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Biomedical subjects

F S Kraly

Publications and source records attributed to F S Kraly.

At least 19 recordsLinked to original sources
PubMed1991

Separate controls for conditioned cephalic phases of acid secretion and drinking in the rat.

Adult male Sprague-Dawley rats, surgically equipped with a stainless steel gastric cannula, were tested in a paradigm known to support conditioning of cephalic phase gastric acid secretion. Rats were tested first under (a) baseline conditions--prepared to sham feed, but no food was offered and none should have been expected; then (b) 5 conditioning trials--prepared and allowed to sham feed sweetened milk; and finally (c) extinction trials--prepared to sham feed milk, but milk was not offered. Combined antagonism of H1 and H2 histamine receptors (using intraperitoneal dexbrompheniramine plus cimetidine) prevented the acquisition of conditioned cephalic phase of acid secretion, but had no effect on acquisition of conditioned water intake. Such histaminergic antagonism also blocked the expression of an established conditioned acid secretory response without effect on conditioned water intake; peripheral cholinergic blockade using atropine methyl nitrate had virtually the same effect as did histaminergic antagonism. The converse was observed following blockade of angiotensin II synthesis using subcutaneous captopril: Established conditioned secretion was unaffected, but conditioned water intake was inhibited. These results dissociate the physiological controls for conditioned responses which occur simultaneously in rats anticipating eating: Peripheral histamine mediates the acquisition and expression of the conditioned cephalic phase of acid secretion, whereas angiotensin II appears to mediate at least the expression of conditioned water intake.

Angiotensin II↗
PubMed1990

Histamine in brain may have no role for histaminergic control of food-related drinking in the rat.

Adult male Sprague-Dawley rats surgically fitted with a cannula positioned in the third cerebral ventricle were tested for drinking after exogenous histamine or after eating with or without antagonism of H1 and/or H2 receptors for histamine using intracerebroventricular (ICV) dexbrompheniramine (DXB; 12.5-50 micrograms) or cimetidine (C; 25-100 micrograms). Histamine (0.06-16 micrograms) given ICV failed to elicit drinking. For rats drinking in response to subcutaneous (SC) histamine, ICV DXB alone did not affect drinking, whereas ICV DXB plus C, and ICV C given alone inhibited drinking. Such inhibition appeared to be relatively selective for drinking elicited by SC histamine, because ICV 50 micrograms DXB plus 100 micrograms C abolished drinking elicited by SC histamine, but failed to inhibit drinking after 12-hr water deprivation. When rats ate and drank after food deprivation, ICV DXB alone and ICV DXB plus C did not significantly inhibit food-related water intake. The inhibition of food-related drinking by ICV 100 micrograms C given alone was accompanied by inhibition of eating. In summary, histamine had unimpressive dipsogenic effects when given ICV, ICV DXB and C inhibited drinking elicited by SC histamine, but ICV DXB and C failed to inhibit food-related drinking in a manner parallel to the selective effects of intraperitoneal injection of these drugs on drinking elicited by eating. This suggests that it is histamine and histamine receptors in the periphery rather than in brain that have the predominant role for a histaminergic mechanism for drinking elicited by eating in the rat, but our findings do not rule out a role(s) for histamine in brain in the control of ingestive behavior.

Animals↗
PubMed1990

Pregastric food-contingent stimulation elicits drinking in the absence of systemic dehydration in the rat.

Adult male Sprague-Dawley rats surgically fitted with a stainless steel gastric cannula were prepared following 24-h food deprivation for sham feeding liquid diet with open gastric fistula. Sham feeding (pregastric food-contingent stimulation) of 5, 10, 20 or 40 ml of liquid diet elicited water intake that was not in proportion to volume of liquid diet sham fed. Rats sham feeding between 1 and 68 ml of sweetened milk showed no evidence of cellular or extracellular dehydration as measured by plasma osmolality and hematocrit, respectively. Subcutaneous injection of 100 mg/kg captopril, a dose sufficient to block conversion of angiotensin I to angiotensin II in brain and periphery, inhibited drinking elicited by sham feeding without effect on sham feeding. These results demonstrate that pregastric food-contingent stimulation elicits water intake that is not in proportion to amount of liquid diet sham fed and that occurs in the apparent absence of systemic dehydration. That such drinking could depend upon endogenous angiotensin II provokes consideration of a role for angiotensin II in the mediation of a pregastric (perhaps histaminergic) mechanism that initiates drinking in advance of postprandial dehydration.

