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Effects of endotoxin on coronary vascular resistance in the isolated blood-perfused rabbit heart
Insights
Endotoxin shock increases coronary vascular resistance (CVR) via blood from affected rabbits, not direct endotoxin addition. This elevated CVR may contribute to heart dysfunction during endotoxin shock.
Area of Science:
- Cardiovascular Physiology
- Endotoxic Shock Research
- Microcirculation Studies
Background:
- Endotoxin shock can lead to myocardial dysfunction.
- The direct and indirect effects of endotoxin on coronary vascular resistance (CVR) are not fully understood.
- Understanding CVR changes is crucial for managing endotoxin shock.
Purpose of the Study:
- To investigate the effect of endotoxin on rabbit coronary vascular resistance (CVR).
- To differentiate between direct and indirect effects of endotoxin on CVR.
- To determine if altered CVR contributes to myocardial ischemia in endotoxin shock.
Main Methods:
- Isolated rabbit hearts were perfused with blood.
- Left ventricular pressure and dP/dt were measured.
- Coronary vascular resistance (CVR) was calculated by dividing coronary perfusion pressure by coronary blood flow.
Main Results:
- Direct addition of endotoxin to perfusate did not alter CVR.
- Perfusate from endotoxin-treated rabbits significantly increased CVR.
- Increased CVR was observed regardless of donor rabbit's blood pressure (normotensive or hypotensive).
Conclusions:
- Blood from endotoxin-treated rabbits, not endotoxin itself, elevates CVR.
- Pathologic increases in CVR may play a role in myocardial ischemia during endotoxin shock.
- Further research is needed to elucidate the mechanisms behind endotoxin-induced CVR changes.
Abstract:
Rabbit hearts were excised and perfused with blood pumped through a cannula placed in the aortic root. A fluid-filled balloon-tipped catheter was positioned in the left ventricle for the measurement of left ventricular pressure and dP/dt. Total coronary vascular resistance (CVR) was calculated by dividing the coronary perfusion pressure by the rate of coronary blood flow. Following stabilization, coronary blood flow was held at a constant rate. Compared to control hearts, endotoxin (E. coli) added directly to the blood perfusate (6 mg/80 ml of circulating blood) had no effect on CVR or left ventricular dP/dt. In contrast, changing the perfusate to blood obtained from rabbits previously given endotoxin (LD100; 6 mg/kg IV) resulted in significantly higher CVR, without depression of left ventricular dP/dt. This increase in CVR was observed not only when the endotoxemic donor rabbits were hypotensive at the time the blood was obtained (4-6 hours following endotoxin administration), but also when the endotoxemic donors remained normotensive (blood withdrawn 30 minutes following endotoxin administration). A pathologic increase in CVR might contribute to the myocardial ischemia and contractile dysfunction observed in endotoxin shock.