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Biomedical subjects

C Jönson

Publications and source records attributed to C Jönson.

At least 19 recordsLinked to original sources
PubMed1992

The mediation of increased duodenal alkaline secretion in response to 10 mM HCl in the anaesthetized rat. Support for the involvement of capsaicin-sensitive nerve elements.

Experiments were performed on chloralose-anaesthetized rats. Bicarbonate secretion by the duodenal mucosa was continuously recorded by use of an in situ-titration technique. Exposing the duodenal segment to 10 mM HCl over 5 min increased the bicarbonate transport by about 65%. This acid-induced secretory response was resistant to neural decentralization by means of bilateral cervical vagotomy and/or splanchnicotomy. Furthermore, in the decentralized state, serosal application of the local anaesthetic lidocaine or tetrodotoxin (TTX) lowered basal duodenal bicarbonate secretion. Despite the presence of lidocaine or TTX, exposure of the duodenal mucosa to 10 mM HCl induced a net increase in secretion with a magnitude similar to that observed in the control situation with intact nerves. A 5-min exposure period of the decentralized duodenal segment to capsaicin (1.2 mg ml-1) raised bicarbonate secretion, a response which also occurred in the presence of lidocaine (serosa). Tachyphylaxis to capsaicin blocked the secretory response to 10 mM HCl and inhibited the response to luminal prostaglandin E2 (1.5 10(-5) M) by 80%. The present results indicate that luminal exposure to 10 mM HCl activates capsaicin-sensitive primary afferents which, locally within the submucosa or epithelium, activate the bicarbonate secretion.

Animals↗
PubMed1991

Hypovolaemia inhibits acid-induced alkaline transport in the rat duodenum via an alpha-2 adrenergic mechanism.

Acid exposure of the duodenal mucosa is a well-known stimulant of the mucosal alkaline secretion. We have previously reported that a minor blood loss inhibits this secretory increment via activation of the splanchnic nerves. In the present study the pharmacological characteristics of the splanchnic neural inhibition of the alkaline secretion were investigated. Duodenal HCO3- secretion was measured by in-situ titration in chloralose-anaesthetized rats. Exposure of the duodenal mucosa to hydrochloric acid (0.01 M, 5 min) increased the secretion by approximately 60%. A 10% decrease in blood volume simultaneously to the luminal acidification abolished the secretory increase, as previously reported. Treatment with either guanethidine or yohimbine blocked the bleeding-induced inhibition of the secretion after acid-exposure. Neither prazosin nor propranolol did prevent such hypovolaemia-induced inhibition of duodenal alkaline secretion. The present results suggest that the splanchnic neural inhibition of acid-induced duodenal HCO3- secretion is mediated via adrenergic nerve fibres and alpha-2 adrenoceptors.

Animals↗
PubMed1990

Effects of cigarette smoke and nicotine on duodenal bicarbonate secretion in the rabbit and the rat.

The effects of short-time exposure to cigarette smoke on duodenal mucosal bicarbonate secretion were studied in anesthetized rabbits and rats. The bicarbonate secretion was measured by continuous titration of recirculating luminal perfusate. In artificially ventilated rabbits, intermittent exposure to cigarette smoke during two 10-min periods caused a marked (approximately 40%) decrease (p less than 0.01) in duodenal bicarbonate secretion. After the exposures, secretion gradually recovered and had returned to the pre-exposure rate after 50 min. The decrease in secretion was associated with decreases in heart rate (approximately 15%) and blood pressure (approximately 30%) that, however, were of shorter duration. Neither reduced amounts of smoke (1/6 or 1/3) nor nicotine (25-1,000 micrograms/kg, intravenously) had any major effect on the bicarbonate secretion. In the spontaneously breathing rat, smoke was administered for 1-2 breaths every 30 s during a 5-min period. This exposure resulted in a significant (p less than 0.05) decrease in bicarbonate secretion and some increase in the blood pressure. Exposure to smoke had no effect on the secretion in rats with both splanchnic nerves cut, suggesting neural sympathetic mediation of the smoke-induced inhibition.

Animals↗
PubMed1990

Vagal and sympathetic control of gastric and duodenal bicarbonate secretion.

