[Effects of trimetaphan on hemodynamics and pulmonary gas exchange--a comparison with those of nitroglycerin and prostaglandin E1].

In recent studies, the changes in arterial and end-tidal carbon dioxide tensions have been shown to correlate linearly with changes in cardiac output during the constant minute ventilation. High and low ventilation to perfusion ratios can also be estimated from blood and expiratory gas analysis. In the present study, the effects of trimetaphan (29 +/- 3 micrograms.kg-1.min-1) on hemodynamics and pulmonary gas exchanges were studied by analyzing these gas tensions in nine sevoflurane/nitrous oxide anesthetized patients, and were compared with those of nitroglycerin (5 micrograms.kg-1.min-1) and prostaglandin E1 (100 ng.kg-1.min-1) which had been reported in the previous study. During trimetaphan administration, arterial pressure decreased. The decreases in both systolic and diastolic arterial pressures were greater than those during nitroglycerin or prostaglandin E1 administration. PaCO2 decreased significantly, whereas it did not change in fixed direction with nitroglycerin infusion and increased with prostaglandin E1 infusion. The magnification of both alveolar-arterial oxygen tension difference and arterial-end-tidal carbon dioxide tension difference during trimetaphan administration was equal to that during prostaglandin E1 administration and smaller than that during nitroglycerin administration. Therefore, it seems that trimetaphan as well as nitroglycerin decreases cardiac output but prostaglandin E1 increases or maintains it in patients under sevoflurane/nitrous oxide anesthesia, that trimetaphan reduces vascular resistance most weakly of the three (trimetaphan < nitroglycerin < prostaglandin E1), and that trimetaphan as well as prostaglandin E1 does not influence pulmonary blood distribution as strongly as nitroglycerin.