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Biomedical subjects

E D Jacobson

Publications and source records attributed to E D Jacobson.

At least 109 records · Page 6Linked to original sources
PubMed1978

Inhibition of canine gastric acid secretion by an H-1 receptor antagonist to histamine.

Histamine H-2 receptors are thought to mediate gastric acid secretory responses, whereas H-1 receptors supposedly regulate mucosal vascular responses to histamine. In an in vivo chambered canine stomach flap preparation, the H-1 receptor antagonist, tripelennamine, injected intraarterially (22.1 mumol/kg) into the stomach flap reduced histamine-stimulated (1.25 micron/kg/min intravenously) acid secretion by approximately two thirds with a secondary reduction in gastric mucosal blood flow. This antisecretory action does not appear to be due to nonspecific mucosal damage. The H-2 receptor antagonist, metiamide, injected intraarterially (2.5 mumol/kg) also inhibited gastric acid secretion by about two thirds as did intravenously injected metiamide (4.5 mumol/kg), whereas intravenously administered tripelennamine (40.8 mumol/kg) was ineffective as an acid secretory inhibitor. Intraarterial tripelennamine reduced the secretory actions of the H-2 agonist, 4-methylhistamine (2.2 micron/kg/min intravenously), while intravenous metiamide depressed the gastric mucosal dilator responses to the H-1 agonist, 2-methylhistamine (5 micron/kg/min intravenously). Both histamine-receptor antagonists also reversed the systemic circulatory depressor effects of histamine and its analogs. These results suggest the need for reevaluation of inferences based upon the assumed specificity of H-2 and H-1 agonists and antagonists.

Animals↗
PubMed1978

Toxicity and mutagenicity of radiation from fluorescent lamps and a sunlamp in L5178y mouse lymphoma cells.

Unfiltered broad spectrum radiation emitted by black light, cool white, and black light blue fluorescent lamps and a sunlamp, is both toxic and mutagenic to L5178Y mouse lymphoma cells when the cells are irradiated in phosphate-buffered saline. The increase in mutant frequency seen after exposure of the cells is linear throughout the range of exposures tested. The linear increase in mutagenesis is observed even at exposure levels which do not cause significant toxicity. To facilitate comparison of the differing rates of mutagenesis derived from exposure-response curves obtained for each light source, we have defined a parameter, joule-equivalent mutagenesis (jem), equal to mutants per 10(5) survivors per joule per square meter. Jem values are calculated using the integrated irradiance of each lamp. Based on jem values, the relative mutagenicity of the various lamps tested (compared with a germicidal ultraviolet lamp) is 3 x 10(-3) for the sunlamp, 1 x 10(-4) for the black light and cool white lamps, and 3 x 10(-5) for the black light blue lamp. The toxic and mutagenic effects of the lamps are in reasonable agreement with their relative spectral output from 290 to 330 nm.

Cell Line↗
PubMed1978

Effects of 16,16-dimethyl prostaglandin E2 on ion transport by isolated rabbit gastric mucosa and rat intestinal epithelial cells.

The actions of 16,16-dimethyl prostaglandin E2 (dmPGE2) were investigated on ion transport in in vitro rabbit fundic mucosa and rat isolated jejunal cells. Addition of dmPGE2 (1.3 X 10(-4)M) to the serosal side of the rabbit mucosa resulted in a significant decrease in the transmural potential difference (PD) and short circuit current (Isc). The transmembrane resistance (R) displayed a significant rise over control values. Furthermore, the net serosa to mucosa flux of chloride ion decreased while the net serosa to mucosa movement of sodium remained unchanged. In the rat intestinal cells, increasing the concentration of dmPGE2 from 10(-10) to 10(-4)M caused a fall in sodium efflux. These data indicate that dmPGE2 alters the rate of active transport of the predominant ion pump of the resting rabbit gastric mucosa and the rate of Na efflux from rat intestinal epithelial cells without apparently affecting the membrane permeability.

Animals↗
PubMed1978

Renal histamine H1 and H2 receptors: characterization and functional significance.

Canine experiments were designed to determine if both histamine H1 and H2 receptors are present in the renal circulation. Renal blood flow (RBF) increased steeply over the first minute of intra-arterial histamine infusion, then increased gradually to a plateau in 3--5 min. Infusion of either histamine + H2 antagonist or of H1 agonist produced the initial rapid increase in RBF, whereas infusion of either histamine + H1 antagonist or of H2 antagonist produced a slower but more sustained increase in RBF. Histamine significantly increased urine flow rate (V), chloride excretion, and glomerular filtration rate (GFR). Infusion of the H2 agonist also increased V and Cl excretion without affecting GFR. By contrast H1 agonist significantly reduced V and Cl excretion and tended to reduce GFR (P less than 0.1 greater than 0.05). Histamine, H1 agonist, and H2 agonist each increased inner cortical more than outer cortical blood flow. These data suggest that 1) H1 and H2 receptors are present in the renal vasculature, 2) changes in intrarenal blood flow distribution are not responsible for histamine-induced diuresis, and 3) H1 receptors are primarily postglomerular while H2 receptors exhibit both pre- and postglomerular distribution.

