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Platelet activating factor alters receptor-coupled function in the isolated perfused rat heart
D D Bensard1, B O Anderson, A Banerjee
1Department of Surgery, University of Colorado Health Sciences Center, Denver 80262.
The Journal of Surgical Research
|October 1, 1992
Summary
Platelet activating factor (PAF) initially depresses heart function in sepsis but enhances response to beta-adrenergic stimulation at lower doses. Higher PAF concentrations did not show this amplified effect.
Area of Science:
- Cardiology
- Pharmacology
- Sepsis Research
Background:
- Sepsis causes myocardial dysfunction, with variable cardiac states suggesting mediator modulation.
- Platelet-activating factor (PAF) is implicated in sepsis pathogenesis and has diverse cellular effects.
Purpose of the Study:
- To investigate PAF's influence on basal and receptor-coupled cardiac mechanical function.
- To assess PAF's effects on myocardial function at different concentrations.
Main Methods:
- Isolated rat hearts were perfused using a modified Langendorf preparation.
- Hearts received vehicle or PAF (20 or 40 microM) followed by isoproterenol stimulation.
- Rate pressure product (RPP) was measured to assess cardiac function.
Main Results:
- Both PAF concentrations rapidly decreased basal RPP compared to controls.
- The initial depressive effect of PAF on RPP was transient.
- Pretreatment with 20 microM PAF enhanced the response to isoproterenol, but 40 microM PAF did not.
Conclusions:
- PAF has a biphasic effect on cardiac function during sepsis.
- Low-dose PAF may sensitize the heart to beta-adrenergic stimulation, while higher doses do not.
- These findings highlight PAF's complex role in sepsis-induced cardiac dysfunction.