The effect of pregnancy on the response to blood loss in a rat model

Abstract

Study objectives: A commonly held belief is that the blunted hemodynamic response to hemorrhage observed in pregnant women is secondary to expanded blood volume. In addition to increased blood volume, pregnancy is also a vasodilated state. Vasodilatation may have deleterious effects on the response to hemorrhage by inhibiting central blood shunting after blood loss. How these conflicting variables of increased blood volume and vasodilatation integrate into a whole body model of maternal hemorrhagic shock has yet to be studied in a controlled experiment. We tested the null hypothesis that there would be no difference in the hemodynamic and metabolic responses to hemorrhage between pregnant (PRG) and non-pregnant (NPRG) rats. Methods: Twenty-four adult female Sprague–Dawley rats (12 PRG and 12 NPRG) were anesthetized with Althesin via the intraperitoneal route. Femoral arteries were cannulated by cut-down. Twelve (six PRG and six NPRG) rats underwent controlled catheter hemorrhage of 25% of their total blood volume. Twelve rats (six PRG and six NPRG) served as non-hemorrhage controls. Mean arterial pressure (MAP) and base excess (BE) were measured pre-hemorrhage and then every 15 min post-hemorrhage for the next 90 min. Data were reported as mean±standard error of the mean (S.E.M.) over the 90-min post-hemorrhage observation period. Group comparisons were analyzed by ANOVA with repeated values post-hoc by Bonferroni. Statistical significance was defined by an α=0.05. Results: PRG and NPRG rats were evenly matched for MAP ( P=0.788) and BE ( P=0.146) pre-hemorrhage. Post-hemorrhage there were no mortalities in either group. Post-hemorrhage both the PRG and NPRG groups experienced significant ( P=0.011) drops in systolic and diastolic blood pressures as compared to their non-hemorrhage controls. Post-hemorrhage there was no significant ( P=0.43) difference in MAP between the PRG (89±2 mmHg) and NPRG (80±2 mmHg) rats. BE also dropped significantly within both PRG ( P=0.004) and NPRG ( P=0.001) groups post-hemorrhage. No significant ( P=0.672) difference was noted in BE between PRG and NPRG groups post-hemorrhage –6.1±0.3 mEq/l and –6.9±0.4 mEq/l, respectively. Conclusion: After a controlled hemorrhage of 25% of total blood volume we found no significant differences in MAP and BE between pregnant and non-pregnant rats. Pregnancy does not affect the response to hemorrhage.