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Nam YT, Takahashi S, Tominaga M, et al. The hemodynamic and metabolic changes in prostaglandin E1-induced hypotension in dogs--a comparative study with trimetaphan-induced hypotension. J Anesth. 1989;3(2):210-7doi: 10.1007/s0054090030210.
Nam, Y. T., Takahashi, S., Tominaga, M., & Yoshitake, J. (1989). The hemodynamic and metabolic changes in prostaglandin E1-induced hypotension in dogs--a comparative study with trimetaphan-induced hypotension. Journal of anesthesia, 3(2), 210-7. https://doi.org/10.1007/s0054090030210
Nam, Y T, et al. "The hemodynamic and metabolic changes in prostaglandin E1-induced hypotension in dogs--a comparative study with trimetaphan-induced hypotension." Journal of anesthesia vol. 3,2 (1989): 210-7. doi: https://doi.org/10.1007/s0054090030210
Nam YT, Takahashi S, Tominaga M, Yoshitake J. The hemodynamic and metabolic changes in prostaglandin E1-induced hypotension in dogs--a comparative study with trimetaphan-induced hypotension. J Anesth. 1989 Sep 01;3(2):210-7. doi: 10.1007/s0054090030210. PMID: 15236040.
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J Anesth. 1989 Sep 01;3(2):210-7. doi: 10.1007/s0054090030210.

The hemodynamic and metabolic changes in prostaglandin E1-induced hypotension in dogs--a comparative study with trimetaphan-induced hypotension.

Journal of anesthesia

Y T Nam, S Takahashi, M Tominaga, J Yoshitake

Affiliations

  1. Department of Anesthesiology, Yonsei University College of Medicine, Severance Hospital, Seoul, Korea.

PMID: 15236040 DOI: 10.1007/s0054090030210

Abstract

The hemodynamic and metabolic changes in hypotensive state induced with prostaglandin E1 (PGE1) or trimetaphan (TMT) infusion were investigated in dogs. Mean arterial pressure was decreased by about 50% with 1.58 microg/kg/min of PGE1 or 45 microg/kg/min of TMT. Heart rate, pulmonary capillary wedge pressure and central venous pressure remained virtually unchanged in the two groups. Cardiac output was well maintained in PGE1 group, whereas cardiac output showed the tendency to decline in TMT group. Greater reduction in systemic vascular resistance was seen in PGE1 group than in TMT group. Pulmonary vascular resistance showed no significant change in PGE1 group, whereas it increased significantly in TMT group. Gradual decreases in arterial pH, PaO2 and base excess and slight but significant increase in PaCO2 was observed in PGE1 group, and these abnormalities recovered 30 min after hypotension. Abnormalities in blood gases and acid-base balance were considerably more severe and prolonged in TMT group compared with those in PGE1 group. Blood lactate and pyruvate concentrations showed no significant changes in PGE1 group, whereas substantial elevation was seen in L/P ratio especially 30 min after induction of hypotension in TMT group. Oxygen consumption showed minimal changes in PGE1 group, whereas a significant decrease was observed in TMT group. The conclusions derived from these results are as follows; 1) PGE1 maintained cardiac output better than TMT, probably because of its direct inotropic action on the heart, and of its greater reduction of systemic vascular resistance than TMT. 2) PGE1 seemed to provide the better blood perfusion throughout the body than TMT. 3) PGE1 showed less possibility to produce the metabolic derangement compared with TMT.

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