Accession Number : ADA140108

Title :   Cardio-Pulmonary Response to Shock.

Descriptive Note : Annual progress rept. 1 Jan 80-31 Mar 81,

Corporate Author : HARVARD MEDICAL SCHOOL BOSTON MA

Personal Author(s) : Hechtman,H B

PDF Url : ADA140108

Report Date : Feb 1981

Pagination or Media Count : 28

Abstract : Investigations are continuing into the relationship of pulmonary prostaglandin production and systemic organ function. Our study preparations are of pulmonary embolism and/or positive end-expiratory pressure (PEEP) which we believe to be analogous to the microembolism and hyperventilation of severe injury. Both embolism and PEEP lead to the production of thromboxanes (Tx) as well as decreases in cardiac contractility. The latter event can be prevented with Tx antagonists. Tx cause the elaboration of a high molecular weight protein fraction which suppresses myocardial Ca(++)-ATPase and reduces activity of Krebs cycle enzymes in cardiac mitochondria. During acute thrombocytopenia serotonin (5-HT) infusion was found to protect against petechiae. Antagonists to 5-HT promoted petechiae. Endogenous or exogenously infused prostacyclin (PGI2) caused a reduction in plasma and increase in platelet 5-HT. Endothelial 5-HT transport was blocked. These findings may underly the ability of PGI2 to enhance permeability. Prostacyclin was found to regulate the production of plasminogen activator. This may be one of the mechanism related to the dramatic effectiveness of PGI2 in reversing the cardiopulmonary abnormalities of pulmonary embolism and in reversing lethal endotoxemia.

Descriptors :   *Heart function tests, *Pulmonary function, *Shock(Pathology), *Pressure breathing, *Embolism, Lung function tests, Prostaglandin, Metabolism, Hyperventilation, Wounds and injuries, Heart, Contraction, Pharmacological antagonists, Myocardium, Phosphates, Mitochondria, Serotonin, Thrombocytopenia, Abnormalities, Coronary disease, Respiratory system, Respiratory diseases, Endotoxemia, Pulmonary edema

Subject Categories : Anatomy and Physiology
      Medicine and Medical Research

Distribution Statement : APPROVED FOR PUBLIC RELEASE