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Anaphylaxis in the monkey: hemodynamics and blood flow distribution
Acta Physiologica Scandinavica
|June 1, 1979
Summary
Severe circulatory shock in monkeys during anaphylaxis was caused by increased pulmonary vascular resistance and acute right heart failure. Blood flow was redirected to vital organs, impacting myocardial performance.
Area of Science:
- Cardiovascular Physiology
- Immunology
- Primate Models
Background:
- Anaphylaxis can lead to severe circulatory compromise.
- Understanding hemodynamic changes during anaphylaxis is crucial for effective treatment.
Purpose of the Study:
- To investigate the hemodynamic, blood flow distribution, and myocardial performance changes during induced anaphylaxis in non-human primates.
- To elucidate the primary causes of circulatory shock in this model.
Main Methods:
- Ovalbumin-sensitized monkeys (Macaca irus) were challenged to induce anaphylaxis.
- Hemodynamic parameters, regional blood flow, and myocardial function were monitored.
- Pulmonary and systemic vascular resistance, cardiac output, and ventricular performance were assessed.
Main Results:
- Anaphylaxis induced severe circulatory shock with decreased systemic and left atrial pressures, and increased pulmonary and right atrial pressures.
- Pulmonary vascular resistance increased tenfold, markedly reducing cardiac output (-75%).
- Blood flow redistributed to vital organs (brain, heart, liver) at the expense of other regions; myocardial flow also redistributed, leading to reduced right and left ventricular stroke work.
Conclusions:
- Increased pulmonary vascular resistance is the initial cause of low outflow state in anaphylaxis.
- Acute right heart failure follows, contributing significantly to the shock state.
- Hemodynamic and myocardial dysfunction are key features of severe anaphylaxis.