The Effects of Propofol and Thiopental on Nitric Oxide Production and Release in Erythrocytes
Status:
COMPLETED
Trial end date:
2024-07-07
Target enrollment:
Participant gender:
Summary
Hypotension is frequently encountered during the use of these commonly used intravenous anaesthetic agents (thiopental and propofol). This is thought to be a consequence of their effects on the sympathetic nervous system, myocardial contractility or vascular tone. However, propofol causes a greater fall in systemic arterial blood pressure than any other drug used for induction of anaesthesia. Propofol causes profound vasodilation, whereas its myocardial depressant effect is not clear. The vasodilatation occurs in both arterial and venous systems. The decrease in systemic arterial blood pressure after thiopental induction is mainly due to peripheral vasodilatation caused by depression of the medullary vasomotor centre and inhibition of the sympathetic nervous system. However, how this peripheral vasodilator effect occurs after both drugs and which mediators accompany it have not yet been fully elucidated. In previous studies, it has been emphasised that systemic vasodilation may be related with increased formation of nitric oxide (NO), a small gaseous and lipophilic molecule which plays an important role in the regulation of vascular homeostasis and haemoregulation. It is important to elucidate the mechanisms that may mediate thiopental- and propofol-mediated vasodilatation in future studies in order to help the methods and treatments that can be developed to prevent hypotension caused by these drugs, which are widely used in clinical practice. Therefore, the aim of this study was to investigate the effects of thiopental and profol on erythrocyte NO synthase activity and erythrocyte-mediated NO release.