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Biomedical subjects

L L Shanbour

Publications and source records attributed to L L Shanbour.

At least 37 records · Page 2Linked to original sources
PubMed1977

Effects of dopamine on endotoxin and hemorrhagic shock in the canine stomach.

Studies were conducted to evaluate the effects of dopamine on gastric electrophysiopathology in endotoxin and hemorrhagic shock. Intraarterial infusion of dopamine (15.5 or 31 microgram/kg/min) in the in vivo stomach preparation produced an immediate decrease in electrical potential difference (PD), which then returned and exceeded control values. No changes in resistance (R) and blood pressure were observed. These electrophysiological responses of the gastric mucosa to dopamine are very similar to the actions of epinephrine. The in vitro studies demonstrated that active transport of Na+ was stimulated with an addition of dopamine or epinephrine (2 X 10(-4) M) to the serosal solutions of the isolated gastric mucosa. In addition, the in vivo studies demonstrated that both 40% hemorrhage and 1 mg/kg of endotoxin given as an intravenous bolus decreased PD and blood pressure and increased R although dopamine was continuously infused intraarterially for 60 minutes prior to and following hemorrhage or endotoxin. Administration of endotoxin at the onset of dopamine infusion decreased both blood pressure and PD initially. While PD showed a complete recovery at a later stage, blood pressure never returned to control levels. These results, combined with previous observations, suggest that: 1) dopamine has no beneficial action on the gastric mucosa during hemorrhagic or endotoxin shock; 2) dopamine acts on the electrophysiology in vivo and Na+ fluxes in vitro in the gastric mucosa in a manner similar to epinephrine; and 3) decrease in blood flow may be responsible for the observed decrease in transmural PD after dopamine and epinephrine in vivo.

Animals↗
PubMed1976

Dopamine effects on the intestinal circulation.

The effects of intra-arterial infusion of dopamine on superior mesenteric artery blood flow, intestinal flow, intestinal oxygen consumption, and capillary density were studied in anesthetized dogs before and after blockade of dopamine receptors with haloperidol and after beta-adrenergic receptor blockade with propranolol. Mesenteric blood flow to a distal segment of the small intestine was measured with an electromagnetic blood flow-meter and intestinal oxygen consumption was calculated from the measured arteriovenous oxygen difference across the intestine and total blood flow. Intestinal capillary density was estimated from the clearance of 86Rb. In normal animals prior to dopaminergic or beta-adrenergic blockade, dopamine caused a dose-related decrease in mesenteric blood flow, intestinal oxygen consumption, and 86Rb clearance. Only the lowest dose of the drug, 1 mug/Kg.-min., did not significantly change the intestinal capillary density. In dogs pretreated with the dopamine receptor, antogonist, haloperidol, dopamine (20 mug/Kg.-min.) caused a significant increase in blood flow and oxygen consumption and did not significantly alter the number of perfused intestinal capillaries. These increases in haloperidol-blocked animals administered dopamine were reversed by propranolol. Our results indicate that dopamine caused smooth muscle contraction in mesenteric arterioles and precapillary sphincters, thereby producing intestinal ischemia and hypoxia. These findings with haloperidol and propranolol indicate that dopamine stimulates at least two different receptors in the canine mesenteric vascular bed: a constrictor receptor blocked by haloperidol and a dilator receptor blocked by propranolol.

Blood Pressure↗
PubMed1976

Mechanism of action of aspirin on canine gastric mucosa.

Using an in vivo chambered canine stomach preparation, exposure of the gastric mucosa to 5, 10, and 20 mM aspirin(pH 3.0) resulted in a decrease in electrical potential difference (PD) and in an increase in resistance (R) within 30 min. In vitro, exposure of the mucosal side of the isolated canine gastric mucosa to 5, 10, and 20 mM aspirin (pH 3.0) for 1 h or of 1 mM aspirin (pH 3.0) for longer than 1 h resulted in marked permeability changes, i.e., increases in the undirectional fluxes of Na+ and Cl-, as well as inhibition of net ion fluxes. These concentrations of nonionized aspirin (pH 3.0) also reduced the R and PD. However, 1 mM aspirin (pH 3.0) or 20 mM ionized aspirin (pH 7.4) depresses the active transport of ion, increases R, but does not increase the ionic permeability. Mucosal adenosine triphosphate (ATP) content is reduced by mucosal instillation of aspirin (pH 3.0). These results demonstrate that the initial action of aspirin is inhibition of ion transport which is followed by an increase in permeability.

Animals↗
PubMed1976

Inhibition of ion transport by bile salts in canine gastric mucosa.