Angiotensin II↗
PubMed1990

Angiotensin II mediates drinking elicited by eating in the rat.

Captopril (CA) was used to block synthesis of endogenous angiotensin II (ANG II) in periphery and/or brain of adult male Sprague-Dawley rats in tests for drinking elicited by eating pelleted chow. Blockade of ANG II-converting enzyme (ACE) in periphery alone (using 0.5 mg/kg CA) increased drinking elicited by eating, whereas simultaneous blockade of ACE in periphery and brain (using subcutaneous 100 mg/kg CA or subcutaneous 0.5 mg/kg plus third ventricular 25 micrograms CA) decreased such drinking. The inhibitory effect of 100 mg/kg CA on water-to-food ratio was prevented by a dipsogenically subthreshold subcutaneous dose (5 micrograms/kg) of ANG II. Blockade of ACE in brain alone (third ventricular 25 micrograms CA) had no effect on food-related drinking. Pharmacological antagonism of ANG II (100 mg/kg CA) together with antagonism of histamine H1 and H2 receptors (using intraperitoneal dexbrompheniramine and cimetidine) were not additive in their inhibitory effects on drinking elicited by eating. Blockade of ACE (100 mg/kg CA) inhibited drinking elicited by subcutaneous histamine, but blockade of histamine receptors failed to inhibit drinking elicited by subcutaneous ANG II. These results support a role for endogenous ANG II under what appear to be physiological conditions for drinking behavior, i.e., when drinking is elicited by eating, and they suggest the working hypothesis of ANG II mediation of a histaminergic mechanism for food-related drinking in the rat.

Angiotensin II↗
PubMed1986

Specific postoperative syndromes after total and selective vagotomies in the rat.

Male Sprague-Dawley rats which survived bilateral subdiaphragmatic vagotomy (with hepatic branch intact) exhibited an acute syndrome of hypophagia, hypodipsia and severe loss of body weight when maintained on solid food and water for 14 days after vagotomy. This postvagotomy syndrome was attenuated when rats were maintained on a liquid diet (116EC) chosen to minimize postvagotomy dysphagia and abnormal gastric retention of food; vagotomized rats were hypophagic and lost body weight, but the degree of weight loss was not so severe as for vagotomized rats eating solid food. When rats with total subdiaphragramatic vagotomy were maintained on palatable sweet milk food, the acute postvagotomy syndrome was abolished; these vagotomized rats ate and drank as much as rats with sham vagotomy and they did not lose weight. When rats that underwent selective hepatic, gastric or coeliac vagotomy were maintained on the sweet milk diet, three different postoperative syndromes occurred: after selective hepatic vagotomy, rats were hyperphagic, hyperdipsic and gained body weight at a greater than normal rate; after selective gastric vagotomy, rats lost weight despite relatively normal food and water intakes; and after selective coeliac vagotomy, there was no change in food or water intakes or body weight. These results demonstrate that a sweet milk diet abolishes the anorexia, hypodipsia and weight loss that usually occur in vagotomized rats maintained on pellets and water. Use of this sweet milk diet revealed different acute syndromes after bilateral and selective vagotomies. The differences among the syndromes suggest that hepatic, gastric and coeliac vagal branches serve different functions in the control of food and water intake and body weight.

Animals↗
PubMed1985

Histamine and serotonin independently elicit drinking in the rat.

Drinking elicited by SC histamine or serotonin (5-HT) was studied in Sprague-Dawley male rats following 0.9% NaCl or combined antagonism of H1 and H2 histamine receptors using dexbrompheniramine (DXB) and cimetidine (C), or following antagonism of 5-HT receptors using methysergide (M). Histaminergic antagonism using IP 1 mg/kg DXB plus 16 mg/kg C abolished drinking elicited by SC 2.5 mg/kg histamine, but it failed to inhibit drinking elicited by the ED50 or by the ED100 for SC 5-HT in the same rats. Serotonergic antagonism using IP 3 mg/kg M abolished drinking elicited by SC 0.63 mg/kg 5-HT, but it failed to inhibit drinking elicited by the ED50 or by the ED100 for SC histamine in the same rats. These findings demonstrate that activation of peripheral 5-HT receptors is not necessary for SC histamine to elicit drinking and that activation of peripheral histamine receptors is not necessary for SC 5-HT to elicit drinking. This demonstrates that histamine and 5-HT activate different receptors to elicit drinking in the rat. The finding that the ED50 for histamine and the ED50 for 5-HT are not additive in their effects on drinking is consistent with the notion that a single mechanism mediates the dipsogenic effects of SC histamine and SC 5-HT in the rat.

