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Biomedical subjects

F S Kraly

Publications and source records attributed to F S Kraly.

At least 37 records · Page 2Linked to original sources
PubMed1984

Preabsorptive pregastric vagally mediated histaminergic component of drinking elicited by eating in the rat.

Preabsorptive stimulation by food was confined to the pregastric (oropharynx and esophagus) segment of the gastrointestinal tract by having male Sprague-Dawley rats sham feed liquid food which then drained out a gastric cannula. This procedure provided a paradigm for studying the effect of preabsorptive pregastric food-contingent stimulation on drinking behavior. Sham feeding elicited drinking that was (a) attenuated by complete bilateral subdiaphragmatic vagotomy (with hepatic branch intact), (b) attenuated by peripheral cholinergic blockade with intraperitoneal atropine methyl nitrate (0.25 mg/kg), and (c) abolished by combined antagonism of H1 and H2 histamine receptors with the use of intraperitoneal dexbrompheniramine (1 mg/kg) and cimetidine (16 mg/kg). These results provide evidence for a preabsorptive pregastric vagally mediated histaminergic component of drinking elicited by eating in the rat.

Animals↗
PubMed1984

Vagotomy does not alter cholecystokinin's inhibition of sham feeding.

Verified bilateral abdominal vagotomy (with hepatic branch intact) did not alter the ability of 20% pure cholecystokinin (CCK) or octapeptide of cholecystokinin (CCK-8) to inhibit sham feeding of liquid diet in dose-response studies for male Sprague-Dawley rats with open gastric fistula. In light of previous reports that 1) abdominal vagotomy blocks the satiety effect of exogenous CCK-8 on real feeding in intact rats and 2) inhibition of sham feeding requires seemingly supraphysiological doses of exogenous CCK or CCK-8, these findings show that the inhibition of sham feeding by CCK and the inhibition of real feeding by CCK are different. This limits the utility of the sham-feeding preparation for examining mechanisms for the satiety action of CCK.

Animals↗
PubMed1983

Histamine plays a part in induction of drinking by food intake.

Drinking occurs around meal time in most mammals. Food-related drinking accounts for approximately 70% of daily fluid intake for rats, but little is known of the mechanisms by which eating elicits drinking. That eating and vagal stimulation elicit the release of histamine from gastric mucosa, together with the fact that drinking elicited by eating or exogenous histamine depends on an intact abdominal vagus, suggests a role for endogenous histamine as a component of food-related drinking in the rat. I report here that the combined antagonism of peripheral H1 and H2 receptors for histamine (1) attenuates drinking elicited by normal food-contingent stimulation of the gastrointestinal tract and (2) abolishes drinking elicited by pregastric food-contingent stimulation during sham feeding in the rat.

Animals↗
PubMed1983

A probe for a histaminergic component of drinking in the rat.

Systemic antagonism of H1 or H2 receptors for histamine attenuated drinking elicited by SC 20 mg/kg histamine in adult male Sprague-Dawley rats. The H1 antagonist dexbrompheniramine (DXB; 0.5-16 mg/kg) and the H2 antagonist cimetidine (C; 0.5-100 mg/kg) each inhibited drinking elicited by histamine when given IP 10 min prior to SC histamine: The lowest doses to produce a statistically significant inhibition of drinking were 2 mg/kg DXB and 32 mg/kg C. While 1 mg/kg DXB alone or 16 mg/kg DXB plus 16 mg/kg C virtually abolished drinking elicited by histamine (1.25-20 mg/kg) in a dose-response study. In addition, such combined antagonism of H1 and H2 receptors failed to elicit drinking in the absence of exogenous histamine and failed to inhibit drinking elicited by deprivation from water for 7 or 24 hr. Because combined systemic antagonism of H1 and H2 receptors can specifically and completely inhibit drinking elicited by exogenous histamine, these findings provide a probe for a histaminergic component of drinking in the rat.

Animals↗
PubMed1983

Histaminergic mechanism for drinking elicited by insulin in the rat.

Sprague-Dawley male albino rats showed in a dose-response study a maximal drinking response to a 5 U/kg dose of SC insulin in a 2-hr test. Drinking elicited by 5 U/kg insulin was reduced to baseline (i.e., no insulin) level by combined antagonism of H1 and H2 receptors for histamine using IP 1 mg/kg dexbrompheniramine plus 16 mg/kg cimetidine. Antagonism of histamine receptors in this fashion was specific for drinking elicited by histamine because such antagonism reduced to baseline level drinking elicited by 2.5 mg/kg SC histamine, but failed to inhibit drinking after 8- or 24-hr water deprivation or drinking after 0.63 mg/kg SC serotonin (5-HT). These results demonstrate a histaminergic mechanism for drinking elicited by exogenous insulin which is consistent with the published report that exogenous insulin can release gastric mucosal histamine in the rat. Moreover, because eating is known to elicit the release of endogenous insulin, the results reported here suggest a working hypothesis that endogenous insulin is a component for drinking around mealtime in the rat.