Studies were conducted with in vivo and in vitro canine stomach preparations. Instillation of 5, 10, and 20 mM bile salts in TES bufer (pH 7.4) into the nonsecreting stomach in vivo caused a progressive decrease in electrical potential difference (PD) and an increase in electrical resitance (R). The rate of acid secretion, determined by the pH-stat method in the histamine-stimulated stomach, decreased with 5 and 20 mM bile salts. Mucosal adenosine triphosphate (ATP) content of the nonsecreting or secreting stomach was reduced by bile salts. In vitro flux studies demonstrated that within the first hour after 1 mM bile salts were added to the mucosal side of the chamber, PD decreased, R increased, and net sodium transport decreased. In the second hour, unidirectional fluxes of sodium increased, indicating an increase in permeability of the gastric mucosa to sodium. These results demonstrate that the initial action of bile salts is inhibition of ion transport, which is followed by an increase in permeability.

Adenosine Triphosphate↗
PubMed1975

Reversibility of effects of very hypotonic fluids on in vitro frog gastric mucosa: a functional and morphological study.

Functional and morphological properties of the in vitro frog gastric mucosa were studied during and after exposure to very hypotonic (approximately 25 mOs M) solutions. Within 20 min the acid secretory rate decreased to zero, but it returned to normal levels after isotonic fluids had been restored. The potential difference (PD) dropped within the first minutes after the exposure to hypotonic solutions, and became inverted. Following the return of isotonic conditions the PD increased to levels higher than in the controls. The electrical resistance increased about 10-fold during the hypotonic period, but decreased to near normal values when isotonic conditions were restored. By light and electron microscopy the cells of the hypotonic mucosae appeared greatly swollen, and the alterations were assessed by morphometric methods. The gland lumina were almost obliterated, and the lamina propria was reduced to about 63% of its former volume. After the return to isotonic conditions normal morphology was restores. It is conceivable that the great increase in resistance duroing the hypotonic period was caused by the occlusion of the gland lumina. Quantitative analyses of the Na, K, and Cl tissue concentrations indicated a large loss of these ions during the hypotonic state. Presumably the epithelial cells in the hypotonic mucosae avoid bursting by rapidly letting large numbers of ions exit, which results in a celulular osmolarity close to that of the bathing fluids.

Animals↗
PubMed1975

Electrophysiological effects of burimamide and 16,16-dimethyl prostaglandin E2 on the canine gastric mucosa.

The electrophysiological effects of two potent inhibitors of gastric acid secretion, burimamide and 16,16-dimethyl prostaglandin E2 (dm-PGE2), were determined in an in vivo histamine-stimulated canine stomach preparation and an in vitro canine gastric mucosal preparation. In the in vivo stomach preparation, intravenous burimamide caused a decrease in acid secretion, an increase in transmucosal potential difference (PD) and the relative resistance (R) was essentially unchanged. Intravenous dm-PGE2 also inhibited acid secretion and increased PD but, in contrast to burimamide, increased R. In the in vitro preparation, the unidirectional flux of sodium from mucosa to serosa increased after dm-PGE2 but not after burimamide. Passive sodium fluxes and unidirectional chloride fluxes were not altered after either agent. These findings suggest that increased active transport of sodium from mucosa to serosa is at least partially responsible for the observed increase in transmural PD with dm-PGE2, an agent which also decreases hydrogen ion transport. With burimamide the increased PD was due primarily to inhibition of hydrogen ion secretion.

Animals↗
PubMed1975

Modulation of stimulated acid secretion by dibutyryl cyclic AMP in the dog stomach.

An in vivo canine gastric chamber preparation was used to determine effects of exogenous cyclic AMP and dibutyryl cyclic AMP on histamine-driven acid secretion and the role of blood flow in these responses. Histamine was infused intravenously at a submaximal rate 1.2 mu/kg-min) followed by the intraarterial infusion of either cyclic AMP (0.15 mg/kg-min) or dibutyryl cyclic AMP (0.15 mg/kg-min. Acid secretion and mucosal blood flow (aminopyrine clearance) were measured at 15-minute intervals, and electrical potential difference was measured continuously. Histamine alone decreased the potential difference from 82 mV to 48 mV within 60 minutes, increased aminopyrine clearance from 1.0 ml/min to 2.4 ml/min and increased acid output to 220 muEq/15 min. All values returned towards control following termination of histamine infusion. Dibutyryl cyclic AMP significantly increased histamine stimulated acid secretion to 350 muEq/15 min, but did not alter mucosal blood flow or electrical potential. Cyclic AMP did not change secretory, circulatory or electrical response to histamine. Therefore, dibutyryl cyclic AMP appears to increase histamine-stimulated acid secretion, and the effect is not mediated by increased mucosal blood flow.

Aminopyrine↗