Blood pressure support during general anesthesia in a renin-dependent state in the rat

E. D. Miller, J. A. Ackerly, M. J. Peach

Research output: Contribution to journalArticlepeer-review

Abstract

Previous work had shown that halothane and enflurane at 1 MAC and ketamine, 125 mg/kg, did not increase plasma renin activity (PRA) in the normal sodium-replete rat. To investigate the renin-angiotensin system with increased PRA, 25 rats were fed a low-sodium diet for five to seven days and divided into four groups: awake; halothane, 1.26 vol per cent; enflurane, 1.75 vol per cent; ketamine, 125 mg/kg, intramuscularly. The protocol consisted of a two-hour awake period, then an hour of stable anesthesia, followed by 30 min infusion of saralasin, an angiotensin II competitive inhibitor. An additional 18 rats had PRA measured by radioimmunoassay before and after an hour of stable anesthesia. Stable anesthesia decreased mean arterial pressure from 122 ± 2 to 69 ± 4 torr for the halothane group, 70 ± 3 torr for the enflurane group, and 103 ± 7 torr for the ketamine group. When saralasin was infused for 30 min, blood pressure decreased to 100 ± 3 torr for the awake group, 40 ± 1 torr for the halothane group, 44 ± 2 torr for the enflurane group, and 73 ± 3 torr for the ketamine group. PRA increased from 4.3 ± 0.5 ng/ml/hr for sodium-replete rats to 12.9 ± 1.7 ng/ml/hr for sodium-depleted rats. After an hour of stable anesthesia, PRA increased in all the anesthetized groups. The authors conclude that the anesthetic agents studied increase renin release in the sodium-depleted rat. The initial renin level may be important in determining whether changes in renin release occur with anesthetic agents.

Original languageEnglish (US)
Pages (from-to)404-408
Number of pages5
JournalAnesthesiology
Volume48
Issue number6
DOIs
StatePublished - Jan 1 1978
Externally publishedYes

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

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