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J Cassuto

Publications and source records attributed to J Cassuto.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1986

Failure of epidural anesthesia to prevent postoperative paralytic ileus.

This study used radiopaque markers and serial abdominal radiographs to assess the effect of epidural anesthesia on postoperative colonic ileus. Epidural anesthesia did not result in significantly faster return of propulsive motility in the colon after surgery as compared with control (P greater than 0.05). In addition, no significant difference was seen between the groups in colonic transit time and time for the first passage of gas and feces. The level of inhibition of sympathetic efferent nerves to the abdominal cavity was assessed by repeated measurements of blood glucose levels during the first postoperative day. Blood glucose levels were found to be significantly lower in the epidural group, demonstrating an inhibition of efferent sympathetic nerves below the level of T-5. Results show lack of effect of continuous epidural anesthesia in the prevention of postoperative paralytic ileus and suggest that mechanisms other than spinal reflexes play a major part in the development and maintenance of intestinal paralysis.

Anesthesia, Epidural↗
PubMed1985

Inhibition of postoperative pain by continuous low-dose intravenous infusion of lidocaine.

Intravenous lidocaine has been reported previously to inhibit postoperative pain when given either as single injections or as short infusions in amounts usually causing adverse reactions. To determine the efficacy of a continuous low-dose (2 mg/kg) intravenous infusion of lidocaine, postoperative pain (visual analogue pain scale) and the requirements for postoperative analgesics were measured in a double-blind randomized trial in 20 patients after cholecystectomy. Lidocaine infusion was started 30 min before the operation and continued for 24 hr after surgery (n = 10). Saline was infused in a comparable group of ten patients. The lidocaine-treated patients had significantly lower pain scores during the first day after surgery (P less than 0.001) and required significantly less meperidine during the first (P less than 0.02) and second postoperative days (P less than 0.01). No adverse reactions to lidocaine were observed. Whole blood levels of lidocaine ranged between 1 and 2 micrograms/ml. The results suggest that low-dose continuous infusions of lidocaine decrease the severity of postoperative pain and are devoid of side effects.

Adult↗
PubMed1984

The involvement of the enteric nervous system in the intestinal secretion evoked by cyclic adenosine 3'5'-monophosphate.

Intestinal fluid secretion was evoked in vivo in rats and cats by introducing dibutyrylcyclic adenosine 3,5-monophosphate (db-cAMP) or theophylline, a phosphodiesterase inhibitor, in the intestinal lumen. The intestines were denervated periarterially. It was demonstrated that three compounds of varying chemical structure and with different modes of action on nerves (tetrodotoxin, lidocaine, hexamethonium) decreased the secretory response 60-70%. It is concluded that the secretion induced by increasing the intracellular cAMP concentrations is in part evoked via the enteric nervous system.

Animals↗
PubMed1983

The involvement of intramural nerves in cholera toxin induced intestinal secretion.

In previous reports we have suggested that nervous reflexes are involved in the pathophysiology of cholera secretion and that these nervous reflexes involve a cholinergic synapse and a neuron with vasoactive intestinal polypeptide (VIP) as neurotransmitter. These proposals were further analyzed in this study. Tetrodotoxin (TTX) and lidocaine applied on the serosal surface inhibited cholera secretion in segments of rat small intestine. Fluid absorption in control rats was not significantly changed. Hexamethonium given i.v. decreased cholera secretion in the cat. No additional inhibition of cholera secretion was observed after giving TTX close i.a. Furthermore, the intestinal secretion evoked by VIP was not influenced by hexamethonium given i.v. or TTX given close i.a. The present observations support the hypothesis of a role for nervous reflexes in cholera secretion. The results suggest that at least a major part of the proposed nervous reflex(es) in cholera have a cholinergic synapse. Furthermore, the VIP-ergic neuron is situated "distal" to the cholinergic neuron in the reflex(es) closer to the effector cells.

Animals↗
PubMed1983

5-Hydroxytryptamine and cholera secretion: a histochemical and physiological study in cats.

The effect of cholera toxin on the content of 5-hydroxytryptamine (5-HT) in the enterochromaffin cells of the cat small intestine was estimated by cytofluorimetry of individual enterochromaffin cells at varying times after exposing the intestinal mucosa to the toxin. The observed changes in 5-HT levels in the enterochromaffin cells were correlated with the simultaneously measured rate of net fluid transport across the intestinal epithelium. Intestinal segments exposed to cholera toxin showed a statistically significant decrease in 5-HT levels of enterochromaffin cells compared with segments exposed to heat-inactivated cholera toxin. A good correlation (r = 0.73) was found between relative 5-HT fluorescence in enterochromaffin cells and net fluid transport across the intestinal epithelium. Thus, a diminished 5-HT content was associated with a decreased rate of fluid absorption or an increased rate of secretion. A hypothesis is presented for explaining the possible role of the enterochromaffin cells in the pathophysiology of cholera secretion.

Animals↗
PubMed1983

The importance of the enteric nervous system for the bile-salt-induced secretion in the small intestine of the rat.

We have investigated the possible involvement of the enteric nervous system in the intestinal secretion induced by sodium deoxycholate. Hexamethonium, lidocaine, and tetrodotoxin significantly inhibited the fluid secretion in extrinsically innervated and denervated rat jejunal segments. Atropine had no effect. We conclude that the sodium-deoxycholate-induced intestinal secretion is partly caused by the activation of local nervous reflexes.

Animals↗
PubMed1982

The effect of nicotinic and muscarinic receptor blockade on cholera toxin induced intestinal secretion in rats and cats.

The effects of hexamethonium (cholinergic nicotinic receptor antagonist) and atropine (cholinergic muscarinic receptor antagonist) on cholera toxin induced secretion were investigated in denervated segments of the small intestine of rats and cats. While there was no effect of atropine, hexamethonium markedly inhibited choleraic secretion and turned it into a net fluid absorption in many animals. This observation further strengthens our hypothesis that the enteric nervous system is involved in cholera secretion.

Animals↗
PubMed1982

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↗
PubMed1982

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↗
PubMed1982

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↗
PubMed1981

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↗
PubMed1981

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↗
PubMed1979

Intramural blood flows and flow distribution in the feline small intestine during arterial hypotension.

The vascular reactions of the parallel-coupled vascular sections of the small intestine were studied during hypotension at two different levels of intestinal arterial inflow pressure, using a 85Kr elimination technique. The regional hypotension was accomplished by partially occluding the superior mesenteric artery with a clamp and maintained for 2 h. At the higher level (50-55 mmHg) total intestinal blood flow decreased but not to the same relative extent as blood pressure due to the autoregulatory capacity of the intestinal vascular bed. The flow autoregulation was also reflected in a decreased blood flow resistance. The distribution of blood to the muscularis and mucosa-submucosa layer, respectively, did not change significantly during or after hypotension as compared to the prehypotensive level, since the relative flow decrease was the same in the mucosa-submucosa and in themuscularis. At the lower arterial pressure level (30-35 mmHg) a more marked decrease of intestinal blood flow and flow resistance was observed as compared to the experiments performed at the 50-55 mmHg pressure level. Moreover, muscularis blood flow was relatively more decreased than blood flow in the mucosa-submucosa implying the fraction of total blood flow diverted to the muscularis was significantly decreased. Despite this redistribution of blood flow, a histological damage was apparent only in the mucosa, particularly at the villous tips.

Animals↗