Search PubMed⌕ Search

Biomedical subjects

M Jodal

Publications and source records attributed to M Jodal.

At least 55 records · Page 3Linked to original sources
PubMed1987

Changes in cyclic 3'5'-adenosine monophosphate tissue concentration and net fluid transport in the cat's small intestine elicited by cholera toxin, arachidonic acid, vasoactive intestinal polypeptide and 5-hydroxytryptamine.

We have analysed tissue cyclic 3'5'-adenosine monophosphate (cAMP) concentration in different fractions of the cat's small intestinal mucosa during secretion elicited in vivo by four different secretagogues: cholera toxin (administered intraluminally), vasoactive intestinal polypeptide (VIP; given i.a.), arachidonic acid (AA; administered intraluminally) and 5-hydroxytryptamine (5-HT; given i.a.). Cholera toxin was found to increase cAMP concentration in the villi but not in the crypts. The VIP, AA and 5-HT did not influence tissue cAMP concentration despite a profuse net fluid secretion. Hexamethonium inhibited secretion elicited by cholera toxin and AA but did not significantly influence tissue cAMP concentration. There is strong evidence for the view that villus and crypt regions of the small intestinal mucosa have different functions, secretion taking place in the crypts and absorption in the villi. However, the lack of cAMP increase in the crypts reported in this study suggests that cholera toxin in this model does not reach the crypts. The results are not in agreement with a role for cAMP in mediating secretion from the crypts, but are compatible with a role of cAMP in inhibiting absorption in the villi. It is suggested that the observed fluid secretion from the crypts elicited by cholera toxin, AA and 5-HT is to a major part mediated by intramural enteric reflexes.

Animals↗
PubMed1987

Mechanisms of neurotensin-induced fluid secretion in the cat ileum in vivo.

Neurotensin (NT) is released from N cells in the small intestinal epithelium. Among other effects NT is known to elicit fluid secretion in the small intestine. This study was carried out in order to elucidate the mechanism by which NT elicits this secretion. Neurotensin infusions at two rates (4.5 and 45 pmol min-1 kg-1 body wt) to isolated segments of cat ileum in vivo, caused a steady rate of net fluid secretion and a release of vasoactive intestinal polypeptide into the mesenteric vein. The secretion was totally inhibited by tetrodotoxin. Hexamethonium, a nicotinic receptor antagonist, inhibited the secretion elicited by the lower but not by the higher dose of NT. Met-enkephalin also inhibited the induced secretion while pyrilamine, a histamine-I receptor antagonist had no effect. No significant change in enteric blood flow was caused by the NT infusion. These results indicate that NT elicits a nervous reflex in the enteric nervous system which, accordingly, turns the transport of the enterocytes into net fluid secretion.

Animals↗
PubMed1987

Autoradiographic location of beta-adrenoceptor subtypes in cat colon smooth muscle.

In order to localize beta-adrenoceptors 125I-(-)pindolol (IPIN) was used in binding to sections from cat colon. The binding characteristics for IPIN to beta-adrenoceptors on colon sections were estimated by demonstrating reversible binding in the presence of isoprenaline and by steroselective binding to the isomers of propranolol. The binding of IPIN to both beta 1- and beta 2-adrenoceptors was shown by biphasic displacement curves in the presence of the selective beta-adrenoceptor compounds betaxolol, ICI 118.551 and procaterol. The colon sections were found to contain proportions of beta 1-adrenoceptors (30-50%) and beta 2-adrenoceptors (50-70%). In the autoradiographic studies, 100% of the developed grains after exposure of IPIN to the photographic emulsion were displaced by 50 microM of isoprenaline. By microscopic counting at autoradiographic grains, 30-40% of the grains were found in the circular smooth muscle, while 60-70% of the grains were found in the longitudinal smooth muscle. A concentration of 2 nM ICI 118.551 completely displaced all grains in the circular smooth muscle and partly displaced those found in the longitudinal smooth muscle. A high concentration of ICI 118.551 (1 microM) displaced all grains above background from the smooth muscle. It is concluded that the circular smooth muscle only contains beta 2-adrenoceptors, while longitudinal smooth muscle may contain a proportion of beta 1-adrenoceptors. Whether such a location of beta adrenoceptors can be related to the beta 1-adrenoceptor-mediated inhibition of colon motility can not be clarified from these studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1987

Influence of sodium deoxycholate on morphology, net fluid transport and motility in the small intestine of the rat.

