The adrenergic influence on intestinal secretion in cholera.
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Adrenergic Fibers↗
Biomedical subjects
M Jodal
Publications and source records attributed to M Jodal.
The effect of carotid occlusion on the rate of net fluid absorption in the small intestine of rats and cats.
The effect on net intestinal fluid absorption of unloading the baroreceptors by bilateral carotid occlusion was studied in rats and cats. It was shown that net fluid uptake from the intestine increased 30-40% upon carotid occlusion. This effect was eliminated by cutting the splanchnic nerves (cats) or by severing the nerves surrounding the superior mesenteric artery (rats). In fact, these denervation procedures resulted in a decreased net fluid absorption upon carotid occlusion. Cutting the vagal nerves did not significantly influence the response to carotid occlusion. It is concluded that the arterial baroreceptors influence net fluid transport in the small intestine, a reflex compensatory mechanism that may be important in different hypotensive situations.
Animals↗
The effect of stimulating somatic afferents on cholera secretion in the rat small intestine.
The effect on rate of cholera secretion in the small bowel of activation of the group III and A delta afferent fibres in the sciatic nerve was studied in rats. Activation of these fibres at 3 Hz for 60 min significantly diminished choleraic secretion from 121 +/- 29 to 25 +/- 9 microliters x min-1 x 100 cm-2 serosal surface (mean +/- SE; n = 9). The effect was apparent after the nerve stimulation. Stimulation of the sciatic nerve had no significant effect on choleraic fluid secretion after interrupting the autonomic nerves to the intestine, nor did it significantly alter net fluid transport in non-choleraic intestine with intact nervous supply. It is proposed that the observations may explain the clinical reports of an effect of acupuncture on cholera secretion.
Afferent Pathways↗
The effect of intestinal fluid transport of exposing the serosa to hydrochloric acid. A study of mechanisms.
Hydrochloric acid (0.1 M) placed on the serosal surface of a jejunal segment evoked an intestinal secretion (rats) or inhibited a net fluid absorption (cats). In rats it was demonstrated that lidocaine (placed on the serosa of periarterially denervated intestinal segments), hexamethonium (given i.v.; innervated or denervated intestines) and indomethacin (given i.v.; denervated intestines) markedly inhibited the acid induced secretion, while atropine (given i.v.) had no effect. In the cat experiments it was shown that tetrodotoxin (given close i.a. to denervated intestines) returned the rate of net fluid absorption to the control value observed before applying acid. It is concluded that exposing the intestinal serosa to an acid solution evokes a fluid secretion that is nervously mediated. Furthermore, it is proposed that prostaglandins are involved in the induction of the fluid secretion probably via a stimulation of nociceptors. It is also suggested that the results may have pathophysiological implications for some types of paralytic ileus.
Animals↗
5-hydroxytryptamine and cholera secretion. Physiological and pharmacological studies in cats and rats.
The intestinal secretion evoked by close intra-arterial infusion of 5-hydroxytryptamine (5-HT) in cats was inhibited by tetrodotoxin, a drug abolishing action potentials. Furthermore, the intestinal secretion produced by placing a 2-mM 5-HT solution in the intestinal lumen of rats was inhibited by hexamethonium, a ganglionic receptor-blocking agent. These observations strongly indicate that 5-HT-induced secretion is, at least in part, neurally mediated. It was also shown that 5-HT receptors are involved in the pathophysiology of choleraic secretion, since the secretion was inhibited by making the experimental animal tachyphylactic against 5-HT. No effects of 5-HT tachyphylaxis were noted on fluid transport in normal intestines. The results are discussed in relation to a new hypothesis for the pathophysiology of cholera secretion.
Animals↗
Evidence for cholera secretion emanating from the crypts. A study of villus tissue osmolality and fluid and electrolyte transport in the small intestine of the cat.
Villus tissue osmolality and fluid and electrolyte transport were measured in intestinal segments exposed to cholera toxin. The osmolality of the luminal fluid was kept at about 100, 300, or 600 mOsm X kg-1 by use of appropriate concentrations of mannitol. A net fluid secretion was seen in all experiments, the magnitude being dependent on the osmolality in the lumen. A secretion of sodium, potassium, and chloride was also seen in all experiments but the secretion rate of electrolytes was independent of the osmolality in the intestinal lumen. The hydraulic conductivity of the villus epithelium, calculated from the lumen and tissue osmolality, was the same as that estimated in the normal intestines. A villus tissue osmolality gradient was apparent in all experiments regardless of the mannitol concentration in the lumen, the tip osmolality being hypertonic while the tissue osmolality at the base was isotonic. This was the case also when the luminal fluid was hypotonic, a finding opposite to what we found in an earlier study on the normal feline intestine. A likely explanation for this observation is that the crypts of Lieberkühn secrete fluid containing sodium chloride, which is absorbed by the villus epithelial cells. Hence, a luminal "circulation" of electrolytes between crypts and villi was suggested in the present experimental circumstances.
