Hemodynamic and respiratory effects of thyrotropin-releasing hormone and epinephrine in anaphylactic shock

Abstract

Thyrotropin-releasing hormone (TRH) has been shown to increase mean arterial pressure during anaphylactic shock. The hemodynamic mechanism of action and the effect of TRH on the respiratory system during anaphylactic shock are not known. A rabbit model of anaphylaxis was used to determine the effect of TRH, epinephrine (EPI), and normal saline (NS) on various cardiovascular and respiratory parameters during anaphylactic shock. Anaphylactic shock was induced by antigen challenge in 31 sensitized animals. After a 25% decrease in mean arterial pressure, they were randomly treated with TRH (2 mg/kg), EPI (0.005 mg/kg), or NS (10 mL/kg). Blood was drawn at baseline and at the end of the experiment for laboratory analysis. Cardiac and respiratory parameters were monitored continuously and measured at baseline, at onset of shock (time zero), and at time intervals for 30 minutes. Animals were treated with repeated doses during the first 15 minutes as needed to maintain mean arterial pressure above shock level. Five of ten TRH-, five of 11 EPI-, and six of ten NS-treated animals survived. The TRH-treated group required fewer doses than the other groups and had increased heart rate, mean arterial pressure, peripheral vascular resistance, respiratory rate, and minute ventilation as well as decreased stroke volume index and lung compliance compared with the NS-treated group. EPI treatment resulted in increased minute ventilation and decreased pulmonary airway resistance compared with NS treatment. The EPI group also had a higher postsurvival epinephrine level than the other groups. No difference in right atrial pressure, cardiac index, acid-base status, pO2, A- a gradient, lung weight, lactate, or norepinephrine levels was found.(ABSTRACT TRUNCATED AT 250 WORDS)