Regional Blood Flows during Induced Hypotension Produced by Nitroprusside or Trimethaphan in the Rhesus Monkey

Abstract

SIVARAJAN M, AMORY DW, McKENZlE SM. Regional blood flows during induced hypotension produced by nitroprusside or trimethaphan in the rhesus monkey. Anesth Analg 1985;64:759-66. 111 monkeys anesthetized with 7070 nitrous oxide and 0.5% inspired halothane in oxygen, uie measured changes in systemic herriadynamics and regional blood pows produced by nitroprusside and trimethaphan. Regional blood flow measurements were made using the radioactive microsphere rechnique. Control measurements were made before infusion of nitroprusside and trirnethaphan into each animal in sequence in amounts adequate to reduce mean arterial pressure to approximately 55 2 5 mm Hg. Measurements were made during each drug infusion after a stable period of bypotension lasting at least 30 rnin. During nitroprusside infusion, cerebral blood flow remained unchanged, but myocardial blood flow increased significantly. Houmer, pressure-rate product, an indirect nieasure of tnyocardial oxygtii consumption, was unchanged, implying that tnyocardial blood f l~z c~ exceeded myocardial oxygen requirement. Duritig trimethaphan infusion, cerebral blood flou, decreased, dthou'yh cerebral metabolic rate for oxygen uias undmnged due to increased oxygen extraction hy the brain. Triniethapkan also produced a decrease in myocardial blood flow that was in proporfion to the decrease in myocardial oxygen requiremetif as indicated by pressure-rate product. Neither drug produced changes in renal or total hepatic blood flows. W e concltrdtp that brain oxygen reserve is decreased during hypotension induced by trimethaphan. Blood flous to other organs are not significantly impaired in monkeys dtirinx hypotension to a mean arterial pressure of approximately 55 mni Hs induced b.y either nitroprusside or trimathayhati.

The effects of endothelium‐dependent vasodilators on cardiac output and their distribution in the anaesthetized rat: a comparison with sodium nitroprusside

“…All the vasodilators tested significantly lowered peripheral blood pressure but only bradykinin decreased total peripheral resistance to a point that attained a level of significance of P < 0.05. Nitroprusside has previously been shown to decrease TPR, for example by 47% in the rhesus monkey (Sivarajan et al, 1985). The somewhat smaller reduction in TPR observed in this study may be explained by the fact that our animals were vagotomized and hence had a high central sympathetic outflow with consequent greatly elevated vascular tone.…”

Protein Kinase C Delta Modulates Endothelial Nitric Oxide Synthase after Cardiac Arrest

“…[21][22][23] However, there are many reports that suggest otherwise. [24][25][26] Sodium nitroprussidemediated enhancement of CBF depends upon where and what type(s) of vasculature one is measuring from. Traditionally, studies involving ex vivo manipulation of cerebral or systemic vessel preparation has been used to study these types of phenomena utilizing pharmacological manipulations (i.e.…”

Cerebrovascular Effects of Sodium Nitroprusside in the Anaesthetized Baboon: A Positron Emission Tomographic Study

“…The literature concerning the cerebrovascular effects of SNP is rather controversial. Most studies failed to show any change in CBF (Fitch et al, 1976;Akerman et al, 1976;Sivarajan et al, 1985;Joshi et al, 2002a) while some have shown an increase in CBF after SNP administration (Candia et al, 1978;Fitch et al, 1988;Hartmann et al, 1989). More generally, when CBF is clearly reduced, either the level of anaesthesia is light and the subject is hypertensive at the basal state (Grubb and Raichle, 1982;Griffiths et al, 1974) or the level of SNP-induced hypotension is remarkably severe (McDowall et al, 1974).…”

“…However, direct cerebral vasodilatation should induce an increase of CBF. The literature, about the overall cerebrovascular effects of SNP is rather controversial: studies report no change, an increase, or a decrease in CBF after an intravenous administration of SNP in humans (Griffiths et al, 1974;Larsen et al, 1982;Pinaud et al, 1989;Bü nemann et al, 1991) and in laboratory animals (McDowall et al, 1974;Fitch et al, 1976Fitch et al, , 1988Akerman et al, 1976;Candia et al, 1978;Grubb and Raichle, 1982;Sivarajan et al, 1985;Hartman et al, 1989;Hamaguchi et al, 1992;Tsutsui et al, 1995;Salom et al, 2000;Joshi et al, 2002a) (for a review see Joshi et al, 2002b). In clinical practice, SNP is used for acute hypertension especially associated with encephalopathy, controlled hypotension during anaesthesia and heart failure.…”