Szelényi Z, Barthó L, Székely M, Romanovsky A A
Department of Pathophysiology, University Medical School, Pécs, Hungary.
Brain Res. 1994 Feb 28;638(1-2):69-77. doi: 10.1016/0006-8993(94)90634-3.
In conscious female Wistar rats with chronic lateral cerebroventricular cannula, the thermoregulatory effects of CCK-8, ceruletide and prostaglandin E1 (PGE1) were studied. In addition, the possible involvement of type A or type B receptors of CCK-8 in thermoregulatory effects of PGE1 and CCK-8 was also investigated. In the normothermic rat an intracerebroventricular (i.c.v.) injection of CCK-8 or ceruletide induced a thermogenic response with tail-skin vasoconstriction and a resulting rise in colonic temperature (Tc). There was a significant negative correlation between the starting level of Tc and the extent of rise in Tc following an i.c.v. administration of PGE1, CCK-8 or ceruletide. Subcutaneously injected CCK-8 caused decreases in Tc in a cool ambient temperature as also described by others. The fever-like response to i.c.v. injected CCK-8 was attenuated by a CCK type B receptor blocker, but not by a CCK type A receptor blocker. Conversely, the hypothermic response to peripherally administered CCK-8 was attenuated by a type A receptor blocker, but not by a type B receptor blocker. Neither of these CCK-receptor blockers influenced the fever caused by an i.c.v. injection of PGE1. It is concluded that in normothermic rats the thermogenic response observed after i.c.v. injection of CCK-8 and ceruletide is the most likely central thermoregulatory change mediated by CCK type B receptors, while the well-known hypothermic response observed after peripheral injection of these peptides might also be explained by their direct effect on variables influencing some of the thermoregulatory effector mechanisms at the periphery.
在清醒的、带有慢性侧脑室插管的雌性Wistar大鼠中，研究了胆囊收缩素-8（CCK-8）、蛙皮素和前列腺素E1（PGE1）的体温调节作用。此外，还研究了CCK-8的A 型或B型受体在PGE1和CCK-8体温调节作用中可能的参与情况。在体温正常的大鼠中，脑室内（i.c.v.）注射CCK-8或蛙皮素会引发产热反应，伴有尾皮血管收缩，进而导致结肠温度（Tc）升高。在i.c.v.给予PGE1、CCK-8或蛙皮素后，Tc的起始水平与Tc升高的程度之间存在显著的负相关。皮下注射CCK-8也会导致在凉爽环境温度下Tc降低，这与其他人的描述一致。对i.c.v.注射CCK-8的发热样反应被CCK B型受体阻滞剂减弱，但未被CCK A型受体阻滞剂减弱。相反，对经外周给予CCK-8的低温反应被A型受体阻滞剂减弱，但未被B型受体阻滞剂减弱。这两种CCK受体阻滞剂均未影响i.c.v.注射PGE1引起的发热。得出的结论是，在体温正常的大鼠中，i.c.v.注射CCK-8和蛙皮素后观察到的产热反应最有可能是由CCK B型受体介导的中枢体温调节变化，而外周注射这些肽后观察到的众所周知的低温反应也可能是由于它们对影响外周一些体温调节效应机制的变量的直接作用所致。
