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Cardiac function and coronary flow in chronic endotoxemic pigs
K J Lee1, S W Dziuban, H van der Zee
1Department of Physiology, Albany Medical College, New York 12208.
Summary
In chronic endotoxemia, depressed myocardial inotropism (heart muscle contractility) was not caused by reduced coronary artery blood flow. Instead, the heart muscle was relatively overperfused, challenging previous hypotheses.
Area of Science:
- Cardiology
- Physiology
- Toxicology
Background:
- Previous research indicated depressed myocardial inotropism in acute and chronic endotoxemia.
- A potential mechanism suggested was reduced myocardial perfusion during endotoxemia.
Purpose of the Study:
- To investigate if reduced inotropism in chronic endotoxemia is associated with decreased coronary artery blood flow.
- To test the hypothesis that myocardial perfusion is reduced in chronic endotoxemia.
Main Methods:
- Fifteen pigs were instrumented to measure cardiac function and hemodynamics.
- Chronic endotoxemia was induced in 12 pigs using Salmonella enteriditis endotoxin via osmotic pumps.
- Cardiac output, left ventricular pressure, coronary artery blood flow, and myocardial dimensions were monitored.
Main Results:
- Survivors of endotoxemia showed elevated heart rate, systolic pressure, and cardiac output, but depressed inotropism (ESPDR and % diameter-shortening).
- Coronary artery blood flow was significantly elevated in endotoxemic pigs, leading to increased coronary blood flow to stroke work ratio.
- Nonsurvivors had reduced cardiac function and hemodynamics, with no increase in coronary blood flow.
Conclusions:
- Depressed myocardial inotropism in chronic endotoxemia is not due to reduced coronary blood flow.
- The findings suggest relative myocardial overperfusion during chronic endotoxemia.
- This challenges the notion that endotoxemia-induced cardiac dysfunction is primarily driven by impaired coronary perfusion.