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Biomedical subjects

D W Powell

Publications and source records attributed to D W Powell.

At least 91 records · Page 5Linked to original sources
PubMed1978

Cholinergic-adrenergic interactions on intestinal ion transport.

The autonomic control of intestinal electrolyte transport has been investigated in the in vitro, short-circuited rabbit ileum with varying doses of carbachol and with neuroeffector blocking agents. Low-dose carbachol (less than 10(-6) M) and high-dose carbachol (greater than 10(-4) M) had different effects on Na and Cl transport. Low-dose carbachol caused a transient increase in the potential difference and short-circult current, stimulated Cl secretion, and inhibited the residual flux (probably HCO3 secretion). This is a muscarinic response since it is inhibited by atropine (10(-6) M). After an initial increase of the potential difference and short-circuit current, high-dose carbachol reduced these electrical parameters, stimulated Na and Cl absorption, and abolished the residual flux. This is a nicotinic response since it is inhibited by hexamethonium (10(-5) M). This nicotinic response is identical to that reported by others with alpha-adrenergic agents and it was inhibited also by phentolamine (10(-7) M). We propose that high-dose carbachol stimulates nicotinic receptors on postganglionic sympathetic fibers present in our preparations causing a release of catecholamines and a resulting alpha-adrenergic response by the intestinal epithelial cell. The physiological significance of this response in the gut remains to be determined.

Animals↗
PubMed1978

Prolonged treatment of menetrier's disease with an oral anticholinergic drug.

There is considerable evidence, both in patients with Menetrier's disease and from animal models of protein-losing gastropathy, that antisecretory drugs can acutely decrease or abolish gastric plasma protein shedding. Serial measurements on serum protein components were performed in a patient with Menetrier's disease before, during, and after long term treatment with propantheline bromide. Total serum protein concentration increased significantly during the treatment period from 4.3 +/- 0.50 to 5.9 +/- 0.55 g per dl during treatment, while albumin increased from a pretreatment value of 2.5 +/- 0.12 to 3.4 +/- 0.16 g per dl. The improvement in serum proteins and symptoms continued after therapy was stopped. Intensive anticholinergic drug therapy should be tried in this disease before resorting to gastrectomy.

Administration, Oral↗
PubMed1978

Transmural electrical potential difference in the mammalian esophagus in vivo.

A simple, safe, accurate, and reproducible technique for measuring the transmural electrical potential difference (PD) of the esophagus has been developed. This technique, a modification of those previously used, allows simultaneous correlation of the PD profile with the pressure profile obtained during routine manometry. With this technique, a subcutaneous reference bridge was shown to detect accurately a lumen-negative electrical orientation for the esophageal PD in three species: rabbit, opossum, and man. A characteristic and reproducible PD profile was present for each species. In the rabbit the gastric PD was low,--12 mv, relative to the body of the esophagus,--26 to -29 mv. In contrast, both opossum and man had relatively high gastric PD's ( -36 to -43 mv) when compared to esophageal PD's ( -12 to -25 mv). In the rabbit and opossum, the PD in the lower esophageal sphincter ( -5 to -6 mv) was less than both gastric or esophageal PD's, whereas in human beings the lower esophageal sphincter PD ( -22 mv) was between gastric and esophageal values. In vitro PD measurements and histological studies of opossum esophagus revealed differences in the epithelium which correlated with the different in vivo PD's.

Adult↗
PubMed1976

Effects of cholera toxin on cellular and paracellular sodium fluxes in rabbit ileum.

The diarrhea observed in patients with cholera is known to be related to secretion of water and electrolytes into the intestinal lumen. However, the exact mechanisms involved in these secretory processes have remained unclear. Although it is clear that purified toxin acts on epithelial cell metabolism, its activity on Na+ transport across intestinal mucosa is equivocal: reported either to prevent net Na+ absorption or to cause net secretion of Na+ from serosa to mucosa. Since total transmural Na+ fluxes across "leaky" epithelia involve very significant movement via a paracellular shunt pathway, we studied the effects of cholera toxin on the cellular and paracellular pathways of Na+ movement. Unidirectional Na+ fluxes were examined as functions of applied potential in control tissues and in tissues from the same animal treated with purified cholera toxin. Treatment of rabbit ileum in vitro with toxin simulated the cellular component of serosa-to-mucosa Na+ flux (from 2.41 +/- 0.49 muequiv./h per cm2 under control conditions to 4.71 +/- 0.43 muequiv./h per cm2 after treatment with toxin, P less than 0.01). The effect of cholera toxin on Na+ movement through the cells from mucosa to serosa appeared to be insignificant. Finally, a marked decrease in the Na+ permeability (P less than 0.01) and no detectable significant changes in transference number for Na+ of the paracellular shunt pathway were observed following treatment with cholera toxin. These results provide direct evidence for the hypothesis that purified cholera toxin stimulates active sodium secretion but has minimal effect on sodium absorption.

