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Effects of vasopressin on the coronary circulation: reserve and regulation during ischemia
Insights
Vasopressin significantly reduced coronary blood flow in dogs, leading to ischemia. However, the coronary vasculature maintained its regulatory capacity, suggesting a distal vasoconstrictor effect.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Vasopressin is a hormone with known vasoconstrictive properties.
- Its specific effects on coronary circulation and potential for inducing ischemia require further investigation.
Purpose of the Study:
- To investigate the impact of intracoronary vasopressin infusion on coronary blood flow and myocardial function in a canine model.
- To assess the coronary vasculature's autoregulatory capacity under vasopressin-induced flow reduction.
Main Methods:
- Intracoronary infusion of vasopressin in 18 dogs.
- Measurement of coronary blood flow, systemic hemodynamics, and regional contractility.
- Assessment of ischemia via lactate production and reactive hyperemia.
Main Results:
- Vasopressin caused a 40% reduction in coronary flow without altering systemic hemodynamics.
- Regional contractility decreased, indicating ischemia, which was reversed by adenosine.
- The coronary vasculature retained autoregulation and showed a reduced hyperemic response.
Conclusions:
- Vasopressin exerts a predominant vasoconstrictor effect on the distal coronary vasculature.
- The coronary circulation demonstrates reserve and regulatory mechanisms even under ischemic conditions induced by vasopressin.
- A myogenic factor may play a role in coronary control, amplified by vasopressin.
Abstract:
In 18 dogs, intracoronary infusion of vasopressin produced a 40% reduction in coronary flow without significantly affecting systemic hemodynamics. The blood flow reduction occurred in a uniform transmural pattern without evidence of a gradient. The reduction in coronary flow resulted in a decrease in regional contractility as determined by isometric strain gauge arches. The decrease in regional contractility was transiently reversed by bolus injection of adenosine into the perfusion line. This suggests that the reduction of blood flow due to vasopressin was causing ischemia. Evidence for ischemia was also supported by measurements of local vein and tissue lactate production. Despite the apparently ischemic conditions, the vascular bed demonstrated evidence for significant reserve and regulation. Pressure-flow relationships performed under control and during vasopressin infusion demonstrated that the coronary vasculature retained its ability to regulate or defend a given level of coronary flow over a range of coronary perfusion pressures. Vasopressin produced a mild decrease in the peak hyperemic flow after a 15-s coronary occlusion and shortened the duration of reactive hyperemia. These overall findings are compatible with a predominant vasoconstrictor effect on the distal coronary vasculature. A role for a myogenic factor in the control of the coronary circulation is suggested, which is amplified by vasopressin.