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L Fändriks

Publications and source records attributed to L Fändriks.

89 records · Page 5Linked to original sources
PubMed1986

Effect of alpha, beta-methylene ATP on distal colonic and rectal motility--a possible involvement of P2-purinoceptors in pelvic nerve mediated non-adrenergic, non-cholinergic contraction.

The possible involvement of purinoceptors in the parasympathetic nervous control of large intestinal motility was investigated in cats anaesthetized with chloralose and treated with adrenolytics. Distal colonic and rectal motor responses to efferent pelvic nerve stimulation (PNS) and drugs injected close i.a., were recorded by a volumetric method. Single dose i.a. injections of alpha, beta-methylene ATP (mATP) induced colonic and rectal contractions which were resistant to atropine, hexamethonium and indomethacin, as well as to the nerve blocking agent tetrodotoxin. Repeated injections of mATP were followed by attenuated motor responses and eventually complete tachyphylaxis to the compound developed. In the presence of atropine, or a combination of hexamethonium and atropine, contractions elicited by PNS were inhibited during mATP tachyphylaxis. In contrast, prior to such anticholinergic drugs, or in the presence of hexamethonium alone, pelvic nerve mediated contractions persisted despite mATP tachyphylaxis, which did not affect the colonic and rectal contractions evoked by acetylcholine or histamine. The results suggest that P2-purinoceptors are involved in non-adrenergic, non-cholinergic large intestinal excitatory motor responses to PNS.

Adenosine Triphosphate↗
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↗
PubMed1986

Sympatho-adrenergic inhibition of vagally induced gastric motility and gastroduodenal HCO-3 secretion in the cat.

Chloralosed cats were acutely vagotomized and their adrenal glands were ligated. The gastric lumen was perfused with isotonic NaCl and gastric motility was recorded as change in hydrostatic pressure within the perfusion circuit. Gastric secretions of H+ and HCO3- were calculated from continuous measurements of pH and pCO2 in the perfusate. Mucosal HCO3- secretion in the distal duodenum was titrated in situ by pH-stat equipment. The experiments were divided into three different groups dependent on the state of sympathetic splanchnic nervous supply: intact; cut on a preganglionic level; blocked with the adrenolytic agent guanethidine. Basal levels for gastric motility, gastric H+ and HCO3- secretions and duodenal HCO3- secretion were more or less similar in all groups. Gastric motility, gastric HCO3- and duodenal HCO3- secretory responses to bilateral vagal stimulation were significantly enhanced in splanchnicotomized or guanethidine-treated animals as compared to controls with intact sympathetic supply. However, no clear differences in gastric H+ secretory responses to vagal stimulation were demonstrated between animals with an intact or disrupted sympathetic innervation. These results suggest a sympatho-adrenergic inhibitory action on vagally induced mucosa-protective HCO3- secretion in the stomach and the duodenum. Furthermore, vagal stimulation in animals with intact splanchnic nerves induced a guanethidine-resistant delayed increase in duodenal HCO3- secretion. The nature of this response was not further analysed.

Adrenal Glands↗
PubMed1986

Simultaneous measurements of gastric motility and acid-bicarbonate secretions in the anaesthetized cat.

Chloralosed cats were acutely vagotomized, their splanchnic nerves cut and the adrenal glands ligated. The gastric lumen was perfused with isotonic NaCl and gastric motility was monitored as changes in hydrostatic pressure within the perfusion circuit. Gastric secretion of H+ and HCO3- were calculated from continuous measurements of pH and PCO2. Methodological tests ex vivo showed good accuracy of the estimations. Recovery of H+ after HCl instillation into the stomach in vivo was almost complete, while HCO3- recovery after NaHCO3 instillations was 85-95%. Pentagastrin (10 micrograms kg-1 h-1 i.v.) stimulated gastric contractile activity and increased gastric H+ secretion 30-fold, while HCO3- secretion decreased somewhat. Carbachol (4 micrograms kg-1 h-1) induced gastric contractions and increased H+ secretion by 400% and HCO3- output by 100-130%. Electrical stimulation of the cut vagal nerves (10 Hz for 10 min) induced well known gastric motor responses and increased gastric H+ secretion 20-fold preceded by a transient doubling of HCO3- secretion. Omeprazole, a selective inhibitor of gastric H+ secretion, decreased the vagally induced H+ secretion, while recorded gastric HCO3- secretion was clearly enhanced. In conclusion, the technique permits simultaneous recordings of rapid alterations of gastric motility and H+ and HCO3- secretions. However, HCO3- secretion was modestly underestimated, probably due to mucosal CO2 absorption.