Animals↗
PubMed1976

Effect of aspirin on normal and cholera toxin-stimulated intestinal electrolyte transport.

The effect of aspirin on normal and cholera toxin-stimulated electrolyte transport has been investigated in vitro, because this drug appears to inhibit cholera toxin-induced intestinal secretion in in vivo animal models. In the Ussing chamber, 10 mM aspirin decreased the control rabbit ileal potential difference and short-circuit current by 50% and increased conductance by 28%. Bidirectional electrolyte flux determinations showed that aspirin significantly increased both Na and Cl absorption and reduced flux (which probably represents HCO3 secretion) to zero. This effect of aspirin appears to be identical to that reported to others with catecholamines as determined with similar techniques. However, alpha-adrenergic blockers did not prevent the electrical effects of aspirin, suggesting that aspirin does not have its effect through release of tissue stores of catecholamines. In the presence of aspirin, cholera toxin increased the potential difference and short-circuit current, and decreased the conductance of rabbit ileum in a fashion qualitatively similar to control tissues. However, aspirin reversed cholera toxin-stimulated Na transport from secretion to absorption, inhibited cholera toxin, induced Cl secretion by 58% and partially, but not significantly, inhibited HCO3 secretion. Thus, the inhibitory effect of aspirin on cholera toxin-induced electrolyte secretion appears to be due to aspirin-stimulated Na and Cl absorption. Although aspirin reduced tissue cyclic AMP concentrations in normal and cholera toxin-stimulated ileum, it also inhibited the electrolyte secretion induced by exogenous cyclic AMP. Thus, if aspirin's stimulatory effect on sodium and anion absorption in normal tissue and its inhibitory effect on cholera toxin-stimulated sodium and anion secretion involves a cyclic AMP-mediated system, the effect must be a step distal to cyclic AMP production or degradation. The exact mechanism of aspirin's effect on normal and cholera toxin-induced electrolyte transport, and its possible usefulness in the treatment of cholera diarrhea, remains to be determined.

Animals↗
PubMed1975

Water and electrolyte transport by rabbit esophagus.

The nature of the transmural electrical potential difference and the characteristics of water and electrolyte transport by rabbit esophagus were determined with in vivo and in vitro studies. The potential difference of the perfused esophagus in vivo was -28 +/- 3 mV (lumen negative). In vitro the potential difference was -17.9 +/- 0.6 mV, the short-circuit current 12.9 +/- 0.6 muA/cm2, and the resistance 1,466 +/- 43 ohm-cm2. Net mucosal-to-serosal sodium transport from Ringer solution in the short-circuited esophagus in vitro accounted for 77% of the simultaneously measured short-circuit current and net serosal-to-mucosal chloride transport for 14%. Studies with bicarbonate-free, chloride-free, and bicarbonate-chloride-free solutions suggested that the net serosal-to mucosal transport of these two anions accounts for the short-circuit current not due to sodium absorption. The potential difference and short-circuit current were saturating functions of bathing solution sodium concentration and were inhibited by serosal ouabain and by amiloride. Thus active mucosal-to-serosal sodium transport is the major determinant of the potential difference and short-circuit current in this epithelium.

Amiloride↗
PubMed1975

Salmon calcitonin and water and electrolyte transport in rabbit ileum.

The administration of SCT, natural and synthetic, has no apparent effect on the ileal water and electrolyte transport in the rabbit. The failure of SCT to influence ileal transport of water and electrolytes in the rabbit, as it does in man, may be due to differences in the rabbit intestinal response to a foreign peptide hormone.

Animals↗