Animals↗
PubMed1978

Endocrine control of appetite: gastrointestinal hormonal effects on CNS appetitive structures.

Permanent semi-microelectrodes were implanted in the ventromedial hypothalamus (VMH), lateral hypothalamus (LH), amygdala (AMYG), medial forebrain bundle (MFB), anterior hypothalamus (AH), inferior colliculus (IC), and caudate nucleus (CN). Average evoked responses were recorded simultaneously from the above sites in freely behaving rats before and after administration of pentagastrin (100 microgram/kg), secretin 1 microgram/kg or cholecystokinin octapeptide (CCK-OP) (1 microgram/kg) in search of satiety signal. Gastrin and secretin had little effect while it appears that CCK may perform a regulatory function in a neurohumoral feedback mechanism.

Amygdala↗
PubMed1977

Histamine, cyclic AMP, and gastric secretion in the dog.

Canine gastric mucosal cyclic AMP content was determined at 1, 5, 30, 60, and 120 min after commencing a 2-hr continuous intravenous infusion of histamine of sufficient dose to elicit a brisk acid secretory response from the dog stomach. The increase in acid output was significant at 30 min and stabilized at the stimulated level for the duration of histamine infusion. By contrast, there was no significant increase in mucosal cyclic AMP content at any time of measurement. Our findings indicate that the acid secretory response of the canine stomach to histamine does not require prior accumulation of cyclic AMP in the mucosal tissue.

Animals↗
PubMed1977

The effect of stored blood on mesenteric oxygen extraction during exdotoxin shock.

Storage of blood in acid-citrate-dextrose (ACD) solution gradually depletes red cell 2,3-diphosphoglycerate (DPG) and increases the affinity of hemoglobin for oxygen. We examined the effect of exchange transfusion of DPG-depleted blood on mesenteric blood flow and oxygen consumption in dogs subjected to endotoxin shock. Two groups of 6 dogs each were anesthetized and subjected to exchange transfusion with either fresh ACD blood or 21-day-old ACD blood prior to administration of Escherichia coli endotoxin (2 mg/kg). Mesenteric blood flow, arteriovenous oxygen content difference and systemic arterial blood pressure were monitored continuously before and for 60 min after endotoxin. Mesenteric blood flow was reduced from 250 +/- 21 ml/min before endotoxin to 114 +/- 15 ml/min at 5 min, 157 +/- 29 ml/min at 30 min, and 112 +/- 17 ml/min at 60 min after endotoxin in the dogs exchanged with fresh blood. Corresponding values for intestinal oxygen consumption were 10.4 +/- 1.0, 7.5 +/- 0.8, 8.4 +/- 1.0, and 6.8 +/- 0.7 ml/min. In dogs transfused with 21-day-old blood, pre-endotoxin blood flow was 208 +/- 2ml/min and declined to 115 +/- 12, 93 +/- 5, and 80 +/- 8 ml/min at 5, 30, and 60 min post-endotoxin. Corresponding values for intestinal oxygen consumption were 8.1 +/- 0.9, 6.6 +/- 0.7, 6.2 +/-0.5, and 5.5 +/- 0.7 ml/min. There was no significant difference (p greater than 0.1) in responses of blood flow or oxygen consumption to endotoxin shock between the two groups of dogs. These findings indicate that exchange transfusion with DPG-depleted blood does not impair oxygen extraction by the ischemic intestine.

Acids↗
PubMed1977

Adsorption of bacteriophages phi 29 and 22a to protoplasts of Bacillus subtilis 168.

Adsorption of bacteriophages phi 29 and 22a to protoplasts of Bacillus subtilis 168 is described. The number of binding sites on bacilli and protoplasts is determined for each phage. Bacilli and protoplasts possess roughly the same number of sites per unit area for phi 29, i.e., approximately 700 sites per bacillus. There are also approximately 700 sites per bacillus for 22a, but only about one-third as many sites per unit area on the protoplast surface. A model for phi 29 adsorption is proposed.

Adsorption↗
PubMed1977

The use of prostaglandin E1 for enhanced visualization of the splanchnic circulation.

A single bolus injection of prostaglandin E1 (5-7.5 microgram) into the superior mesenteric, hepatic or pancreatico-duodenal arteries was employed as a pharmacoangiographic aid in 22 patients. Good quality arterial phase and greatly enhanced portal venograms were obtained. No significant complications were observed. The authors found the technique useful in diagnosis of primary and metastatic lesions in the liver and pancreas.

