The Role of Cholecystokinin 1 Receptor in Prolactin Inhibited Gastric Emptying of Male Rat

BACKGROUND/AIMS: Prolactin (PRL) is essential for the lactating mammals, while cholecystokinin (CCK) does inhibit gastric emptying (GE). Present study attempted to determine whether both peptides interacted on the male rat GE, particularly the role of putative CCK1 receptor. METHODS: Acute hyperprolactinemia of male rats was induced by the intraperitoneal injection of ovine PRL (oPRL) in several divided doses 15 minutes before motility study. Rat chronic hyperprolactinemia was induced by the graft of 2 pituitary glands into the capsule of left kidney, while control rats received cerebral cortex graft only. Motility study was conducted 6 weeks later after graft surgery. Fifteen minutes after the intragastric feeding of radiochromium, rat was sacrificed to measure GE via the distribution of radioactivities within stomach and intestine. Among the CCK1 receptor blocking study using lorglumide, rats were divided to receive the regimens in terms of oPRL-vehicle plus lorglumide-vehicle, oPRL plus lorglumide-vehicle, oPRL-vehicle plus lorglumide and oPRL plus lorglumide. Plasma CCK level was measured using a homemade radioimmunoassay kit. RESULTS: Compared to vehicle treatment, acute hyperprolactinemic rats under highest dose (2.0 mg/kg) of oPRL treatment showed delayed GE (70.6% +/- 3.0% vs 42.1% +/- 6.6%, P < 0.05). Chronic hyperprolactinemic rats under graft surgery also showed inhibited GE (70.5% +/- 1.7% vs 54.5% +/- 4.7%, P < 0.05). Both models finally obtained elevated plasma CCK levels (P < 0.05). Lorglumide itself did not influence GE, however, delayed GE under oPRL treatment was restored following the concomitant lorglumide treatment. CONCLUSIONS: Our study suggests that PRL may delay male rat GE via a mechanism of endogenous CCK activation involving the peripheral CCK1 receptor.

Mechanism of Action of Cholecystokinin on Colonic Motility in Isolated, Vascularly Perfused Rat Colon

BACKGROUND/AIMS: It is generally believed that cholecystokinin (CCK) stimulates colonic motility, although there are controversial reports. It has also been suggested that postprandial peptide YY (PYY) release is CCK-dependent. Using a totally isolated, vascularly perfused rat colon, we investigated: (1) the roles of CCK and PYY on colonic motility, (2) to determine if CCK modulates PYY release from the colon to influence the motility and (3) to clarify whether the action of CCK and PYY on colonic motility is mediated via the influence of cholinergic input. METHODS: An isolated whole rat colon was used. Luminal pressure was monitored via microtip catheter pressure transducers from proximal and distal colon. After a control period, CCK-8 or PYY was administerd intraarterially with or without an anti-PYY serum, loxiglumide or atropine at 12, 60 and 240 pM. Each dose was given for a period of 15-minute and the contractile response was expressed as % changes over basal. PYY concentration in the portal effluent was determined by radioimmunoassay. RESULTS: Exogenous CCK-8 increased colonic motility which paralleled the increase in PYY release in the portal effluent. Exogenous PYY also significantly increased colonic motility although it was less potent than CCK. The stimulating effect of CCK-8 was significantly inhibited by an anti-PYY serum, and was completely abolished by loxiglumide, and almost completely abolished by atropine. CONCLUSIONS: CCK increases colonic motility via CCK1 receptor and it is mediated partly by PYY. Cholinergic input is required for the increased motility by either PYY or CCK.

Cholecystokinin octapeptide inhibits carotid sinus baroreflex in anesthetized rats / 生理学报

The purpose of this study was to determine the effect of cholecystokinin octapeptide (CCK-8) on carotid sinus baroreflex in 36 anesthetized male rats by isolated carotid sinus perfusion in vivo. The results obtained are as follows. (1) By perfusion with CCK-8 (0.1, 0.5, 1.0 micromol/L), the functional curve of baroreflex was shifted to the right and upward, with a decrease in peak slope (PS) (p<0.001) and a reflex decrease (RD) in mean arterial pressure, while the threshold pressure (TP) and saturation pressure (SP) were significantly increased. Among the functional parameters of carotid sinus baroreflex, the changes in RD, PS and TP were dose-dependent. (2) Pretreatment with proglumide (100 micromol/L), a nonselective CCK receptor antagonist, the inhibitory effect of CCK-8 (0.5 micromol/L) on the baroreflex was significantly attenuated. (3) Pretreatment with L-NAME (100 micromol/L), an inhibitor of nitric oxide (NO) synthase, did not affect the inhibitory action of CCK-8 (0.5 micromol/L). (4) Preperfusion with Bay K 8644 (500 nmol/L), an agonist of calcium channel, could attenuate the effect of CCK-8 (0.5 micromol/L). It is suggested that the inhibitory action of CCK-8 on the baroreflex may be mediated by the activation of its receptors in the carotid sinus baroreceptor, leading to an inhibition of stretch-sensitive channels and a decrease in Ca(2+) influx. However, NO released from the endothelium seems not to be involved in the mechanism of this effect.

Plasma cortisol levels in captive wild felines after chemical restraint

Eight Panthera onca (Po), 13 Felis concolor (Fc), Felis yagouaroundi (Fy) 7 Felis tigrina (Ft) and 5 Felis pardalis (Fp) specimens from SÒo Paulo State zoos were used. All animals were restrained with darts containing 10 mg/kg ketamine and 1 mg/kg xylazine. Venous blood samples were collected as soon as possible (within 15-20 min) and serum was frozen until the time for cortisol quantification. Cortisol was determined using a solid phase radioimmunoassay with and intra-assay coefficient of 8.51 percent. Data were analyzed statistically by the Kruskal-Wallis test, followed by Dunn´s multiple comparisons test, and the one-sample t-test, with the level of significance set at P<0.05. Data are reported as means + SEM. Cortisol levels differed among the captive felines: Po = 166 + 33a, Fc = 670 + 118b, Fy = 480 + 83b, Ft = 237 + 42ab, Fp = 97 + 12a nmol/l (values followed by different superscript letters were significantly different (P<0.001). Since most of the veterinary procedures on these species involve chemical restraint, these results show the necessity of preventive measures in order to minimize the effect of restraint stress on more susceptible species.

Inmovilazación de venados cola blanca (Odocoileus virginianus) utilizando una mezcla de xilazina y ketamina / Immobilization of white-tailed deer (Odocoileus virginianus) with ketamine- xilazine mix

Con la finalidad de evaluar la utilidad de usar una mezcla a dosis constantes (250 mg de xilazina + 100 mg de keatmina/animal) para inmovilizar venados cola blanca (Odocoileus virginianus), se utlizó un rifle "Dist-Inyect" calibre 32 con adaptador de cargas explosivas 22 para proyectar el dardo vector de la mezcla de drogas. Después de una inyección por vía intramuscular (IM), se logró inmovilizar 5 animales entre los 6 min. y 37 min. (prom. 28 min).Con la aplicación por vía endovenosa de 0,1-02 mg. de sulfato de atropina/Kg. de peso corporal, los venados se recuperaron satisfactoriamente entre los 89 min. y 150 min. Tomando como base las ventajas expuestas en el trabajo, se conclute que aún a concentraciones bajas constantes, la mezcla es sumamente útil, confiable y segura para inmovilizar venados silvestres. Para mejorar la técnica se recomienda aumentar en un 20 por ciento la concentración de ambas drogas y usar clorhidrato de yohimbina como antídoto