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Biomedical subjects

D Mailman

Publications and source records attributed to D Mailman.

17 recordsLinked to original sources
PubMed1990

Binding and solubility of oleic acid to laboratory materials: a possible artifact.

The possibility that significant amounts of fatty acids were dissolved in or bound to the surfaces of common laboratory materials was examined. The uptake or adsorption of radioisotopically labeled oleic acid and cholic acid by plastic tubing of Tygon, Teflon, and polyethylene, and Pyrex, and borosilicate glass, and steel was measured. 3H-oleic acid and 14C-cholic acid were used in the presence of different concentrations of unlabeled oleic acid, cholic acid, and/or bovine serum albumin. Concentrations, composition, pH, and perfusion rates were varied. Relatively large amounts (10-95%) of oleic acid (25 microM) were lost by dissolving in plastic and adsorption to glass or metal. The degree of losses decreased in the presence of compounds in the perfusion solution which could bind or dissolve oleic acid. In contrast, cholic acid was not lost to plastic, glass or metal. The magnitude of and influence of perfusion rate, composition, pH, and sequence of perfusion solutions on oleic acid losses were sufficiently large that the results of certain studies, such as those of unstirred water layers of albumin - stimulated fatty acid uptake by hepatocytes may need to be reexamined.

Adsorption↗
PubMed1990

Villous motility and unstirred water layers in canine intestine.

The possibility that villous motility reduces the mucosal unstirred water layer by mechanical stirring was examined. The frequency of contraction of villi was measured by using videomicroscopic techniques while a segment of anesthetized canine jejunum or ileum with its nerve and blood supply intact was maintained in a sealed chamber through which Tyrode solution was perfused. Radioisotopically labeled inulin, H2O, and butyric and lauric acid were used to measure net and/or unidirectional fluxes from the chamber. The unidirectional absorptive transport of H2O and butyric acid but not lauric acid by jejunal segments was significantly correlated with flow through the chamber. Plasma volume expansion increased villous motility but decreased the absorption of H2O and lauric acid. Absorption of butyric acid from the ileum was little different than from the jejunum although the degree of villous motility was less and net water absorption was greater from the ileum. Absorption of butyric acid into dead tissue indicated that passive diffusion into the tissue accounted for between 7 and 25%, depending on flow rate, of the absorption in intact tissue and that nonspecific binding was low. It was concluded that villous motility did not stir the unstirred water layers and was not directly associated with altered transport.

Animals↗
PubMed1989

Effects of intraarterial, intravenous, and intraluminal neurotensin on canine ileal sodium and water absorption and blood flow.

Neurotensin is a regulatory peptide which is found primarily in the ileum and is secreted into the blood and lumen. The physiologic effects of neurotensin are uncertain but in certain pathologic states neurotensin increases to levels which can have effects on many organs. The effects of intravenous, intraarterial and intraluminal neurotensin (0.075-7.5 micrograms/min) on fed canine ileal sodium and water fluxes, potassium secretion, and blood flows were studied. Intravenous and intraarterial infusion of neurotensin increased net sodium, potassium, and water secretion, due to increased secretory fluxes, and increased hematocrits. Intraarterial neurotensin was not more effective than intravenous neurotensin except for stimulating potassium secretion. Neurotensin increased potassium secretion at 0.075 micrograms/min IA, increased sodium and water secretion at 0.75 micrograms/min IA and IV, and increased hematocrit at 7.5 micrograms/min IA and and IV. Total and absorptive site blood flows and arterial and venous pressures were not changed. Intraluminal neurotensin had no effects at any infusion rate. Neurotensin can increase potassium secretion at physiologic levels by a local effect and can increase sodium and water secretion at high physiological-pathological levels through a hormonal mechanism. The secretion is not dependent on cardiovascular changes.

Animals↗
PubMed1989

Effects of oleic acid and bile salts on canine villous motility.

