CIRCULATING NEGATIVE INOTROPIC AGENT(S) FOLLOWING PULMONARY-EMBOLISM

  • 1 January 1982
    • journal article
    • research article
    • Vol. 91  (4) , 402-408
Abstract
Pulmonary emboli may impair myocardial performance, causing declines in cardiac index (CI) and right and left ventricular stroke work (LVSW) because of mechanical events. Embolism also leads to the generation of a humoral factor(s) that may reduce cardiac contractility. Eleven mongrel dogs were infused with 0.5 g/kg clot. Decreases in CI and LVSW were observed 1 h after embolization. The stable metabolites of prostacyclin and thromboxane (Tx) A2-6-keto-PG[prostaglandin]F1.alpha. and TxB2, respectively-increased within 30 min (P < 0.005, P < 0.001) and then decreased. These changes did not correlate with the declines in CI or LVSW. Plasma from embolized animals used to bathe an isolated rat papillary muscle reduced developed tension (Tpd) (P < 0.01) and decreased calcium ATPase (Ca2+-ATPase) activity of a myofibril preparation (P < 0.001) obtained from rat dardiac muscle. The correlation between the reduction of Tpd and myofibril Ca2+-ATPase activity was 0.72 (P < 0.001). The decline in Ca2+-ATPase was also related to the decreases in CI (r = 0.59, P < 0.001) and LVSW (r = 0.57, P < 0.001). Five animals pretreated with indomethacin prior to embolization had no decrease in LVSW as compared with controls (P < 0.001). Postembolism plasma did not depress papillary muscle Tpd and did not lower Ca2+-ATPase activity of myofibrils. Anesthesia itself did not alter cardiopulmonary function. Apparently pulmonary emboli cause the release of a negative inotropic agent(s) into plasma that affects energy availability in the heart and reduces contractility. The production of this agent(s) is inhibited by indomethacin pretreatment.