This report summarizes data concerning the extrinsic neural control of bicarbonate secretion by the gastric and duodenal mucosa. Parasympathetic vagal effects have been studied in experimental animals and in man by means of direct electrical vagal stimulation, sham-feeding procedures and intracerebroventricular peptide injections. The results show that the vagal nerves have a stimulatory effect on gastroduodenal bicarbonate secretion. Furthermore, both conventional nicotinic and muscarinic cholinoceptor, as well as non-cholinergic transmission, mediate the vagal effect. Sympathetic splanchnic nerve effects have been investigated by means of nerve sections, direct electrical stimulation, reflex activation and stereotaxic electrical hypothalamic stimulation. The data show that the splanchnic nerves have a predominantly inhibitory action on gastroduodenal bicarbonate secretion by use of peripheral adrenergic neurones and receptors of the alpha-2 subtype. The role of the adrenal glands is not fully understood. It is concluded that gastroduodenal bicarbonate secretion is under autonomic neural control, mainly in the classical antagonistic fashion; the parasympathetic vagal nerves stimulate bicarbonate output, whereas the sympathetic splanchnic nerves are mainly inhibitory.

Acid-Base Equilibrium↗
PubMed1990

Effects of acute administration of omeprazole or ranitidine on basal and vagally stimulated gastric acid secretion and alkalinization of the duodenum in anaesthetized cats.

Experiments were performed on acutely vagotomized cats during chloralose anaesthesia. In order to avoid sympathoadrenergic influences, the adrenal glands were ligated and the splanchnic nerves were cut bilaterally in all animals. The gastric lumen was perfused with saline and the H+ secretion was calculated from pH measurements in the perfusate. HCO3- secretion by the duodenal mucosa was titrated in situ. Omeprazole (4 mg kg-1 i.v., dissolved in PEG400, 40% w/v) did not influence basal or vagally induced HCO3- secretions, but inhibited by about 80% the H+ secretory response induced by electric vagal stimulation. Acute administration of ranitidine (5 mg kg-1 i.v.) transiently lowered arterial pressure, an effect which was followed by a sustained compensatory tachycardia. Ranitidine raised basal duodenal HCO3- secretion by 50% and inhibited vagally induced gastric H+ secretion by about 70%, whereas vagally induced HCO3- secretion was not influenced. The results suggest that vagal nerve stimulation raises the duodenal bicarbonate secretion via a mechanism independent of the level of gastric H+ secretion.

Anesthesia↗
PubMed1990

Effects of hypovolemia on blood flow, arterial [HCO3-], and HCO3- output in the rat duodenum.

The effects of bleeding-induced hypovolemia on duodenal blood flow (microsphere technique), arterial [HCO3-], and duodenal HCO3- secretion (in situ titration) were investigated in chloralose-anesthetized rats. A 10% decrease in blood volume reduced duodenal HCO3- secretion by 44%, duodenal blood flow by 31%, and arterial [HCO3-] by 11%. In a group with cervically cut vagal nerves, basal duodenal HCO3- secretion was greater than 50% lower compared with controls. Basal blood flow and arterial [HCO3-] were on similar levels as in nonvagotomized animals. Furthermore, bleeding failed to lower duodenal alkaline output in rats with cut vagal nerves, although blood flow and arterial [HCO3-] were reduced to a similar extent as in the vagally intact controls. In a yohimbine-treated group, a 10% bleeding reduced duodenal blood flow by 28% and arterial [HCO3-] by 7% without influencing duodenal HCO3- secretion. We suggest that the hypovolemia-induced inhibition of duodenal alkaline secretion is not caused by a decrease in blood and/or arterial [HCO3-]. Instead, other factors may be of importance, for example, neural effects on enteric secretomotor neurons or directly on the secreting epithelium.

Animals↗
PubMed1989

Splanchnic nerve activation inhibits the increase in duodenal HCO3- secretion induced by luminal acidification in the rat.

Acid exposure of the duodenal mucosa increased duodenal HCO3- secretion by approximately 60%. When the acid exposure was performed simultaneously with an arterial bleeding of 0.6 ml/100 g body wt (10% of the total blood volume), the increase in duodenal HCO3- secretion was totally abolished. When the acid exposure and bleeding procedures were performed at the same time in rats with bilaterally cut splanchnic nerves, alkaline secretion increased by 60%, as it did in the unbled rats. Direct electrical stimulation of the splanchnic nerves (10 Hz, supramaximal intensity) inhibited the stimulatory effect of duodenal acid exposure on alkaline secretion. Taken together, the data suggest that the sympathetic nervous system, because of splanchnic nerve activation, inhibits the acid-induced increase in duodenal HCO3- secretion.

Animals↗
PubMed1989

Influences of the sympatho-adrenal system on gastric motility and acid secretion and on gastroduodenal bicarbonate secretion in the cat.