Intestinal fluid secretion and motility were induced by luminal perfusion of rat small intestine with sodium deoxycholate, a dihydroxy bile salt for 1-3 h. Changes in intestinal morphology were studied simultaneously with the changes in fluid transport and motility. The results suggest that the bile salt causes epithelial lesions which may lead to a reduced fluid absorption in the villi, thereby explaining part of the total change in net fluid transport caused by the bile salt. Pyrilamine and indomethacin did not influence the bile salt-induced secretion. Based on earlier studies, it is proposed that the major part of the bile salt-evoked secretion is mediated via activation of intramural nervous reflex(es), which also stimulate the intestinal smooth muscle cells.

Animals↗
PubMed1987

Mechanisms underlying the small intestinal fluid secretion caused by arachidonic acid, prostaglandin E1 and prostaglandin E2 in the rat in vivo.

Prostanoids were given intraluminally (PGE2) or infused close intra-arterially (PGE1 and PGE2) or arachidonic acid was administered intraluminally to denervated jejunal segments of the rat in vivo. These experimental manoeuvres caused a net fluid secretion, although a 1,000-fold higher concentration of the prostanoids was needed from the luminal than from the vascular side. I.v. hexamethonium or serosally applied lidocaine diminished the induced fluid secretion suggesting that the prostanoids act mainly by eliciting local secretory reflexes in the enteric nervous system. This nerve-mediated secretion is not accompanied by any increase in tissue cAMP. However, at higher i.a. concentrations of PGE2 there seems to be a non-neurogenic effect on the enterocytes associated with an increase in tissue cAMP.

Alprostadil↗
PubMed1986

The adrenergic nervous control of fluid transport in the small intestine of normotensive and spontaneously hypertensive rats.

Intestinal net fluid transport in normotensive Wistar Kyoto rats (WKR) and spontaneously hypertensive rats of the Okamoto strain (SHR) were studied during 'rest', during electrical stimulation of the regional sympathetic fibres as well as after acute denervation and alpha-adrenergic receptor blockade (phentolamine). During 'rest' no statistically significant difference in fluid transport rate could be demonstrated between WKR and SHR. Cutting the left splanchnic nerve, severing the periarterial nerves or giving phentolamine turned net fluid absorption to net fluid secretion in most SHR, whereas fluid absorption was little influenced in WKR by these procedures. Stimulating the left splanchnic nerve (2, 4, 8 Hz) markedly increased net fluid uptake or decreased net fluid secretion in SHR in a frequency-dependent manner. A small effect was seen in WKR at a stimulation rate of 4 Hz. The 'spontaneous' fluid secretion in denervated intestinal segments of SHR was accompanied by a net chloride secretion. Giving hexamethonium i.v. turned net fluid and chloride secretion into water and ion absorption, suggesting that the secretion was evoked by secretory nervous pathways in the enteric nervous system. It is concluded that the 'spontaneous' fluid and electrolyte secretion seen in denervated intestines of SHR is normally 'concealed' by an augmented rate of firing in the regional adrenergic nerve fibres controlling fluid and electrolyte transport. The possible importance of the 'spontaneous' intestinal secretion in SHR in the pathophysiology of arterial hypertension is tentatively discussed.

Adrenergic Fibers↗
PubMed1986

The net fluid secretion caused by cyclic 3'5'-guanosine monophosphate in the rat jejunum in vivo is mediated by a local nervous reflex.

