Hypotension Caused by Extracorporeal Circulation

Abstract

Background-Cardiopulmonary bypass and hemodialysis often cause hypotension. We investigated a possible role of pump-induced platelet activation with consequent serotonin release. Methods and Results-In rats, a heparin-coated extracorporeal shunt was placed between the proximal part of a carotid artery and the distal part of a femoral artery. Autoperfusion did not affect platelets or hemodynamics. Pump perfusion, however, immediately elicited strong platelet aggregation, whereas aortic pressure rapidly fell to 60Ϯ12% (meanϮSD) of its prepump value, partially recovered, and then progressively decreased to 70Ϯ12% at 2 hours. Femoral resistance doubled and then decreased to 59Ϯ11%. The initial changes in aortic pressure and femoral resistance were proportional to the amount of platelet aggregation, were accompanied by a rise (6-fold) in plasma serotonin levels downstream of the pump, but not in the aorta, and could be mimicked by serotonin-infusion into the leg. All hemodynamic changes were prevented or largely reduced by blockade of 5-hydroxytryptamine (5-HT) 2 receptors with pizotifen or ritanserin. The hypotension and femoral resistance decrease could also be prevented or abolished by inhibiting the production of nitric oxide (NO), an intermediate in 5-HT 2B receptor-induced vasodilation. When the extracorporeal blood was pumped into the aortic arch instead of the femoral artery, the hypotensive effect was similar and also NO dependent, but it was absent with venous return. Conclusions-Pump perfusion with arterial return of the blood causes hypotension by endothelial NO-release, which in turn is triggered by serotonin from activated platelets.

Migraine Modulation and Debut after Percutaneous Atrial Septal Defect Closure: A Review

“…Aggregating platelets normally release a number a substances including thromboxane A2, adenosine diphosphate and serotonin. In addition, serotonin released from aggregating platelets serves as a vasoconstrictor, but under normal conditions, and as aggregation subsides, reduced levels of serotonin can lead to vasodilation (119). It has been hypothesized that alteration in plasma serotonin level causes MH (MO or MA), and that platelet aggregation and heightened serotonin induce vasoconstriction causing reduction in blood flow and the neuronal manifestation of aura (14).…”

Reduction in Platelet Activation by Citrate Anticoagulation Does Not Prevent Intradialytic Hemodynamic Instability

“…Therefore, it is not entirely clear whether the HD dal -induced increase in PF4 results exclusively from platelet activation in the ECC or from the combination of platelet activation and release from endothelium-bound PF4. In rats, we demonstrated [12] that hemodynamic alterations during extracorporeal circulation were proportional to the amount of shear stress induced platelet aggregation and the subsequent rise in plasma serotonin levels. As all hemodynamic changes could be prevented by blockade of 5-hydroxytryptamine-2 receptors and by inhibition of NO formation, the observed fall in the BP was ascribed to serotonin-induced endothelial NO release.…”

“…In rats, we have previously shown that shear stress elicited platelet aggregation and subsequent serotonin release induce hypotension via endothelial NO release in a roller pump perfused extracorporeal circulation model [12]. Others [13] demonstrated a reduction in platelet activity at lower core temperatures in studies on cardiopulmonary bypass surgery.…”

Nitric Oxide Synthase Inhibitor (MTR-105) during Open-Heart Surgery

“…The effectiveness of NOS inhibition is plausible since current data suggest that NO mediates vasodilatation following CPB and rewarming, perhaps stimulated in part by release of proinflammatory cytokines [1, 2]. NO production is directly associated with temperature-dependent regulation of systemic vascular resistance during CPB: serum NO concentrations are significantly higher when CPB perfusion solution is tepid than when it is hypothermic [5].…”

“…Effects of CPB and the associated systemic hypothermia and rewarming, putatively mediated at least in part by cytokine release, routinely cause marked systemic vasodilatation, often resulting in profound (and rapidly developing) hypotension [1, 2]. Overproduction or excessive release of nitric oxide (NO) has been implicated in the development of this response [3, 4].…”