Cardio-Pulmonary Response to Shock.
Abstract
The general objectives of this laboratory have been to study cardiopulmonary abnormalities associated with shock and trauma, with a focus on the intermediary role of lung and circulating blood cell metabolism. Pressure breathing, pulmonary embolism and acid aspiration, by altering arachidonic acid metabolism were found to depress cardiac contractility and alter the distribution of systematic blood flow. The roles of prostacyclin (PG12) and thromboxane (Tx) A2 in these settings were quantitated by radioimmunoassay and use of selective antagonists. These same prostanoids, along with platelet serotonin, also moderated changes in pulmonary function, particularly physiologic shunt, physiologic dead space and pulmonary vascular resistance. The secondary consequence of injury, the recruitment of an inflammatory reaction, was found to be a significant determinant of increased microvascular permeability both in acid injury of the lungs and heat injury to the skin. In both instances, neutrophil accumulations and permeability edema could be attenuated by inhibition of Tx synthesis. These data indicate that the prostanoids exert direct and indirect actions in moderating cardiopulmonary function following injury.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 30, 1983
- Accession Number
- ADA150943
Entities
People
- H. B. Hechtman
Organizations
- Harvard University