Experiments were performed on acutely vagotomized cats during chloralose anaesthesia. Gastric H+ and HCO3- secretions were calculated from the pH and PCO2 in a luminal perfusate. Gastric motility was reflected by changes in hydrostatic pressure within the luminal perfusion system ('intragastric pressure'). Duodenal HCO3- secretion was monitored by pH titration in situ. Animals with an intact sympatho-adrenal system (group 1) were compared with others subjected to splanchnicotomy (group 2), adrenal gland ligation (group 3), and splanchnicotomy plus adrenal gland ligation (group 4). Basal gastric H+ secretion, as well as vagally induced H+ secretory responses, did not differ significantly between groups. Basal gastric HCO3- secretion was lower in all groups with a manipulated sympatho-adrenal system compared to the intact controls. Vagally induced increases in gastric HCO3- secretion were enhanced in the splanchnicotomized groups (groups 2 and 4). Basal as well as vagally induced increases in intragastric pressure and duodenal HCO3- secretion were enhanced in animals subjected to splanchnicotomy, with or without simultaneous adrenal gland ligation (groups 2 and 4). Adrenal gland ligation per se had no such effects. The results suggest that the adrenal glands exert a stimulatory action on basal gastric HCO3- secretion. Basal intragastric pressure and basal duodenal HCO3- secretion are inhibited by post-ganglionic sympathetic neurons, not involving the adrenal glands. Also, vagal excitatory effects on gastric motility, as well as on gastric and duodenal HCO3- secretions, are inhibited by such a direct neural mechanism.

Adrenal Glands↗
PubMed1989

Increased duodenal HCO3- output after blood volume expansion in the rat: an effect mediated by atrial natriuretic peptide (ANP)?

Duodenal HCO3- secretion was measured by in-situ titration in chloralose-anaesthetized rats. The effects of hypervolaemia, induced by i.v. injections of an albumin infusion, on duodenal HCO3- secretion were investigated. A 10% increase in blood volume increased duodenal HCO3- secretion by about 50%, and this effect was unaffected by splanchnicotomy. If the splanchnicotomy was combined with cervical vagotomy, the basal HCO3- secretion was lower but the increase in secretion after 10% blood volume expansion with albumin was still 50%. If the same increase in blood volume was produced in splanchnicotomized and vagotomized rats in which the right atrial appendix had been removed, a procedure that markedly reduces the ANP (atrial natriuretic peptide)-producing cells, no increase in secretion could be observed. Intravenous injections of alpha-r-ANP (10 micrograms kg-1 and 30 micrograms kg-1) increased duodenal HCO3- secretion in a dose-dependent fashion. Based on the present findings, we suggest that hypervolaemia increases duodenal HCO3- secretion via release of ANP from the heart.

Animals↗
PubMed1989

Hypothalamic inhibition of duodenal alkaline secretion via a sympatho-adrenergic mechanism in the rat.

Experiments were performed on rats anaesthetized with chloralose. A duodenal segment was perfused with recirculating isotonic saline, and alkalinization of this perfusate (HCO3- secretion) was measured by continuous pH-stat titration. Stereotaxic electric unipolar stimulations were performed in the perifornical region of the hypothalamus. Stimulation points eliciting an increased arterial pressure were stimulated for a period of 15 min. Duodenal HCO3- secretion decreased in 19 out of 25 experiments and increased in four out of 25 experiments. Inhibitory responses to hypothalamic stimulation were blocked either by thoracic epidural anaesthesia or by the adrenolytic agent guanethidine, suggesting a spinal pathway to the duodenum, presumably in the thoracic splanchnic nerves, and involvement of adrenergic neurons.

Anesthesia, Epidural↗
PubMed1988

Afferent electrical stimulation of mesenteric nerves inhibits duodenal HCO3- secretion via a spinal reflex activation of the splanchnic nerves in the rat.

The experiments were performed on male Sprague-Dawley rats anaesthetized with chloralose. Duodenal HCO3- secretion was measured in situ by pH-stat titration. The nerves bundles surrounding two randomly chosen mesenteric vessels were electrically stimulated (3 Hz, supramaximal intensity) in the afferent direction. This was done in order to mimic the intestino-intestinal spinal reflex activation of the splanchnic sympathetic fibres. The procedure reduced duodenal HCO3- secretion by 20% together with an increase in mean arterial pressure and heart rate. Duodenal HCO3- secretion decreased similarly in control rats and in those subjected to a cervical cord transection, whereas animals with bilaterally cut splanchnic nerves did not respond to such mesenteric nerve stimulation. Pharmacological pretreatment with guanethidine or yohimbine, but not prazosin, inhibited the reduction in duodenal HCO3- secretion. Thus the data suggest that electrical stimulation of mesenteric afferent nerves inhibits duodenal HCO3- secretion via a spinal reflex activation of splanchnic sympathetic nerve fibres to the duodenum, and that the response is mediated via alpha 2 adrenoceptors.

