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Biomedical subjects

O Lundgren

Publications and source records attributed to O Lundgren.

At least 127 records · Page 7Linked to original sources

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↗

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↗

Role of splanchnic resistance vessels in overall cardiovascular homeostasis.

The reactions of splanchnic resistance vessels elicited reflexly from cardiovascular baroreceptors, volume receptors, and chemoreceptors are briefly reviewed. Unloading the baroreceptors and/or the volume receptors evokes a chiefly neurogenic constriction of resistance vessels in the splanchnic region. There is no significant change in the post- to precapillary resistance ratio to evoke any change in mean capillary hydrostatic pressure. In contrast, the post- to precapillary resistance ratio of the skeletal muscle vascular bed falls, thus lowering mean capillary pressure and causing an autotransfusion of the cardiovascular system. Stimulating the chemoreceptors induces vascular effects in the splanchnic organs and the skeletal muscle similar to that of unloading the baroreceptors. In hemorrhagic hypotension an integrated response from the different receptors is observed. No change occurs in the post- to precapillary resistance ratio in the splanchnic area even during prolonged hemorrhagic hypotension.

Animals↗

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↗

Countercurrent exchange of progesterone and antipyrine between human utero-ovarian vessels, and of antipyrine between the femoral vessels in the cat.

The utero-ovarian vein and ovarian artery in surgical specimens were cannulated and perfused in a countercurrent manner with isotonic, buffered solutions, fortified on the venous side with progesterone or radiolabelled methylantipyrine. Both substances were gradually transferred from the vein into the artery in the majority of the experiments while albumin was not exchanged. The results point to the existence of a countercurrent exchange mechanism in the human ovarian pedicle. Hardly detectable amounts of methylantipyrine were transferred from femoral vein to artery in the cat.

Animals↗

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↗

Gastric blood flow and distribution in anesthetized cat and man as studied by an inert gas elimination method.

Gastric blood flow and its intramural distribution were studied in anesthetized cat and man by recording the elimination of intra-arterially injected krypton-85. The elimination was monitored with two external detectors--a scintillation detector recording the disappearance of gamma-activity from the entire gastric wall and a G-M tube recording the disappearance of beta-activity from the muscle layer only. Total and muscle layer blood flow could be calculated from the washout curves, and, knowing these variables, the blood flow to the mucosa-submucosa could be indirectly calculated. Gastric blood flow in the cat and man closely resembled each other, both in magnitude and distribution. Total blood flow in man 'at rest' was 12 +/- 4 ml/min and 100 g tissue (mean +/- S.D.; no. = 20), muscle blood flow amounting to 7 +/- 3 and mucosa-submucosa flow to 16 +/- 8 ml/min and 100 g muscle and mucosa-submucosa tissue, respectively. The distribution to the muscle layer was 26 +/- 14% and to the mucosa-submucosa 74 +/- 14% of total gastric blood flow.

Anesthesia, General↗

Gastric blood flow and distribution: the effect of pentagastrin in anesthetized cat and man as studied by an inert gas elimination method.

Using a krypton-85 elimination method previously described, the effect of pentagastrin on gastric blood flow has been studied in 28 anesthetized patients, 12 control patients, and 16 patients with duodenal ulcer disease. Both in control and duodenal ulcer patients a significant increase in total blood flow was found, reflecting an increase of flow in the mucosa-submucosa layer of the corpus. In normal subjects a 5-fold increase in flow was found in this tissue layer, whereas the corresponding increase in duodenal ulcer patients was 12-fold. Concomitantly, a significant decrease of flow distribution to the muscle layer was seen. In the antrum pentagastrin did not cause any significant changes in either mucosa-submucosa or muscle layer blood flow. No qualitative differences in the response to pentagastrin, with regard to the gastric blood flow, was found between normal subjects and duodenal ulcer patients.

Adult↗

Mucosal lesions in the feline small intestine in septic shock.

The incidence and possible pathogenic mechanisms in the development of small intestinal mucosal lesions in experimental septic shock were investigated in cats. Mucosal lesions were found in 50% of the animals following a standardized bacteremia, and 15% had pronounced mucosal damage. The development of these lesions was not correlated with intestinal vasoconstriction or to portal hypertension but with decreased systemic arterial blood pressure during the last hour of the experiments. The correlation between mucosal damage and arterial hypotension in septic shock supports the view that these lesions are caused by hypoxia secondary to an increased efficiency in the countercurrent exchange mechanisms of oxygen in the villi.

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↗

An evaluation of the functional implications of the intestinal mucosal lesions in shock.

Small intestinal mucosal lesions are reported in clinical shock and are commonly found in experimental shock. Experimental series in which shock is induced by regional intestinal ischemia or IV infusion of live Escherichia coli in cats or by graded intestinal vascular occlusion in rats are described. In all series mucosal damage was related to pronounced hypotension or mortality. In the cat models myocardial dysfunction was demonstrated in vivo by IV volume load and recording of changes in left ventricular filling pressure as related to cardiac performance. Following intestinal ischemia in cats and intestinal vascular obstruction in rats the intestinal venous plasma was found to contain cardiotoxic factors when tested in vitro. It is proposed that the development of small intestinal mucosa lesions in shock tends to further aggravate hypotension by causing intestinal release of cardioinhibitory material.

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↗