The effects on canine villous motility of mucosal Tyrodes solution containing oleic acid (10 mM) and/or either taurocholic or cholic acid (15 mM) in the presence or absence of IV atropine (1 mg/kg) was used to assess the neural mediation of the effects of luminal nutrients. Villous motility was measured over 12 min periods by in vivo videomicroscopy of segments of jejunum. Neither bile salt had effects alone but villous motility increased after oleic acid was added to taurocholate and decreased after oleic acid was added to cholate. Villous motility increased when taurocholate and oleic acid were present initially and returned to control levels when removed. Villous motility was not affected by cholate and oleic acid but villous motility decreased when they were removed from the Tyrodes solution. Atropine blocked the increase in villous motility caused by taurocholate and oleic acid. Bile salts can modify the effect of oleic acid on villous motility and a cholinergic step is involved in the stimulation of motility.

Animals↗
PubMed1988

Villous motility: relationship to lymph flow and blood flow in the dog jejunum.

Villous contraction frequency, lymph flow, blood flow, and arteriovenous oxygen difference were measured in dog jejunum. Venous pressure elevation and plasma dilution were used to increase capillary fluid filtration. Both perturbations produced concomitant increases in villous contraction frequency and lymph flow. A highly significant correlation (r = 0.83, p less than 0.001) was obtained between villous contraction frequency and lymph flow. This finding, coupled with the observation that stimulation of net fluid absorption increases villous contraction frequency, suggests that villous motility is increased by a myogenic response elicited by increments in interstitial fluid pressure. In another series of experiments local arterial pressure was reduced in 20-mmHg steps from 120 to 20 mmHg. Although blood flow fell proportionately to arterial pressure, villous contraction frequency and oxygen uptake were maintained at a normal level when arterial pressure was between 120 and 60 mmHg. Villous motility and oxygen consumption fell progressively as arterial pressure was reduced below 60 mmHg. This observation indicates that ischemia does not alter villous contraction frequency unless blood flow is reduced below the level necessary to maintain normal tissue oxygenation.

Animals↗
PubMed1988

Effects of atropine and tetrodotoxin on neurotensin-induced ileal sodium transport in the dog.

1. Neurotensin was infused intravenously, in the presence or absence of intravenous atropine or intraarterial tetrodotoxin, into dogs anaesthetized with sodium pentobarbitone. Net and unidirectional fluxes of sodium and blood flows in the ileum were measured. Arterial and mesenteric venous blood pressures, haematocrits and plasma total solids were also determined. 2. Neurotensin caused a transient increase in net sodium absorption which was not associated with significant changes in unidirectional fluxes. This was followed by prolonged net secretion which was associated with an increase in unidirectional sodium secretion and a smaller decrease in sodium absorption. Potassium secretion was also increased when net sodium secretion increased. 3. Neurotensin increased haematocrit and total solids and decreased arterial pressure at the same time that secretion occurred. 4. Atropine blocked all the cardiovascular effects of neurotensin and reduced its early effects on both absorption and secretion but not the later effects on secretion. Tetrodotoxin only blocked the increase in absorption but not the secretion or the cardiovascular effects. 5. It was concluded that there is a cholinergic step in the cardiovascular effects of neurotensin and that the early effects of neurotensin on secretion are due to active secretion supported by fluid leakage from the plasma. The later effects of neurotensin on secretion do not have a cholinergic step and are due primarily to an active secretion. The increased absorption is mediated partly through intrinsic nerves of the gut.

Animals↗
PubMed1988

Neurohumoral control of villous motility.

A quantitative videomicroscopic method was used to examine neurohumoral control of villous motility. Intraduodenal instillation of saline, 0.4% hydrochloric acid, or acidified predigested food did not cause a significant change in villous contraction frequency in an isolated segment of jejunum. Villous motility in the jejunum of fed dogs, from which the chyme had been removed, was not greater than that in fasted dogs (2.9 +/- 0.3 vs. 3.4 +/- 0.5 contractions/min). Furthermore, acid extracts of the duodenal mucosa did not produce an increase in jejunal villous motility when injected intravenously. These data argue against the existence of a humoral stimulant of villous motility (villikinin). Vagotomy caused only a small (20%) and transient (10 min) decline in villous motility. Vagal stimulation at 5, 10, and 20 Hz caused villous motility to increase by 24 +/- 7, 23 +/- 9, and 32 +/- 10%, respectively. Atropine blocked the effects of vagal stimulation. Section of the periarterial (sympathetic) nerves did not alter villous contractile activity. Stimulation of the periarterial nerves at 5, 10, and 20 Hz caused villous contraction frequency to decline by 41 +/- 5, 45 +/- 5, and 38 +/- 10%, respectively. This inhibition appears to involve both alpha- and beta-adrenergic receptors and a reduction in blood flow. Neither atropine, alpha-blockade, nor beta-blockade produced a sustained alteration in basal contraction frequency.

