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Biomedical subjects

E D Jacobson

Publications and source records attributed to E D Jacobson.

At least 127 records · Page 7Linked to original sources
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

Effects of vasoconstrictors on intestinal vascular resistance and oxygen extraction.

To delineate the mechanism through which vasoactive compounds alter intestinal oxygen consumption and to determine the pharmacological nature of the receptors involved, we quantitated the effects of vasoconstrictors on arteriovenous oxygen difference and on vascular resistance in isolated constant-flow perfused canine small bowel. Norepinephrine (NE) and sympathetic stimulation (SS) increased vascular resistance and depressed O2 extraction. These effects were not altered by beta-blockade, but were abolished by alpha-blockade. Since capillary filtration coefficients at constant-pressure perfusion and 86Rb extraction at constant flow are reported to diminish during NE and SS, it follows that these agents reduce O2 extraction by an alpha-adrenergic closure of precapillary sphincters. Vasopressin had similar effects which were not affected by adrenergic blocking agents. Epinephrine (Epi) in high doses or after propranolol produced the same effects as NE and SS. By contrast, Epi in low doses increased O2 and 86Rb extraction. This response to low doses of Epi was not affected by phentolamine, but was reversed by propranolol. We conclude that Epi in high doses or after propranolol depresses intestinal O2 extraction by the same mechanism as NE and SS, but the mechanism through which Epi increases intestinal O2 extraction is unclear.

Animals↗
PubMed1976

Evaluation of (14C)aminopyrine clearance for determination of gastric mucosal blood flow.

This study has demonstrated high correlation between the radiometric and spectrophotometric determinations of gastric mucosal aminopyrine clearance. The radiometric method is technically easier, allows a larger number of samples to be determined and is safer to the subject. The clearance of small amounts of [14C]aminopyrine was unaffected by large doses of unlabeled aminopyrine showing that mucosal extraction is not concentration limited. Small amounts of [14C]aminopyrine may provide an excellent tool for examining the role of mucosal blood flow in the pathogenesis of gastric disease in man.

Aminopyrine↗
PubMed1976

Re-evaluation of the role of cyclic AMP in histamine-induced gastric acid secretion.

The 600 x g particulate fraction of gastric mucosal scrapings from rats was incubated with 3H-metiamide which saturated available binding sites at a concentration of 1 muM. Scatchard plots showed a single component with a Kd value of 0.2 muM. Unlabelled cimetidine and histamine competed with 3H-metiamide binding. The 600 x g particulate fraction also contained all of the hormone and sodium fluoride sensitive adenylyl cyclase. Adenylyl cyclase activity was not altered by histamine, pentagastrin or carbachol but was increased during incubation with prostaglandin E1, secretin and epinephrine. These findings do not support the hypthesis that gastric secretion is mediated by intracellular accumulation of cyclic AMP.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1976

Cyclic AMP and gastric secretion: the illusive second messenger.

We have surveyed the literature which bears upon the contention that accumulation of intracellular cyclic AMP is a necessary intermediate event between secretagogue and secretion of acid by the stomach. In our view, the evidence in favor of this hypothesis is wanting for these three reasons: (i) the evidence does not fit with better established information about regulation of gastric secretion and about hormonal actions on the cyclic AMP system; (ii) technological problems involved in the biological preparations employed and in the assay procedures used make the evidence nearly uninterpretable; and (iii) there exists a body of contradictory evidence at least as convincing as that which favors the thesis. These three arguments against acceptance of the theory are not definitive and are not intended to dissuade investigators interested in gastric mucosal metabolism from their quest. And, although we are not at this time adherents of the preceding hypothesis, we are also not unmindful of its basic appeal, which has attracted numerous scientists into a study of the metabolic correlates of gastric acid secretion. Unfortunately the general appeal of the second messenger hypothesis is such as to make it almost a paradigm of gastric secretory physiology in the seventies, in Kuhn's sense of that word (118). The disadvantages of paradigms are that they tend to obscure negative evidence among their adherents, and they arouse controversies more marked by heat than by light.

Animals↗
PubMed1975

Interaction of protoplasts, L forms, and bacilli of Bacillus subtilis with 12 strains of bacteriophage.

The interaction of 12 phage strains with bacilli, protoplasts, and L forms of Bacillus subtilis 168 and with eight of its mutants and two of its lysogens is described qualitatively and quantitatively. After removal of the cell wall from B. subtilis 168, 11 of the 12 phage strains can still adsorb to the protoplasts, nine kill their wall-less host cells, and five multiply in the naked bacteria, forming plaques on L form lawns. Individual gene mutations can have similarly pleiotropic effects, strongly dependent upon the plating medium. Thus, the gta A mutation, which causes loss of glucosylation of the wall teichoic acid, results in loss of wall adsorption sites for phi (but not membrane sites) and for phi105. Phages phi25, SP82G and phie can still adsorb to gta A bacilli and plaque in unstabilized and sorbitol-stabilized lawns of this mutant, but they can not plaque in sucrose-stabilized lawns. The lysogenized wild type, B. subtilis 168 (SPO2), also exhibits a pleiotropic pattern, showing different levels of resistance to phages SPO2, phi1, phie, and phi25. Its resistance pattern is very similar to that of wild-type protoplasts. On the basis of such patterns, the bacterial mutants and strain B. subtilis 168 (SPO2) could be ordered into four classes and the phage strains classified into four to six groups. Together, they form four to six interaction complexes, based partly on adsorption sites and perhaps partly on metabolic blocks in phage development.