Animals↗
The effect of hexamethonium on the secretion induced by sodium deoxycholate in the rat jejunum.
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Animals↗
Release of vasoactive intestinal polypeptide from the cat small intestine exposed to cholera toxin.
During a four hour observation period vasoactive intestinal polypeptide (VIP) is released in increasing amounts from the feline small intestine exposed to cholera toxin. As VIP is known to be located almost exclusively in the intestinal nerves, the present findings strongly suggest that cholera toxin activates the enteric nervous system. The findings of this and other studies performed in this laboratory lead to the proposal that the choleraic secretion is, at least in part, secondary to the activation of intramural nervous reflexes in the gut.
Animals↗
On the role of intramural nerves in the pathogenesis of cholera toxin-induced intestinal secretion.
Intestinal secretion was produced in anesthetized cats and rats by exposing isolated intestinal segments to cholera enterotoxin. Giving, for example, tetrodotoxin, a nerve-conduction-blocking agent, or adding lidocaine, a local anesthetic agent, to the solution in the intestinal segments markedly inhibited the rate of choleraic secretion, and in most experiments a net absorption of fluid was observed. The results suggest that intramural nervous mechanisms are involved in the pathogenesis of choleraic secretion.
Anesthetics, Local↗
The effect of Apamin on nonadrenergic, noncholinergic nervous vasodilatations in the cat small intestine.
The intestinal vasodilation evoked by mechanical mucosal stimulation or by transmural electrical field stimulation was abolished by close i.a. injection of Apamin, a polypeptide originally isolated from bee venom. Apamin also blocked the vasodilatation induced by close i.a. infusion of vasoactive intestinal polypeptide (VIP). It is suggested that Apamin is a VIP receptor antagonist.
Animals↗
Villous tissue osmolality, water and electrolyte transport in the cat small intestine at varying luminal osmolalities.
Villous tissue osmolality and net transport for water, sodium, potassium and chloride were determined in the feline small intestine when exposing the mucosa to solutions with different mannitol concentrations (0, 100, 315 and 600 mmol/l). Tissue osmolality at the villous tip varied with luminal osmolality. At the villous base, on the other hand, tissue osmolality remained around the plasma osmolality regardless of the osmolality of the luminal fluid. Transport rates for water were affected in the way predicted from the lumen to tissue osmolality difference. A net flux from tissue to lumen was always recorded for the studied electrolytes. The hydraulic conductivity (Lp) of the intestinal epithelium with dilated intercellular spaces was estimated from the present results to be around 30 x 10(-12) cm x s-1 x Pa-1. When the intercellular spaces were collapsed Lp was estimated to be 15 x 10(-12 cm x s-1 x Pa-1.
Animals↗
Vasoactive intestinal polypeptide, 5-hydroxytryptamine and reflex hyperaemia in the small intestine of the cat.
1. The release of vasoactive intestinal polypeptide (VIP) into venous blood from the small intestine of the cat was studied when mechanically stimulating the intestinal mucosa and during close intra-arterial infusions of 5-hydroxytryptamine (5-HT) or isopropylnoradrenaline. The studies were performed on anaesthetized cats given atropine.2. Mechanical stimulation of the intestinal mucosa induced a vasodilatation and a release of VIP into the intestinal venous blood. Intra-arterial administration of tetrodotoxin was given in doses that blocked the vasoconstrictor effect of the regional sympathetic nerve fibres. This also abolished the vascular response and the release of VIP into blood upon mechanical stimulation.3. Close intra-arterial administration of 2-bromo-lysergic acid diethylamide reduced the VIP release and the intestinal vasodilatation upon mucosal stimulation to largely the same extent.4. Close intra-arterial infusions of 5-HT produced a marked release of VIP from the intestine and a moderate vasodilatation. Close intra-arterial infusions of isopropylnoradrenaline, which caused a pronounced intestinal vasodilatation, evoked only a small release of VIP.5. The results are compatible with the hypothesis that the vasodilatation in the gut, induced by mechanical mucosal stimulation, is mediated via an intramural nervous reflex containing a neurone capable of releasing VIP. It is proposed that the nervous reflex is activated by the release of 5-HT from the enterochromaffin cells evoked by mechanical stimulation of the mucosa.
Animals↗
The effect of lidocaine on the secretion induced by cholera toxin in the cat small intestine.
The intraluminal administration of lidocaine, a local anaesthetic agent, inhibits the net loss of fluid into the intestinal lumen produced by cholera toxin in the cat. It is suggested that the activation of a nervous reflex is involved in the pathogenesis of cholera.
Animals↗
Effects of vasoactive intestinal polypeptide on blood flow, motility and fluid transport in the gastrointestinal tract of the cat.