Animals↗
PubMed1986

Vagal and splanchnic neural influences on gastric and duodenal bicarbonate secretions. An experimental study in the cat.

HCO3(-)-secretion by the gastroduodenal epithelium is probably an important factor in the mucosal defence against luminal H+. The aim of this study was to establish the existence of autonomic nervous influence on gastroduodenal HCO3(-)-secretion and to present some pharmacological characteristics. Experiments were performed on chloralosed cats with ligated adrenals. The vagal nerves were cut at the cervical level and arranged for electrical stimulation. The sympathetic splanchnic nerves were either cut or left intact. A gastric perfusion technique was developed which allowed simultaneous measurements of gastric motility and H+ and HCO3(-)-secretions, the latter being estimated from measurements of pH and pCO2 in the perfusate (isotonic NaCl). This technique was evaluated both ex vivo and in vivo. A distal segment of the duodenum was cannulated in situ and the lumen was perfused with recirculating isotonic NaCl. HCO3(-)-secretion into the perfusate was titrated by the pH-stat technique. Stimulation of the vagal nerves increased gastric and duodenal HCO3(-)-secretions and these responses were blocked completely by hexamethonium and partly inhibited by atropine. Vagally-induced increases in gastric and duodenal HCO3(-)-secretion were inhibited by: an intact splanchnic nerve supply, peripheral stimulation of the cut splanchnic nerves, and alpha-2-adrenoceptor stimulation with clonidine. In animals with intact splanchnic nerve supplies, the administration of the adrenolytic agent guanethidine or the alpha-2-adrenoceptor antagonist yohimbine revealed increases in gastric and duodenal HCO3(-)-secretion in response to vagal stimulation. Neither the alpha-1-adrenoceptor blocker prazosin nor the beta-adrenoceptor antagonist propranolol had any such effect. Furthermore, the inhibition of vagally induced gastric and duodenal HCO3(-)-secretion by splanchnic nerve stimulation or clonidine treatment was blocked by yohimbine. It can be concluded that peripheral autonomic nerves influence both gastric and duodenal HCO3(-)-secretion. The vagal nerves convey an excitatory pathway involving nicotinic, as well as muscarinic, cholinoceptor-mediated transmission. Furthermore, the present data suggest the existence of a sympatho-inhibitory mechanism for which the primary point of action involves alpha-2-adrenoceptors, presumably at a neural site.

Adrenergic alpha-Agonists↗
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↗
PubMed1985

Non-nicotinic, non-adrenergic excitatory motor fibres in the preganglionic sympathetic supply to the feline colon. An axon reflex arrangement associated to thin sensory neurons, involving substance P?

Experiments were performed on chloralosed cats with ligated adrenals. The peripheral ends of the preganglionic sympathetic nerves to the colon were stimulated and colonic motility was monitored by a volumetric method. Electric nerve stimulation with various intensities elicited inhibitory motor responses and occasionally contractions. Hexamethonium and/or guanethidine blocked all inhibitory actions and revealed pure excitatory responses at high stimulation intensities. These colonic contractions were inhibited by atropine. However, atropine-resistant contractions were sometimes observed, predominantly in the colorectal region. Thoracic sympathetic nerves affected the motility in the proximal colon only, while lumbar sympathetic nerves acted on both proximal and distal parts. Strength-duration relationships and sensitivity to local heating suggest that the excitatory responses are due to an antidromic activation of thin, possibly afferent nerve fibres. Small doses of substance P injected close i.a. induced colonic contractions unchanged by hexamethonium and/or guanethidine but sensitive to atropine. The neurally-induced colonic contractions are suggested to be due to an antidromic activation of thin sensory neurons which in the periphery release substance P, in turn activating cholinergic motor neurons, thus constituting an axon reflex arrangement. The possibility of a similar axon reflex mechanism, associated to thin afferents, activating adrenergic inhibitory neurons at the prevertebral ganglionic level is discussed.