Animals↗
PubMed1983

Diurnal variation for inhibition of eating by bombesin in the rat.

Sprague-Dawley male albino rats ate sweet milk at the midpoint of the day or night phase of a 12:12 light/dark cycle 1 min after IP 0.9% NaCl or synthetic bombesin (BBS; 2-32 micrograms/kg) following 24-hr food deprivation. Exogenous BBS inhibited food intake in a dose-related manner during the day; a linear regression line accounted for 85% of the total variance for percentage suppression of food intake by BBS in 30 min. In contrast, inhibition of eating by BBS at night was not dose-related; a linear regression line accounted for only 16% of the variance. Rats were tested under identical conditions following 3-hr food deprivation. Exogenous BBS (4-64 micrograms/kg) inhibited food intake in a dose-related manner at night; a linear regression line accounted for 92% of the total variance. In contrast, inhibition of eating by BBS during the day was not as orderly; a linear regression line accounted for only 44% of the variance. The 8 micrograms/kg dose was twice as potent for inhibition of eating of 25% GIBCO 116EC liquid diet than it was for inhibition of eating sweet milk at the midpoint of the day phase. These results describe diurnal variation in potency of exogenous BBS for inhibition of food intake in the rat. Whether BBS is more or less potent at night than during the day depends upon the particular dose, degree of hunger of the rat, and probably the type of food being eaten.

Animals↗
PubMed1982

Histamine-elicited drinking is dependent upon gastric vagal afferents and peripheral angiotensin II in the rat.

While transection of either the anterior (including hepatic) or posterior (including coeliac) vagal trunk failed to alter drinking in response to subcutaneous histamine (0.312--20 mg/kg), selective gastric vagotomy severely attenuated drinking after systemic histamine (1.25--40 mg/kg) in male Sprague-Dawley rats. The dose-response curve for rats with gastric vagotomy was shifted to the right. Vagotomy increased the threshold dose nearly tenfold and more than doubled the ED50. Because the effect of vagotomy on histamine-elicited drinking was not mimicked by cholinergic blockade of vagal efferents using atropine methyl nitrate (10 mg/kg), these results demonstrate that gastric vagal afferents are necessary for a normal drinking response to systemic histamine. When gastric vagotomy was combined with intragastric SQ14,225 (to inhibit the conversion of peripheral angiotensin I to angiotensin II) drinking after systemic histamine was abolished. These results suggest that gastric vagal afferents and angiotensin II are necessary for systemic histamine to elicit drinking in the rat.

Angiotensin II↗
PubMed1982

A vagally mediated histaminergic component of food-related drinking in the rat.

Histamine elicited drinking in a dose-related manner typically within 5 min after subcutaneous injection in male albino rats. Threshold for increased drinking was 1.25 mg/kg, and 2.5 mg/kg elicited half of the maximal drinking response that followed 20 mg/kg. Histamine was not differentially potent for drinking in the day or night phase of the diurnal cycle. Bilateral subdiaphragmatic vagotomy, with the hepatic branch left intact, severely attenuated drinking in response to systemic histamine: Vagotomized rats drank later and less than did normal rats after doses of histamine between 1.25 and 40 mg/kg. This attenuation was attributed to the destruction of vagal afferent fibers because histamine-elicited drinking was not affected by blockade of vagal efferents with the peripheral anticholinergic atropine methyl nitrate. Drugs antagonistic to peripheral H2 histamine receptors specifically inhibited drinking in response to histamine: Intraperitoneal cimetidine or metiamide delayed and decreased drinking after sc histamine and temporarily decreased drinking after hypovolemia produced by sc polyethylene glycol, but these H2 antagonists failed to inhibit drinking after water deprivation, cellular dehydration, or isoproterenol. Finally, cimetidine or metiamide inhibited drinking in temporal association with a meal of liquid or solid food without decreasing food intake. These results constitute the first evidence for a peripheral histaminergic determinant of food-related drinking in the rat.

Afferent Pathways↗
PubMed1982

Nocturnal food-related hyperdipsia in the adult spontaneously hypertensive rat.