Abdomen↗
PubMed1977

Histamine H1- and H2-receptor vasodilation of canine intestinal circulation.

Studies were conducted in anesthetized dogs to determine whether the mesenteric vasodilator response to histamine is mediated by H1 receptors alone or whether H2 receptors are also involved in the response. Evidence favoring a role for both receptors included: 1) the vasodilator response to histamine was inhibited by either the H1-receptor antagonist, tripelennamine, or the H2-receptor antagonist, metiamide; 2) both the H1 agonist, 2-methylhistamine, and the H2 agonist, 4-methylhistamine, induced dilator responses in the mesenteric circulation; and 3) two temporal patterns of vasodilation could be distinguished, namely a transient spike and subsequent fade of blood flow (seen with either the H1 agonist or with histamine after H2-receptor blockade) and a sustained and stable increase in flow (seen with either the H2 agonist or with histamine after H1 blockade). Metiamide appeared to be a potent inhibitor of the mesenteric vasodilator response to histamine at least equal to tripelennamine.

Action Potentials↗
PubMed1977

Cyclic nucleotide metabolism and vasodilation in canine mesenteric artery.

The uptake and extracellular and intracellular metabolism of radioisotopically labeled cyclic 3',5'-adenosine monophosphate (cAMP) and dibutyryl cAMP (DBcAMP) was determined in canine mesenteric arteries incubated in vitro. Intracellular tissue uptake was measured by radioisotope counting and labeled metabolites separated by thin-layer chromatography. Extracellularly, cAMP was extensively metabolized to AMP, adenosine, and Pi. DBcAMP was metabolized to monobutyryl cAMP (MBcAMP) intracellularly. Vasodilation of the mesenteric circulation in vivo was produced by cAMP, its metabolites and DBcAMP. DBcAMP caused greater vasodilation than cAMP but had a response time to its peak effect of 12 min versus 90 s for cAMP. The vasodilator properties of cAMP and DBcAMP were related to their metabolism. It was concluded that the vasodilation caused by cAMP was due to cAMP metabolites produced by extracellular metabolism.

Adenosine↗
PubMed1977

Rat gastric mucosal adenylyl cyclase.

Prostaglandin E1, epinephrine, secretin, and glucagon are known inhibitors of gastric acid secretion, and each agent stimulated mucosal membrane (600 X g pellet) adenylyl cyclase activity from the corpus of the rat stomach. This adenylyl cyclase activity was also stimulated by 5'-guanylyl-imidodiphosphate and sodium fluoride but not by guanosine-5'-triphosphate. By contrast, the gastric acid secretagogues, pentagastrin, histamine, and carbachol, had no effect on basal or prostaglandin E1-stimulated mucosal adenylyl cyclase activity. Most of the sodium fluoride- and hormone-stimulated adenylyl cyclase of the corpus mucosa was contained in the 600 X g membrane fraction. The enzyme exhibited Michaelis-Menten kinetics with respect to the concentration of ATP, with an apparent Km of 0.25 mM. Histamine did not stimulate rat mucosal adenylyl cyclase activity under a variety of conditions, but did stimulate the same enzyme in guinea pig gastric fundic mucosa, an enzyme also activated by prostaglandin E1. These studies do not support the hypothesis that cyclic AMP mediates the actions of gastric acid secretagogues on the parietal cell in the rat.

Adenylyl Cyclases↗
PubMed1977

Activation of rat gastric mucosal adenylyl cyclase by secretory inhibitors.

Prostaglandin (PG) E1, E2, A1, and A2 stimulated rat gastric corpus mucosal membrane adenylyl cyclase activity. PGE1 (Kalpha congruent to 8 muM) affected the maximum velocity but not the affinity of the enzyme for ATP and maximum PGE1 activation was not affected by histamine H1 or H2 receptor antagonists. 5'-Guanylyl-diphosphoimide (Gpp(NH)p), but not GTP, stimulated both the basal and PGE1-stimulated adenylyl cyclase activities, although the percentage stimulation by maximal PGE was the same with or without Gpp(NH)p. NaF stimulation was also additive to that of PGE1. Secretin also stimulated gastric mucosal adenylyl cyclase activity (Kalpha congruent to 30 nM). Maximal secretin activation was not additive to that of PGE1, suggesting a coupling to the same adenylyl cyclase catalytic site. These studies suggest that mucosal membranes may contain beta-adrenergic receptors. The adenylyl cyclase activating agents used in this study, PGE1, secretin, and the catecholamines, are all known inhibitors of gastric acid secretion, suggesting a possible involvement of cyclic AMP in the inhibition of acid secretion in the rat stomach.

Adenosine Triphosphate↗