Afferent Pathways↗
PubMed1988

Splanchnic nerve stimulation inhibits duodenal HCO3- secretion in the rat.

Sympathoadrenergic inhibition of HCO3- secretion by the duodenal mucosa was studied in chloralose anesthetized rats. Duodenal HCO3- secretion was measured in situ by pH-stat titration. Direct efferent electrical stimulation of the cut splanchnic nerves (10 Hz, supramaximal intensity) inhibited the duodenal alkaline output by approximately 50%. This inhibitory response was blocked by the administration of either the adrenolytic agent guanethidine or the alpha 2-adrenoceptor antagonist yohimbine. However, neither the alpha 1-adrenoceptor antagonist prazosin nor the beta-adrenoceptor antagonist propranolol blocked the response to splanchnic nerve stimulation. The present data suggest that electrical splanchnic nerve stimulation inhibits duodenal HCO3- secretion via activation of adrenergic nerve fibers and alpha 2-adrenoceptors within the peripheral nervous system.

Animals↗
PubMed1987

Effects of splanchnic nerve stimulation and of clonidine on gastric and duodenal HCO3- secretion in the anaesthetized cat.

Experiments were performed on chloralose-anaesthetized cats with ligated adrenals. The vagal and splanchnic nerves were cut and arranged for peripheral electric stimulation. The gastric lumen was perfused with isotonic saline and gastric H+ and HCO3- secretions were calculated from pH/pCO2 measurements in the perfusate. Gastric motility was recorded as changes in hydrostatic pressure in the perfusion circuit. Mucosal HCO3- secretion into the duodenum was monitored in situ by pH-stat titration. Vagal stimulation (10 Hz for 10 min) increased gastric and duodenal HCO3- secretions, as well as gastric motor activity and H+ secretion. Splanchnic nerve stimulation (10 Hz for 10 min) did not affect gastric H+ and HCO3- secretions, but tended to decrease gastric motor tone and basal duodenal HCO3- secretion. Splanchnic nerve stimulation simultaneously with vagal stimulation inhibited gastric contractions and the rise in gastric H+ and duodenal HCO3- secretions observed in response to vagal stimulation alone, but had little effect on the rise in gastric HCO3- secretion. However, such vago-splanchnic stimulation in the presence of the alpha 2-adrenoceptor blocker yohimbine induced gastric contractions, H+ secretory and duodenal HCO3- secretory responses with magnitudes similar to those induced by vagal stimulation alone, whereas the gastric HCO3- secretory response was larger than by vagal stimulation alone. The alpha 2-adrenoceptor agonist clonidine (50 micrograms kg-1 h-1, i.v.) inhibited the gastric contractions and increases in gastric and duodenal HCO3- secretion in response to vagal stimulation, but did not influence vagal stimulation of gastric H+ secretion. The results suggest the existence of a peripheral sympatho-inhibitory action on gastric and duodenal HCO3- secretion involving alpha 2-adrenoceptors. Also splanchnic neural stimulatory effects on gastric and duodenal HCO3- secretion may exist.

Animals↗
PubMed1987

Effects of adrenoceptor antagonists on vagally induced gastric and duodenal HCO3- secretions in the cat.

Experiments were performed on chloralosed cats with ligated adrenal glands. The cervical vagi were cut and arranged for electric stimulation. The gastric lumen was continuously perfused, and the secretions of H+ and HCO3- were calculated from pH/pCO2 measurements in the perfusate. Gastric motility was recorded as changes in hydrostatic pressure within the perfusion system. Mucosal HCO3- secretion into a duodenal segment, distal to the papilla of Vater and Brunners gland area, was titrated in situ by a pH-stat equipment. Animals pretreated with various adrenoceptor blockers or splanchnicotomy were compared with control animals with intact sympatho-adrenergic system. Basal gastric motor activity, H+ and HCO3- secretions, as well as duodenal HCO3- secretion were not influenced by prazosin, propranolol or splanchnicotomy. Yohimbine increased significantly basal gastric HCO3- secretion, but did not influence basal gastric motor activity, H+ secretion or duodenal HCO3- secretion. Vagal stimulation in yohimbine-treated or splanchnicotomized animals induced significantly larger gastric contractions, HCO3- secretory and duodenal HCO3- secretory responses than in the controls, whereas these responses to vagal stimulation were small in prazosin- or propranolol-treated animals. Vagally induced gastric H+ secretory responses were significantly larger in propranolol-treated animals than in controls, whereas prazosin-treated, yohimbine-treated or splanchnicotomized animals in this regard did not differ from the controls. The results suggest the existence of a sympathetic, probably alpha-2-adrenergic, inhibition of vagally induced gastric contractions as well as of the gastric and duodenal HCO3- secretions.