Adsorption↗
PubMed1975

The use of prostaglandin E1 to enhance the angiographic visualization of the splanchnic circulation.

Superior mesenteric angiograms were obtained in a series of dogs before and again after the injection of a 1-ml bolus of prostaglandin E1 (0.1-1.0 mug/kg) through the angiographic catheter. The prostaglandin E1 produced, on the average, a 100% increase in the superior mesenteric arterial blood flow with only minimal changes in the heart rate, systemic arterial pressure, and portal venous pressure. Opacification of the portal venous system was consistently enhanced after the prostaglandin E1. The arterial phase was preserved by increasing the rate of contrast administration.

Animals↗
PubMed1975

Effect of vasoactive agents on intestinal oxygen consumption and blood flow in dogs.

A comparison study of several vasoconstrictor and vasodilator agents was conducted measuring changes in intestinal blood flow and oxygen consumption during 10-min periods of intra-arterial infusion. Blood flow was measured in a branch of the superior mesenteric artery of anesthetized dogs with an electromagnetic blood flow meter, and the arteriovenous oxygen content difference across the gut segment was determined photometrically. Vasopressin (4 x 10(-3) and 7x 10(-4) U/kg-min) diminished blood flow 60 and 28% and reduced oxygen consumption 54 and 22%, respectively (all P less than 0.001). In a dose which did not lower blood flow, vasopressin still caused a decline in oxygen consumption (P less than 0.01). Epinephrine (5 x 10(-2) mug/kg-min) decreased blood flow 19% (P less than 0.001) but did not reduce oxygen consumption. After beta-adrenergic blockade, however, the same dose of epinephrine decreased blood flow 41% and oxygen consumption 33% (both P less than 0.001). Responses to angiotension II, calcium chloride, and prostaglandin F2alpha resembled effects of vasopressin rather than those of epinephrine, namely decreased blood flow and decreased oxygen consumption. The vasodilator agents, prostaglandin E1, is isoproterenol, and histamine, increased (P less than 0.001) both blood flow (130, 80, and 98%, respectively) and oxygen consumption (98, 64, and 70%, respectively). Vasopressin, angiotensin II, calcium chloride, and prostaglandin F2alpha appear to contract arteriolar and precapillary sphincteric smooth muscle indiscriminately to evoke both intestinal ischemia and hypoxia. Epinephrine is the exceptional constrictor in this case, producing diminished blood flow without a reduction in oxygen uptake.

Animals↗
PubMed1975

Experimental use of prostaglandin E1 in nonocclusive mesenteric ischemia.

Nonocclusive mesenteric ischemia was produced in dogs by intraarterial infusion of digoxin and by hemorrhage of 1/3 of total blood volume. Both methods produced a substantial drop in the superior mesenteric arterial blood flow rate. In each case, a superior mesenteric arterial infusion of 0.1 mug./kg. per minute of prostaglandin E1 allowed the blood flow rate to increase to above the control level without significantly altering heart rate or systemic arterial pressure. The improved arterial blood flow rates were accompanied by a reversal of the diffuse mesenteric vasoconstriction that was seen in the ischemic state. These findings were demonstrated by superior mesenteric arteriography performed prior to and following the production of mesenteric ischemia and again following the infusion of prostaglandin E1.

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

Pharmacologic effects of gastrointestinal hormones on intestinal oxygen consumption and blood flow.

The vasoactive effects of cholecystokinin-octapeptide (CCK-OP), pentagastrin, synthetic secretin, glucagon, and acetylcholine were assessed in the intestinal circulation of the dog. In pharmacologic doses of glucagon, CCK-OP, and, to a lesser degree, pentagastrin significantly increased blood flow and oxygen consumption. Atropine blocked the vasodilator effects of CCK-OP, pentagastrin, and acetylcholine but did not block those of glucagon. Neither the alpha-adrenergic blocker, phenoxybenzamine, nor the beta-adrenergic blocker, propranolol, blocked the vasodilator response to pentagastrin. Synthetic secretin had no significant effect on either blood flow or oxygen consumption in the intestinal segment. The vasodilator response to CCK-OP and pentagastrin appears to be mediated specifically through cholinergic receptors.

Acetylcholine↗