Male adult spontaneously hypertensive rats (SHR) ate the same but drank more and had a higher water to food ratio (W:F) than did Wistar-Kyoto (WKY) rats in 24-hr when they had continuous access to standard laboratory pellets and tap water. When rats ate in the day phase of a 12:12 light/dark cycle after 24-hr food deprivation, SHR rats ate and drank the same ad did WKY rats in a 60-min test. When the same rats ate at night after 24-hr food deprivation, however, SHR rats were hyperdipsic: They ate the same as did WKY rats, but SHR rats drank more and had a higher W:F. This relative hyperdipsia reflected the increased ability of ingestion of food to stimulate drinking in SHR, because when food was absent for a 60-min test at night SHR drank the same as did WKY rats. Three dipsogens which are candidate components for eating-elicited drinking in the rat, cellular dehydration, histamine and angiotensin II, elicited drinking differentially in SHR and WKY rats: SHR drank more than did WKY rats in response to (1) cellular dehydration produced by IP hypertonic saline, (2) large doses of SC histamine, and (3) SC angiotensin II. These results demonstrate that SHR exhibit a nocturnal food-related hyperdipsia which may reflect differential sensitivity to stimuli important for eating-elicited drinking such as increased osmolality and endogenous histamine or angiotensin.

Angiotensin II↗
PubMed1980

Nocturnal hyperphagia in the rat is characterized by decreased postprandial satiety.

Rats eat more at night than during the day. This work investigated whether this nocturnal hyperphagia is characterized by increased hunger, decreased postprandial satiety, or both. Rats were presented with liquid food after 3-hr food deprivation at the midpoint of the night or day phase of a 12:12 hr light/dark cycle. Quinine adulteration of food produced equal percentage suppression of first meal size (MS) and of 60-min intakes in the night and the day. This suggests that rats are equally hungry after 3-hr food deprivation in the night and the day. In contrast to apparently equal hunger, rats were less satiated by ingested food after 3 hr of food deprivation at night than during the day. This conclusion is based on the observations that the postprandial intermeal interval (IMI) was significantly shorter at night and that the satiety ratio (IMI/MS) was smaller at night. This nocturnal decrease in the satiating potency of ingested food was demonstrated for two specific preabsorptive satiety mechanisms: (a) the pregastric satiety mechanism(s) stimulated by sham feeding and (b) cholecystokinin, the putative satiety hormone released by food contacting the mucosal surface of the upper small intestine. All the results suggest that the diurnal variation of food intake in rats is primarily the result of diurnal variation in the potency of postprandial satiety mechanisms.

Animals↗
PubMed1978

Abdominal vagotomy disrupts food-related drinking in the rat.

Rats with complete subdiaphragmatic bilateral transection of the abdominal vagus (Vgx-C) showed disordered food-related drinking when drinking water in temporal association with a meal of dry food after 5-hr food deprivation and when drinking water in association with a liquid meal after 24-hr food deprivation. The Vgx-C rats drank after significantly longer latencies and drank significantly less water in 1 hr than did sham-vagotomized (Sham) rats after eating the same size meal (solid or liquid) as Shams. Rats with incomplete vagal transection (Vgx-I) ate and drank like Shams. Water intake of Sham and Vgx-I rats correlated positively with the meal size of solid food, but the water intake of Vgx-C rats did not. The failure of Vgx-C rats to drink water normally when food was ingested was not due to failure of a food stimulus to reach the intestine, because Vgx-C and Sham rats emptied equivalent volumes of liquid food from the stomach into the intestine within 10 min of food entering the stomach. These results indicate that the abdominal vagus is an important neurological substrate for food-related drinking in the rat.

Animals↗
PubMed1978

Effect of cholecystokinin on meal size and intermeal interval in the sham-feeding rat.

After 3-hr food deprivation, rats with gastric fistulas ate liquid food with the fistula closed (normal feeding) or open (sham feeding). Meal size (MS) was larger, latency to rest (LR) after a meal was longer, and intermeal interval (IMI) was shorter during sham feeding than during normal feeding. The putative satiety signal cholecystokinin (CCK, 20% pure) decreased MS and LR and increased IMI during sham feeding. After CCK (30 U/kg) the MS, LR, and IMI were the same during sham feeding as during normal feeding. The synthetic octapeptide (OCT) of CCK, which has the known biological actions of the complete hormone, reproduced the effects of CCK (30 U/kg) on MS and LR but not on IMI. Ingestive behavior was not nonspecifically suppressed by CCK or OCT because water drinking was not inhibited by CCK or OCT. The CCK and OCT were also tested for their ability to serve as unconditioned stimuli (UCS) for the formation of a conditioned taste aversion (CTA) in the 3-hr food-deprived sham-feeding rat. The OCT (30 U/kg) did not serve as a UCS for a CTA in the same sham-feeding conditions in which OCT produced normal MS and LR. Impure CCK (30 U/kg), however, did serve as a UCS for a CTA under these conditions. The differential effectiveness of CCK and OCT for IMI and CTA may be due to non-CCK factors in the impure extract of CCK. These experiments demonstrate that the preabsorptive food-contingent stimuli of sham feeding plus exogenous CCK are sufficient for normal short-term satiety under certain conditions, and they provide further evidence consistent with the hypothesis that cholecystokinin produces satiety in rats.

Animals↗