Animals↗
PubMed1978

Effects of vasoactive intestinal polypeptide on intestinal absorption and blood flow.

1. Intestinal absorption and blood flow in anaesthetized dogs was determined after I.V. infusion of vasoactive intestinal polypeptide (VIP) (1.75-175 ng/min) to determine the contribution of the cardiovascular changes to transport. 2. 22Na and 3H2O were utilized to determine the unidirectional fluxes of Na and H2O from saline perfused through the ileal lumen and the clearances of 3H2O were used to determine total and absorptive site blood flow. 3. Net Na and H2O absorption were reversed to secretion by VIP at 175 ng/min due to a significant decrease in unidirectional absorptive fluxes and smaller increases in secretory fluxes. 4. Arterial pressure and absorptive site blood flow were reduced in proportion to the changes in Na and H2O fluxes. 5. Total and absorptive site blood flow decreased and the blood flow resistances increased. 6. Prior treatment with guanethidine to suppress sympathetic effects did not greatly affect the responses to VIP. Prior treatment with atropine to suppress cholinergic effects inhibited most of the effects of VIP. 7. Absorptive site blood flow was linearly related to absorptive fluxes of Na and H2O but with different slopes for results from atropinized dogs as compared to those from dogs given VIP alone or VIP plus guanethidine. 8. It was concluded that VIP reduces gut absorption through a generalized cardiovascular effect and also through a mechanism which depends on the release of ACh by the gut.

Animals↗
PubMed1977

Effects of glucagon on canine intestinal sodium and water fluxes and regional blood flow.

1. Glucagon (0-05 or 0-5 microng/kg. min) was infused into a mesenteric artery of a canine ileal segment from which transport was measured (direct infusion) or into a mesenteric artery of an adjacent non-perfused segment (indirect infusion). Unidirectional Na and H2O fluxes and arterial and mesenteric vein pressures and total and absorptive site blood flows were measured. 2. Direct glucagon infusion increased the absorptive and secretory fluxes of Na and H2O and absorptive site blood flow, and decreased absorptive site resistance and arterial and mesenteric vein pressure. Indirect glucagon infusion had the opposite effects. 3. Neither the direct arterial infusion of histamine (0-1-53 microng/kg. min) nor the I.V. infusion of glucose (0-2 g/min) or insulin (0-1 micron/kg) or glucose plus insulin, mimicked the effects of glucagon. 4. The unidirectional secretory and absorptive fluxes of both Na and H2O were linearly related to the calculated capillary pressure during glucagon infusion. 5. It was concluded that the effects of glucagon on gut transport were due to effects exerted through the cardiovascular system.

Animals↗
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↗
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↗
PubMed1975

The effect of saline and hyperoncotic dextran infusion on canine ileal salt and water absorption and regional blood flow.

1. The unidirectional Na and H2O fluxes, vascular pressures and total and absorptive site blood flows in the canine ileum were determined before and during I.V. saline infusion and subsequent I.V. infusion of hyperoncotic dextran. The intestinal perfusion solutions were isotonic saline or isotonic saline and mannitol, but the effects of I.V. saline or I.V. hyperoncotic dextran infusion were generally the same for both luminal solutions. 2. Continuous I.V. infusion of saline caused a continuous increase in the unidirectional flux of Na and H2O into the ileal lumen, an increase in total blood flow, and an increase in venous pressure. 3. The net absorption of Na and H2O was decreased by I.V. saline infusion. 4. The unidirectional fluxes of Na and H2O out of the lumen, arterial pressure, and absorptive site blood flow were not affected by I.V. saline infusion. 5. I.V. hyperoncotic dextran infusion reversed most of the effects of saline infusion. 6. The unidirectional fluxes of Na and H2O into the lumen were significantly correlated with Starling forces during I.V. saline infusion. 7. It was concluded that intestinal transport of salt and water was subject to regulation by physical forces at the capillary level.

Animals↗