Animals↗
PubMed1985

Histamine plays no part in schedule-induced polydipsia in the rat.

Twelve Sprague-Dawley male albino rats were tested with or without combined antagonism of peripheral H1 (using 2 mg/kg dexbrompheniramine IP) and H2 (using 32 mg/kg cimetidine IP) receptors for histamine prior to (a) drinking after 2.5 mg/kg histamine SC, (b) drinking after 24-hr water deprivation, and (c) drinking during the acquisition and maintenance of schedule-induced polydipsia (SIP) with a 45 mg Noyes pellet delivered every 90 sec. Such antagonism of histamine receptors abolished drinking elicited by exogenous histamine without inhibiting drinking after water deprivation. Moreover, histaminergic antagonism failed to prevent the acquisition and maintenance of SIP and failed to alter the distribution of contacts with the drinking spout during interpellet intervals. These findings demonstrate no role for endogenous systemic histamine in SIP.

Animals↗
PubMed1985

Histamine: a role in normal drinking.

Little is known about the physiological mechanisms that control normal drinking and, in particular, drinking around mealtime. This problem has recently been penetrated by experiments evaluating a role for histamine in drinking elicited by eating. This work supports the hypothesis of a preabsorptive, pregastric, vagally-mediated, histaminergic component of drinking elicited by eating in the rat.

Animals↗
PubMed1985

Disordered drinking in developing spontaneously hypertensive rats.

Eating and drinking in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were measured at 5-17 wk of life. The SHR drank significantly more water in 24 h than WKY as early as wk 9, spilled more dry food than did WKY, and exhibited an inverse relation between 24-h water intake and dry food spilled. When eating a meal of dry food after 12 h food deprivation, SHR drank earlier and drank more in a 1-h test than WKY rats. Moreover, SHR exhibited (as early as wk 7) a striking pattern of interrupting eating to drink. This pattern was not present when SHR ate liquid food, and it was attenuated by infusion of water through a cheek fistula. Adult SHR (22 wk) salivated less than WKY in response to intraperitoneal 3.25 mg/kg pilocarpine nitrate. When developing SHR and WKY were maintained on liquid and solid food, SHR gained disproportionately more weight than WKY during development. When young SHR were permitted to drink no more water than WKY rats, the development of hypertension was retarded, and body weight gain was slowed. Because restricted access to food, which produced an equivalent slowing of body weight gain as did restricted access to water, also retarded development of hypertension, it appears that restricted access to water retards development of hypertension due to delayed growth. These results demonstrate that hyperdipsia, apparently caused by deficient salivary function, is not necessary for the development of hypertension in SHR.

Animals↗
PubMed1984

Histamine plays a major role for drinking elicited by spontaneous eating in rats.

The effects of combined antagonism of H1 (using 1 mg/kg dexbrompheniramine IP) and H2 (using 16 mg/kg cimetidine IP) receptors for histamine prior to (a) drinking after 2.5 mg/kg histamine SC, (b) drinking after 1-hr water deprivation, and (c) drinking during spontaneous eating were examined at 1 hr into the dark phase of a 12:12'-hr light/dark cycle for 14 Sprague-Dawley male rats. Such antagonism of histamine receptors abolished drinking elicited by exogenous histamine without affecting drinking after water deprivation. Histaminergic antagonism did not affect spontaneous eating, but it appeared to abolish drinking prior to a meal (for only those 3 rats which exhibited such drinking), delayed the latency to initiate drinking after initiating a meal, and inhibited drinking which occurred during and after eating but prior to postprandial resting (i.e., satiety for food). Because antagonism of peripheral histamine receptors inhibited food-related drinking by over 60%, these results provide indirect support for the hypothesis that the preabsorptive food-contingent vagally-mediated release of gastric mucosal histamine plays a major role in spontaneous food-related drinking in the rat.

Animals↗
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↗