The tissue concentration of cyclic 3'5'-guanosine monophosphate (cGMP) has been shown to increase in the small intestine when net fluid secretion is evoked by the heat-stable enterotoxine of Escherichia coli. Lipophilic cGMP analogues are also known to elicit intestinal fluid secretion. It is therefore believed that an increase in intracellular cGMP concentration in enterocytes mediates this secretion. The present study reports that the fluid secretion, elicited by placing two different cGMP analogues, dibutyryl-cGMP and 8-Br-cGMP, in the intestinal lumen of anaesthetized rats in vivo, is significantly inhibited by atropine, hexamethonium and lidocaine. It is proposed that cGMP activates a reflex in the enteric nervous system which, in part, explains the observed fluid secretion.

Acetylcholine↗
PubMed1986

Blood flow distribution, lymph flow, villus tissue osmolality and fluid and electrolyte transport after exposing the cat small intestine to sodium deoxycholate.

The effect of luminal perfusion of a dihydroxy bile salt (sodium deoxycholate) on net fluid transport, intestinal haemodynamics, lymph flow, electrolyte transport and villus tissue osmolality was studied in cat jejunum. Furthermore, the effects of hexamethonium and tetrodotoxin, two drugs influencing nervous activity, were investigated. Concomitant to net fluid secretion, the bile salt increased mucosal blood flow whereas capillary filtration coefficient and lymph flow remained unchanged. Net sodium and chloride transport changed from absorption to secretion. The change of sodium transport was due to both an increased flux from tissue to lumen and a reduced flux in the opposite direction. Villus tissue hyperosmolality was reduced. None of the effects on intestinal haemodynamics correlated with the change in net fluid transport. Furthermore, hexamethonium and tetrodotoxin inhibited the secretion of fluid and electrolytes without influencing the induced changes in intestinal haemodynamics. It is concluded that the bile salt induces intestinal fluid secretion by stimulating an active secretory process in the crypts via enteric nerves. A minor part of the total change in net fluid transport may be due to a reduced uptake in the villi.

Animals↗
PubMed1986

Intestinal fluid and electrolyte transport in man during reduced circulating blood volume.

The effect on intestinal net transport of fluid and electrolytes of a reduced circulating blood volume was studied in the human jejunum with the triple lumen perfusion technique. The blood volume was reduced by changing the lower extremities from an elevated to a dependent position combined with a venous stasis. The tilting manoeuvre, probably resembling a bleeding of about 600-800 ml, significantly increased net absorption of fluid, sodium and chloride while glucose transport was unaffected. Concomitantly the blood flow decreased and vascular resistance increased in the forearm vascular bed. The results are consistent with the hypothesis that activity in the sympathetic nervous system initiated from unloading of the cardiopulmonary volume receptors enhances intestinal absorption of fluid and electrolytes. The results also indicate that the human intestines are an important target organ in the compensatory mechanisms activated during hypovolaemia due to - for example, haemorrhage.

Adult↗
PubMed1986

Involvement of the enteric nervous system in the intestinal secretion induced by sodium deoxycholate and sodium ricinoleate.

Rat small intestine was continuously perfused for up to 3 h with two different concentrations of sodium deoxycholate (4 and 8 mM) or with sodium ricinoleate (6 mM). The 4-mM bile salt solution produced a secretion that developed to a maximal rate within 3 h, whereas the maximal rate was reached within 1 h with the 8-mM bile salt solution. Hexamethonium, a ganglionic blocker, and lidocaine, a local anesthetic, always reduced the net fluid secretion to approximately zero irrespective of the rate of bile-salt-induced secretion, the concentration of the bile salt, or the perfusion time. Fluid secretion induced by sodium ricinoleate was, like the bile-salt-induced secretion, markedly inhibited by hexamethonium and lidocaine but not by atropine. It is concluded that the rate of secretion induced by the bile salt is related to the monomer concentration of free bile salt molecules in close proximity to or within the intestinal epithelium. The intestinal fluid secretion is mainly due to stimulation of an active secretory process via an activation of enteric nerves. Sodium ricinoleate evokes secretion via similar nervous reflex mechanisms.

