The effect of arginine vasopressin (AW) on the contents of cAMP and cGMP in the isolated right atria and ventricular muscle strips was observed at the concentration possessing negative inotropic effect on the cardiac muscle (0.8ng/ml). Results showed that although there were accumulation of both cAMP and cGMP stimulated by AVP in the cardiac muscle, the increase of cGMP was more pronounced with the rise of cGMP/cAMP ratio from the control value 024 (atria) and 0.29(ventricle) to 0.45 and 0.41 respectively after treatment with AVP. Coupled with the known effect of cGMP in mediating the negative inotropic effect in the heart, cGMP is also a possible mediator of the negative inotropic effect of AVP in the heart. The significance of increase in cAMP stimulated by AVP awaits further studies.

Indexes of cardiovascular function and survival time were obser-vedin rats given the following antagonists respectively after scald injury: anti-p-endorphin serum at 10?l, Naloxone at 2mg, ICI174864 at 0.2mg, or TRH at 2 mg, and half of the doses were administered at 1, 2, 3h after scald. The results showed that the cardiac indexes (dP/dtmax, -dP/dtmax and LVSP)were improved, the decrease of mean arterial pressure ( MAP ) and heart rate ( HR ) were delayed after the injections of anti-p-endorphin serum, naloxone or ICIi748e4, and survival time was significantly prolonged in anti ? - endorphin serum group. TRH had little effect on cardiac indexes, MAP and HR were maintained at high level at earlier period, but sharply sloped down in about 210 min after burn. The result suggests that intraventri-cular administration of anti-?-endorphin, naloxone or ICI174864 had much benefit on scald shock, but TRH was uncertain at least in the treatment of scald shock.

Methods including stimulation, cauterization, of nuclei and measurement of pain threshold were used to clarify the role of paraventricular nucleus of hypothalamus (PVH) in pain regulation. Results showed that electrical or L-glutamate sodium stimulation of PVH could elevate the pain threshold in the rat dose-dependently, electrical cauterization of PVH could reduce the pain threshold; and removal of the pituitary gland could not influence the effect of L-glutamate sodium on pain threshold. These results suggest that PVH may play an important role in pain regulation.

The immune function of rats was markedly suppressed following burn injury. At 24 h after burn, the lymphoproliferative response to Con A and IL-1 and IL-2 production in burned rats were significantly reduced, as compared with control animals. At 72 h after burn the immune parameters as above were at the lowerest levels. At 120 h after burn, a slight elevation of immune function was observed, but still lower than the levels of controls. The results of radioimmunoassay of ?-endorphin and dynorphin A in plasma showed that the concentration of ?-endorphin in plasma was not markedly changed after burn except at 2 h after injury, and that of dynorphin A in plasma was reduced markedly after burn injury. The dynamic change of circulating dynorphin A in plasma was coincident with that of immune function. Our results suggest that burn-induced immunosuppression may be related to decrease of circulating dynorphin A levels.