-. 1 mmHg in the untreated animals (P < 0.05). Plasma renin activity of 1.58 .+-. 0.25 ng .cntdot. ml-1 .cntdot. h-1 in the treated group was significantly less than 2.59 .+-. 0.21 ng .cntdot. ml-1 .cntdot. h-1 in the untreated rats (P < 0.05). With the induction and maintenance of stable anesthesia, blood pressure decreased to 82 .+-. 2 mmHg with halothane, 92 .+-. 4 mmHg with enflurane, and 104 .+-. 4 mmHg with ketamine in the treated animals. Plasma renin activity did not increase in either treated or untreated animals. Similar degrees of blood pressure decreases were seen in untreated animals. With the infusion of saralasin, a further decrease of approximately 20 mmHg in blood pressure was seen, in both the treated and untreated rats anesthetized with halothane. In treated rats anesthetized with enflurane or ketamine, no depressor response to saralasin was seen, which is in marked contrast to the response seen in untreated animals. The plasma renin response in the treated animals was blunted. Using this animal model, partial peripheral sympathectomy apparently does not result in deleterious effects when rats are anesthetized with halothane, enflurane or ketamine.