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Early (ES) vs. late (LS) hemorrhagic shock: response of cardiac contractility [(dp/dt)max] and ex vivo Na+,K+‐ATPase (NKA) activity to resuscitation (R)
Author(s) -
Oliver J. D.,
Atkins J. L.,
Schooley J. F.,
Wang L.,
Pamnani M. B.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1385
Subject(s) - contractility , medicine , ex vivo , resuscitation , hemorrhagic shock , shock (circulatory) , cardiology , anesthesia , blood pressure , in vivo , biology , microbiology and biotechnology
Methods Anesthetized male Wistar rats underwent isobaric hemorrhage to a mean arterial pressure (MAP) = 40 mmHg. Late‐shock (LS+R) rats were bled until 25% return of peak shed blood volume (pSBV), then underwent R with normal saline to a target=80 mmHg. Early‐shock (ES+R) rats underwent bleeding until 50% of predicted pSBV, and then underwent R to the same target. Hemodynamic parameters were recorded by intrasvascular catheters. The rats were sacrificed, the left ventricle was harvested for NKA, and plasma levels of endogenous NKA‐inhibitor (NKA‐I) were assessed. Baseline and Start of R values of NKA and NKA‐I were obtained from matched groups of unbled and bled but non‐R rats. Results 7/8 of ES+R vs. 2/8 of LS+R rats were successfully resuscitated to target ( p =0.04). (dp/dt) max fell equally in both groups with hemorrhage but returned to baseline with R. In both ES and LS, NKA‐I decreased in correlation with an increase in tissue NKA; NKA increased further in LS after R. Conclusion Failure to reach target MAP with R after prolonged hemorrhage is not explained by changes in (dp/dt) max . However, hemorrhage induces changes in NKA and NKA‐I that are not reversed by R.