Animals↗
PubMed1985

Mechanisms underlying the intestinal fluid secretion evoked by nociceptive serosal stimulation of the rat.

Intestinal net fluid transport was measured in vivo continuously with a gravimetric method. Chemical stimulation of the jejunal serosa with hydrochloric acid (0.1 M), ethanol (20%), cat bile or 7-deoxycholic acid (10 mM) evoked an intestinal fluid secretion. Hexamethonium (10 mg/kg b.wt.i.v.) or serosal application of lidocaine (1% solution) partially blocked this secretory response. Bradykinin and prostaglandin E1, two important inflammatory mediators, elicited fluid secretion when applied to the serosal surface at a concentration of 10(-4) M. This secretion was also partly inhibited by hexamethonium. Furthermore indomethacin (10 mg/kg b.wt. i.v.) or pyrilamine (10 mg/kg b.wt. i.v.), a H1-receptor blocker, partly inhibited the secretory response caused by chemical stimulation of the serosa while cimetidine (1 mg/kg b.wt. i.v.), a H2-receptor blocker, had no effect. Freeze sectioned samples from chemically stimulated intestines were examined by fluorescence microscopy. A leakage of i.v. administrated Evans blue labelled albumin into the interstitial space of the serosa and the outer layer of the muscularis was found. It is concluded: The intestinal fluid secretion studied is mainly elicited by nociceptive stimulation of nerves in the serosa or the outer muscularis. The reflex may be activated by the local release of histamine, kinins and prostaglandins. The reflex studied is part of an inflammatory response.

Animals↗
PubMed1985

The enteric nervous system participates in the secretory response to the heat stable enterotoxins of Escherichia coli in rats and cats.

Intestinal secretion was evoked in periarterially denervated jejunal segments of anesthetized rats and cats by exposing the intestines to the heat stable (ST) toxins from a strain of Escherichia coli producing both STa and STb toxins. The secretion was significantly inhibited and to about the same relative extent by the addition of each one of the three following drugs: hexamethonium (i.v., rats), lidocaine (applied on the serosal surface, rats) and tetrodotoxin (intra-arterial, cats). Atropine inhibited fluid secretion in some experiments. It is proposed that a nervous mechanism is mediating part of the secretory response to Escherichia coli heat stable toxins, since three different drugs, which influence nervous activity in different ways, significantly diminished the secretory response. A model for the secretory nervous reflex(es) within the enteric nervous system is proposed; Escherichia coli heat stable toxins activate a "receptor cell" in the epithelium, which then stimulates surrounding dendritic nerve endings via the release of unknown substance(s). A nicotinic receptor is involved but further characteristics of the nervous reflex(es) remain to be elucidated.

Animals↗
PubMed1985

Evaluation of laser Doppler flowmetry in the assessment of intestinal blood flow in cat.

Laser Doppler flowmetry with a differential detector system has been used in the assessment of blood flow in the feline small intestine. Simultaneous mucosal and serosal laser Doppler flowmeter recordings were compared with total blood flow of a bowel segment measured by an optical drop-recorder unit in 6 cats. Blood flow through the muscularis layer was estimated using the 85Kr washout technique. A correlation coefficient of r = 0.96 (mucosal recordings = 90, serosal recordings = 80, p less than 0.001) was obtained between laser Doppler flowmeter output signals and total blood flow at different levels of vascular tone, regardless of whether the flowmeter recordings were made from the mucosal or the serosal side of the bowel wall. At intense vasodilation, the flowmeters showed a tendency to underestimate blood flow. The flowmeter signals were at variance with the muscularis blood flow but were clearly correlated to the calculated mucosal-submucosal blood flow. The uneven blood flow distribution in the intestinal wall did not affect the ability of the flowmeters to reflect total blood flow from either side of the bowel wall. A calibration curve could be constructed for approximate interpretation of the laser Doppler signals in absolute flow units. However, further experiments in humans and further development of the technique must be performed to elucidate clinical applications of the method.

Animals↗