Effects of Cardiopulmonary Bypass and Prostacyclin on Plasma Catecholamines, Angiotensin II and Arginine‐Vasopressin

Abstract

Infusion of prostacyclin during cardiopulmonary bypass (CPB) reduces platelet activation, diminishes postoperative blood loss and decreases arterial blood pressure. In spite of continuous prostacyclin infusion, there is a delayed gradual rise in arterial pressure and resistance from low initial levels. We measured epinephrine (E), norepinephrine (NE), serotonin (5-HT), angiotensin II (ATII) and arginine-vasopressin (AVP) in plasma and carried out hemodynamic studies in 19 patients operated for coronary vascular disease. Eight patients served as a control group and were subjected to routine CPB. Eleven patients received prostacyclin 50 ng/kg/min during CPB. E and NE increased four- to sixfold during CPB from about 0.5 ng/ml (P less than 0.001). There was no difference between the groups. During CPB AVP increased sixfold from about 20 pg/ml in both groups (P less than 0.001), decreased early after CPB and increased again to high levels 3 h after CPB. The combined action of E, NE and AVP is of likely importance for the rise in systemic vascular resistance and/or need of vasodilation during CPB in the control group. ATII did not increase in the control group, but increased fourfold to about 20 pg/ml (P less than 0.01) during CPB in the prostacyclin group. The addition of AT II to E, NE and AVP seems responsible for the gradual return of arterial pressure and resistance during prostacyclin infusion. Postoperative hypertension and/or need of vasodilation 3 h after CPB was associated with high AVP levels in both groups. Hypotension caused by prostacyclin infusion did not increase E, NE or AVP above levels produced by CPB and moderate hypotension alone.

Heparin-enhanced plasma phospholipase A2 activity and prostacyclin synthesis in patients undergoing cardiac surgery.

“…When PLA2 acts upon lipids containing arachidonic acid in the sn-2 position the resulting free arachidonic acid can serve as a substrate for cyclooxygenases and lipoxygenases. Platelet damage or excess secretion of humoral factors such as catecholamines or angiotensin II during cardiac surgery (14)(15)(16) has been implicated in the elevation of cellular PLA2 activity. Complement activation during CPB (17) causes chemotaxis and leukosequestration, together with the production of oxygen free-radicals by neutrophils, which is thought to affect PLA2 activity (18).…”

Prostacyclin and iloprost: Equal efficiency in preserving high energy phosphates in the dog heart following coronary artery ligation

“…On the other hand, an excitation of the efferent cardiac sympathetic nerve fibers, which occurs after CAL (20) and is followed by a release of catecholamines, may be important for the rise in cardiac cyclic AMP. Whereas PGI2 or iloprost seem not to influence the latter catecbolamine release (34), a moderate effect of prostacyclin, lowering the blood noradrenaline level, has been demonstrated recently (10). Neither PGI2 nor iloprost administration caused a normalization in the cyclic AMP level to the preligation value, which has been found in the range of 0.5 to 0.7 pmol/mg wet weight in tissue freeze-clamped immediately after thoracotomy (3,7,17).…”

Vasopressin Therapy for Vasoplegic Syndrome Following Cardiopulmonary Bypass

“…Whether endogenous serum vasopressin levels are adequate to sustain the systemic blood pressure and the response to the stressful postsurgical course is not known with certainty, decreased vasopressin serum levels have been observed in patients with hypotensive septic shock 15 . Studies of vasopressin during cardiac operations have shown increased serum levels during cardiopulmonary bypass, and a marked decrease of these levels in the early and late postoperative period 19,20 . These reduced postoperative levels may be insufficient to achieve an adequate stress response.…”