The effect of close intraarterial infusions of vasoactive intestinal polypeptide (VIP) on gastric motility, intestinal fluid transport and colonic motility were studied in the cat. Regional blood flow was also followed in all experiments. In the stomach VIP produced a gastric relaxation and a blood flow increase. The motility response was similar to that observed when eliciting the vago-vagal reflex relaxation by distending the esophagus. In the small intestine a hyperemia and a decrease of net water uptake was observed. When infusing small amounts of VIP a decrease of net water uptake was seen without any change of intestinal blood flow. Large amounts of VIP produced a transient secretory state in the small intestine. In the colon a hyperemia was seen immediately upon starting the infusion of the drug. After 2-3 min of infusion a contraction of the colon was apparent. The administration of atropine to the animal did not significantly affect any of the responses produced by VIP. The results are discussed in relation to VIP as a possible neurotransmitter in the gastrointestinal tract.
Animals↗
Vascular anatomy and tissue osmolality in the filiform and fungiform papillae of the cat's tongue.
The vascular anatomy of the filiform and fungiform papillae of the feline tongue was studied by i.a. injection of India ink. Vascular loops of various appearances were found in the types of papillae studied, i.e. the large and the small filiform papillae and the fungiform ones. Such hairpin loops may function as countercurrent exchangers and to test this hypothesis tissue osmolality was determined in the papillae, while exposing them to various isotonic electrolyte solutions. The large filiform papillae with a vascular arrangement similar to that of intestinal villi exhibited a marked osmolar gradient from tip to base when exposed to a solution containing both glucose and sodium. If sodium and/or glucose was excluded from the solution, tissue osmolality was significantly decreased. This was also the case when the chloride ions of the solution was substituted with sulphate. The small filiform papillae are only provided with one or a few capillary loops. They exhibited a less marked osmolar gradient than the large ones and one of the different electrolyte solutions decreased the gradient. In the fungiform papillae a tissue hyperosmolality at the tip was also demonstrated. It is proposed that the papillary epithelium is provided with active transport mechanism(s) and that the papillary vessels function as countercurrent multipliers. The functional importance of these mechanisms are tentatively discussed.
Animals↗
The effect of vasodilatation and sympathetic nerve activation on net water absorption in the cat's small intestine.
The rate of net water uptake from the feline small intestine has been investigated during control conditions, during graded infusions of the vasodilator drug isopropylnoradrenaline, and during electrical stimulation of the regional sympathetic nerve fibres to the gut. Net water absorption rate was largely unaffected by intestinal vasodilatation. The fraction of the absorbate transported via the lymphatics remained also constrant at 20-40% of the total absorption regardless of blood flow rate. Stimulating the sympathetic nerve fibres to the small intestine increased, however, net water absorption rate. The increase was particularly pronounced when blood pressure was kept constant during the period of stimulation. The absorption rate was on an average almost doubled at a stimulation frequency of 8 Hz during constant pressure conditions. The mechanism(s) explaining this nervous control of water absorption are tentatively discussed.
Adrenergic Fibers↗
Importance of sodium and glucose for the establishment of a villous tissue hyperosmolality by the intestinal countercurrent multiplier.
The intestinal countercurrent multiplier has earlier been shown to create an increased tissue osmolality in the villi (Jodal et al. 1978). In the present paper the importance of varying the luminal contents on the creation of the villous hyperosmolality was investigated using the cryoscopic technique described by Jodal et al. (1978). The perfusion solutions used contained 0, 25 or 147 mmol Na/l and were either provided with mannitol or glucose (30 mmol/l). It was demonstrated that sodium was of particular importance for the establishment of the villous hyperosmolality while glucose only contributed significantly at low luminal sodium concentrations. It is therefore proposed that glucose only in the absence of sodium in the luminal perfusate may effectively participate in the generation of the villous tissue hyperosmolality via the countercurrent multiplication mechanism.
Animals↗
Villous tissue osmolality and intestinal transport of water and electrolytes.
The villous tissue hyperosmolality created by the intestinal countercurrent multiplier has been proposed to be of importance for fluid transport across the intestinal epithelium in vivo. This study was performed to test this hypothesis. Net transport of fluid and electrolytes (sodium, potassium and chloride), as well as unidirectional fluxes of water and sodium were determined in the small intestine of the cat. The villous osmolality was altered by varying the composition of sodium and glucose in the isotonic solutions perfusing the intestinal lumen. Net transport of fluid was correlated to tissue osmolality mainly due to an increase of the unidirectional flux of water from lumen to tissue with augmented tissue osmolality. The results are thus consistent with the view that the intestinal countercurrent multiplier is of essential importance for net water transport. A correlation was found between net water and net sodium intestinal transport. A similar correlation was also demonstrated between net sodium and net chloride absorption rates in the jejunum while in the ileum net loss of sodium into the intestinal lumen was not accompanied by any corresponding loss of chloride ions. This observation suggests the presence of a sodium independent transport mechanism for chloride in the ilium but not in the jejunum.
Animals↗