SUMMARY1. Acutely, opioids inhibit oxytocin secretion. To study the responses of oxytocin neurones during chronic opioid exposure, forty-five lactating rats were infused continuously from a subcutaneous osmotically driven mini-pump via a lateral cerebral ventricle with morphine sulphate solution from day 2 post-partum for 5-7 days; the infusion rate was increased 2-or 2-5-fold each 40 h from 10 ,ug/h initially up to 50 ,ug/h; controls were infused with vehicle (1 ,u/h, twenty-eight rats) or were untreated (eight rats).2. Maternal behaviour was disrupted in 27 % of the morphine-treated rats; in rats that remained maternal morphine did not affect body weight or water intake but increased rectal temperature by 0-82 + 0-14 'C (mean+S.E.M.) across the first 4 days.3. Weight gain of the litters of maternal morphine-treated rats was reduced by 32 % during 7 days, predominantly in the first day of treatment when milk transfer was also reduced. Observation of pup behaviour during suckling showed decreased frequency of milk ejections on only the second day of morphine treatment. Plasma concentration of prolactin after 6 days was similar in maternal morphine-treated and control rats, but reduced by 90 % in non-maternal morphine-treated rats, indicating normal control of prolactin secretion by suckling in morphine-treated rats.4. Oxytocin and vasopressin contents, measured by radioimmunoassay, in the supraoptic and paraventricular nuclei and in the neurohypophysis were similar between fourteen maternal morphine-treated, twelve vehicle-treated and eight untreated lactating rats; thus exposure to morphine did not involve increased production and storage of oxytocin.5. Distribution of L3H]morphine infused intracerebroventricularly into six virgin female rats for 6 days was measured by scintillation counting of tissue extracts. Morphine concentration in the hypothalamus and neurohypophysis was 2-7 and 12 8 jug/g, respectively, and in blood plasma 0 75 ,ug/g. Tolerance was not due to failure of morphine infusion. In addition, naloxone (5 mg/kg s.c.) provoked typical withdrawal reactions ('wet dog' shakes, defaecation, burrowing) in lactating rats infused with morphine for 5 days.6. Pups were suckled onto seven maternal morphine-infused and five vehicle-V. C. RA YNER AND OTHERS infused rats anaesthetized with urethane for recording of intramammary and arterial blood pressures after treatment for 5 days. The incidence and pattern of milk ejections, and mammary gland sensitivity to oxytocin were similar in the two groups. Tolerance to the inhibition of suckling-induced oxytocin secretion by intracerebroventricular (i.c.v.) morphine did not extend to acute intravenous morphine (2-5 or 5 mg/kg).7. In fourteen out of fifteen morphine-infused rats under urethane anaesthesia, intravenous naloxone HCl (5 mg/kg) quickly provoked a large, fluctuating increase in intramammary pressure lasting 41-5+ 15 min (mean±+S.D.); this excitation of presumptive oxytocin secretion was independent of suckling and was not seen in twelve vehicle-infused ra...
We show a difference in alpha-MSH and AgRP in lean and obese subjects that correlates closely with body fat at baseline. We demonstrate an increase in plasma AgRP during a 6-day fast in lean individuals that is coincident with a decrease in plasma leptin. This increase in AgRP was not due to weight loss per se as there was no change in AgRP as a result of the same weight loss in the VLCD intervention in lean individuals. The source of the increase in plasma AgRP and its physiological function in the periphery remains to be elucidated but we suggest that the dynamics of the change in plasma leptin may determine the elevation in fasting plasma AgRP in lean subjects.
SUMMARY1. The pattern of small intestinal digesta transit was studied in six young pigs (20-30 kg) by simultaneous electromyography and radiology. Pigs showed migrating myoelectric complexes (m.m.c.s) in the small intestine both when fasted and after feeding. The m.m.c.s were modified by feeding; quiescence was much reduced in duration and irregular spiking activity (i.s.a.) was prolonged; m.m.c.s were not disrupted and phases of regular spiking activity (r.s.a.) were still seen after feeding.2. The r.s.a. phase could be recognized on the screen and in spot films from both fasting and fed pigs as a band of intense rhythmic contractions pinching off the intestine and propelling all intestinal contents ahead of it. The r.s.a. moved caudad clearing the small intestine of digesta and leaving an empty quiescent intestine behind it. It was particularly characteristic in the fasted pig where it was usually associated with the progression of a gas bubble. 6. Two patterns of transport into the large intestine were seen. Usually digesta was transported by peristaltic rushes starting 100-200 cm from the ileo-caecal junction. The rush then continued through 1-11 turns of the spiral colon; occasionally the terminal ileum emptied by slow peristalsis. In this case there was no colonic rush and digesta went into the caecum.
SUMMARY1. The physiology of the internal anal sphincter of the vervet monkey was investigated.2. Strips of sphincter in vitro contracted to noradrenaline and adrenaline; adrenoceptors were mainly a-excitatory. Strips of rectal circular muscle relaxed to noradrenaline and contained both inhibitory a-and fi-adrenoceptors.3. All strips contracted to acetylcholine. After hyoscine or atropine, high doses of acetylcholine relaxed all strips by stimulating intramural inhibitory neurones as relaxations were blocked by tetrodotoxin and hexamethonium. Nicotine and DMPP gave relaxations with similar characteristics.4. It was concluded that relaxations to acetylcholine, nicotine and DMPP were not adrenergic as relaxations still occurred in strips from sympathetically denervated or reserpinized animals. The block of these relaxations by propranolol and guanethidine was considered to be unrelated to their actions as adrenergic blocking drugs.5. All strips relaxed to field electrical stimulation (1-5 Hz) through stimulation of intramural inhibitory neurones as tetrodotoxin blocked these relaxations. Adrenergic blocking drugs, prior reserpinization or prior section of the hypogastric nerves did not block these responses. The relaxations were not therefore adrenergic.6. 5-Hydroxytryptamine relaxed all strips but was not the transmitter in relaxations to acetylcholine, DMPP or nicotine, nor to field electrical stimulation, as desensitization of strips to 5-HT did not alter these responses.7. The circular smooth muscle of the internal anal sphincter had a dense terminal adrenergic innervation which rapidly decreased orad.8. In vivo, hypogastric nerve stimulation relaxed the rectum but contracted the sphincter. Sacral nerve root stimulation caused an after-contraction in both rectum and sphincter. In vivo, a close arterial injection of adrenaline or noradrenaline inhibited the spontaneous contraction waves of the rectum, but contracted the sphincter. Both these responses were blocked by phentolamine. 9. It was concluded that the internal anal sphincter is a discrete high pressure zone which has excitatory cholinergic and adrenergic innervations and an inhibitory non-adrenergic innervation.
The effect of insulin on the myoelectric activity of the small intestine was determined in conscious pigs. Animals were implanted with electrodes along the small intestine, a strain gage on the stomach and catheters in both saphenous arteries. Feeding modified the migrating myoelectric complex (MMC), a cyclic pattern of action potential activity of the small intestine characteristic of fasting. The first period of regular spiking activity (RSA) on the duodenum after feeding was delayed and was not followed by quiescence. Plasma insulin and glucose concentrations during the first three MMC after feeding were highest just before periods of duodenal RSA. Injection or infusion of insulin into fasted pigs with production of hypoglycemia caused disruption of stomach motility and duodenal electrical activity. The duodenal MMC was not altered when glucose to prevent hypoglycemia was infused together with insulin or when glucose was infused alone. These studies suggest that insulin is not directly responsible for the postprandial modification of MMC activity as insulin infusions only modify the MMC when hypoglycemia occurs.
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