CARDIAC CONTRACTILITY (DP/DTMAX) AND RESPONSE TO RESUSCITATION (RES) AFTER HEMORRHAGE (HEM)

Abstract

Hypothesis: Severity of HEM may change the hemodynamic response to RES by altering dp/dtmax. Methods: Anesthetized male Wistar rats underwent isobaric HEM to a mean arterial pressure (MAP) = 40 mmHg. Late-shock (LS) rats were bled until 25% return of peak shed blood volume (pSBV), then underwent RES with saline to a target = 80 mmHg. Early-shock (ES) rats were bled to 50% of predicted pSBV, followed by RES. dp/dtmax was continuously recorded by intraventricular catheter. At termination, Na+,K+-ATPase activity (NKA) was measured from harvested left ventricle and skeletal muscle, and plasma levels of endogenous NKA inhibitor (NKAI) were assessed. Results: 7/8 of ES vs. 2/8 LS rats were successfully resuscitated to target (p = 0.04). 1/8 ES vs. 4/8 LS had an increase in MAP (+response) with RES but did not reach target. 2/8 LS rats had a decompensatory fall in MAP (−response) with onset of RES. On post-hoc analysis, in ES and LS+response, dp/dtmax fell with HEM from baseline to start of RES but returned to baseline with RES. For LS−response, there was a nonsignificant decrease in dp/dtmax by start of RES, but no change with RES. Levels of NKA and NKAI were not different between ES, LS+response, and LS−response. Conclusion: Failure of RES after prolonged HEM may be related to a suboptimal cardiac response to RES; however, this is not explained by intrinsic changes in NKA or NKAI.Table