Animals↗
PubMed1985

On the transmission of sacral parasympathetic nervous influence on distal colonic and rectal motility in the cat.

Experiments were performed on cats anaesthetized with chloralose and treated with adrenoceptor blocking agents. Distal colonic and rectal motility were selectively recorded by a volumetric method. The effects of muscarinic and ganglionic nicotine receptor blockade on motor responses induced by graded efferent electrical pelvic nerve stimulation (PNS) were studied. Stimulation at low current strength evoked contractions in both the colon and the rectum, which were sensitive to atropine and to hexamethonium. High intensity stimulation elicited distal colonic contractions resistant to both atropine and hexamethonium. Similar excitatory responses to high strength PNS were also observed in the rectum, though not in all experiments. Stimulation at intermediate intensities evoked distal colonic and rectal relaxations which were resistant to atropine but blocked by hexamethonium. The results indicate that PNS influences colonic and rectal motility by activation of at least three discrete non-adrenergic nervous pathways: (1) low-threshold excitatory fibres involving nicotinic and muscarinic transmission, (2) high-threshold excitatory fibres with a non-muscarinic, non-nicotinic transmission mechanism, (3) inhibitory fibres with an intermediate stimulus intensity threshold, exerting their effect by a non-muscarinic mechanism involving a nicotinic step.

Animals↗
PubMed1983

Inhibition of antidromically induced stimulation of gastric motility by substance P receptor blockade.

Electrical stimulation of the feline vagal or splanchnic nerves after hexamethonium blockade of nicotinic ganglionic transmission produces gastric contractions, suggesting antidromic activation of thin afferents. The present experiments were performed to examine whether substance P is involved as a transmitter in such gastric responses. Cats were anesthetized with chloralose, laparotomized and the adrenals were ligated. The left greater splanchnic nerve, proximal to the celiac ganglion, and the left or right cervical vagal nerve were dissected, cut and placed on electrodes for peripheral stimulation. Gastric motility was monitored with a balloon. Hexamethonium was administered i.v. as well as i.a. to the stomach. Nerve stimulations produced powerful gastric contractions, which were antagonized by large doses (approximately 0.8 mumol) of substance P administered i.a. to the stomach. Similarly, the gastric contractions elicited by vagal or splanchnic nerve stimulations were reduced to at least 60% of control by the specific substance P antagonist (D-Pro2, D-Trp7,9)-SP administered i.a. (0.4-1.3 mumol). The present results support the concept that substance P is associated with gastric excitatory motor responses, possibly elicited by antidromic activation of thin afferent nerve fibres.

Animals↗
PubMed1982

Gastric atropine-sensitive excitation by peripheral vagal stimulation after hexamethonium. Antidromic activation of afferents?

Experiments were performed in chloralosed cats with ligated adrenals with recording of arterial blood pressure, heat rate and gastric volume, the latter with a balloon method. Electric activation of the peripheral cut vagus at low and high intensity induced gastric excitatory and relaxatory responses, respectively. Hexamethonium blocked the stimulation-bound bradycardia but now high intensities induced excitatory gastric responses, resistant to alpha- and beta-adrenergic blocking agents and naloxone but sensitive to atropine. Heating of the intact vagus, to selectively activate thin afferents, resulted in gastric inhibition, due to vago-vagal reflex activation. When the nerve had been proximally cut, local nerve heating induced excitatory gastric responses, with the same pharmacological characteristics as those caused by electric nerve stimulation. The observations suggest that the hexamethonium-resistant gastric excitatory responses to peripheral vagal stimulation are due to antidromic activation of thin afferents which are proposed to function in axon reflexes affecting gastric motility.

Animals↗