PubMed Health⌕ Search

Biomedical subjects

C Jönson

Publications and source records attributed to C Jönson.

25 records · Page 2Linked to original sources
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↗
PubMed1985

Blockade of substance P receptors inhibits non-nicotinic, non-adrenergic colonic contractions induced by stimulation of the lumbar sympathetic nerves to the feline large intestine.

Experiments were performed on chloralosed cats, pretreated with guanethidine and hexamethonium and with ligated adrenals. The motility of an arterially isolated colonic segment was monitored by a volumetric method. Colonic contractions were induced either by electric stimulation of the centrally cut lumbar splanchnic nerves, or by close i.a. injections of acetylcholine (ACh). Close i.a. injections of substance P (SP) were performed in order to test the degree of SP-receptor blockade. Blockade of colonic SP-receptors, either by close i.a. administration of large amounts of SP itself or by Spantide, a competitive SP-receptor antagonist, markedly reduced or abolished the neurally induced colonic contractions, while responses to ACh were unchanged. These results indicate a role for SP, or a closely related peptide, as an intermediate neurotransmitter in the neurally induced colonic responses. Thus, the present study gives support to the hypothesis that non-nicotinic, non-adrenergic colonic contractions, in response to electric stimulation of sympathetic nerves, are due to an antidromic activation of sensory neurons with peripheral excitatory collaterals which release SP, in turn activating the colonic smooth muscle, mainly via a muscarinic mechanism.

Acetylcholine↗