Adrenergic alpha-Antagonists↗
PubMed1987

Bleeding inhibits vagally induced duodenal HCO3- secretion via activation of the splanchnic nerves in anaesthetized rats.

This study was performed on chloralosed rats in order to examine the influence of a minor blood loss on duodenal HCO3- secretion. The HCO3- output was measured by in situ titration in a duodenal segment. Blood loss of 0.3 ml per 100 g body wt (approximately 5% of total blood volume) and 0.6 ml per 100 g body wt (approximately 10% of total body volume) reduced duodenal HCO3- secretion by about 18 and 31%, respectively. Adrenal ligation increased basal output of HCO3- but did not affect the bleeding-induced response. Thoracic epidural anaesthesia or splanchnicotomy did not affect the basal secretion but markedly reduced the depression of duodenal HCO3- secretion due to blood loss. Vagotomy lowered basal duodenal HCO3- secretion and blood loss did not reduce alkaline output in these animals. However, electric stimulation of the cut vagal nerves raised the duodenal HCO3- secretion to a similar level as in rats with intact vagal nerves. In this group blood loss reduced the duodenal HCO3- output as in rats with intact nerves. It is suggested that a small blood loss, via an activation of the sympathetic nervous system, reduces the vagally controlled part of the duodenal HCO3- secretion and that this effect is conveyed in the splanchnic nerves.

Adrenal Glands↗
PubMed1987

Bleeding-induced decrease in duodenal HCO3- secretion in the rat is mediated via alpha 2-adrenoceptors.

This study was performed on chloralosed rats in order to examine the influence of a minor blood loss on duodenal HCO3- secretion. The HCO3- output was measured by in situ titration in a duodenal segment. Blood loss of 0.6 ml per 100 g body wt (approximately 10% of total blood volume) reduced duodenal HCO3- secretion by about 30%. Pretreatment with guanethidine did not affect basal output of HCO3- but markedly reduced the bleeding-induced response. The alpha 2-adrenoceptor antagonist yohimbine did not affect the basal secretion but almost abolished the depression of duodenal HCO3- secretion due to blood loss. Pretreatment with the alpha 1-adrenoceptor antagonist prazosine or the beta-adrenoceptor antagonist propranolol did neither change basal duodenal HCO3- secretion nor the bleeding-induced decrease in duodenal HCO3- secretion. It is suggested that a small blood loss by means of a reflex activation of the sympathetic nervous system, and via the release of transmitter substances from adrenergic nerve endings, reduces the duodenal HCO3- secretion. The inhibitory effect is mainly due to activation of alpha 2-adrenoceptors.

Animals↗
PubMed1986

Vagal stimulation of duodenal HCO3(-)-secretion in anaesthetized rats.

The present study was designed to examine the influence of the vagal nerves on mucosa protective duodenal HCO3(-)-secretion in chloralosed rats. The HCO3(-)-secretion was measured by in situ titration in a duodenal segment devoid of Brunner glands. Cervical vagotomy lowered duodenal HCO3(-)-secretion and stimulation of the cut vagal nerves (10 Hz for 15 min) increased this secretion. Both basal and vagally stimulated duodenal HCO3(-)-secretions were more pronounced in rats with ligated adrenal glands. Atropine did not influence basal duodenal HCO3(-)-secretion, whereas indomethacin and hexamethonium lowered basal secretion in vagotomized rats with ligated adrenal glands. Compared with untreated controls, vagally induced secretory responses were unchanged by atropine, 50% smaller in indomethacin treated rats and almost abolished in rats treated with hexamethonium. The study suggests that the vagal nerves exert an excitatory effect on duodenal HCO3(-)-secretion which is mainly mediated via nicotinic, non-muscarinic transmission, in part dependent on prostaglandin synthesis. Furthermore, the results indicate that the adrenal glands exert an inhibitory action on both the basal and vagally induced mucosa protective HCO3(-)-secretion.

Adrenal Glands↗