Effect of PGE 2 on pulmonary C‐fiber response to hyperthermia in rats

Abstract

Body temperature frequently increases to ~41°C during strenuous exercise or severe fever. Local tissue hyperthermia is known to occur during inflammatory reaction, and an increase in airway temperature has been reported in asthmatic patients (Am J Respir Crit Care Med. 165:181, 2002). A recent study in our lab (J Physiol. 565:295, 2005) showed intrathoracic hyperthermia induces the hypersensitivity of pulmonary C-fibers. In this study, we investigated whether the response of pulmonary C-fibers to hyperthermia is altered by prostaglandin E2 (PGE2), one of the major autacoids released in the lung during airway inflammation. Single-unit afferent activities of pulmonary C-fibers were recorded in anesthetized, artificially ventilated rats when the intrathoracic temperature (Tit) was maintained at normal (~36 °C; N) and hyperthermia levels (~41 °C; H) by the perfusion of heated saline into the thoracic chamber for 3 min. After 20 min of recovery, the fiber activities were recorded again during the perfusion of PGE2 (3 μg/kg/min, 3 min) at these two Tit, N and H. Our studies show: 1) During PGE2 perfusion, baseline fiber activities were higher than the control at both N and H levels of Tit. Furthermore, the hyperthermia-induced increase in baseline activity was also significantly augmented by PGE2 (P < 0.01). 2) The responses of pulmonary C-fibers to both lung inflation (15 and 30 cmH2O) and right atrial injection of capsaicin (1 μg/kg) during the perfusion of PGE2 increased in a similar pattern as that of the baseline. In conclusion, PGE2 markedly potentiates the hyperthermia-induced hypersensitivity of vagal pulmonary C-fibers to lung inflation and capsaicin. (Supported by NIH HL 67379)