[Discoordination of gastroduodenal myoelectrical activity during immobilization stress in rabbits].
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Biomedical subjects
Publications and source records attributed to V I Ovsiannikov.
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Distension of the ileal segment was shown to induce its contraction in isolated portion of the cat ileum, the response being abolished by M-cholinergic blockade and preserved after N-cholinergic blockade. Blockade of the beta-adrenoreceptors or their stimulation did not affect the peristaltic reflex. The findings suggest that the excitatory beta-adrenoreceptors are not directly involved in the first phase of peristaltic reflex.
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Experiments were performed on unanaesthetized rabbits. It has been shown that beta-adrenergic stimulation by isoprenaline can lead to decreasing as well as increasing of spike activity of the ileum. Pretreatment with propranolol completely prevented both effects of isoprenaline. Administration of isoprenaline both during M-cholinergic and N-cholinergic blockades resulted in decreased spike activity alone. These results suggest that isoprenaline-induced increase in spike activity is mediated by excitatory beta-adrenoceptors localized on the presynaptic cholinergic interneurons of the enteric nervous system.
Acute experiments were performed on the isolated intestinal loop, vascularly perfused with arterial blood by means of the constant flow perfusion pump. Contractile activity of the ileocecal sphincter and proximal parts of the large intestine was estimated by the maximal isometric tension and total (integrated) contractile activity. Isoprenaline (1-2 mg) induced contractile responses of the colonic segment and ileocecal sphincter. These responses were abolished or dramatically diminished by the blockade of beta-adrenoceptors, muscarinic, and nicotinic cholinergic receptors. Data obtained support the idea, that the large intestine and ileocecal sphincter have excitatory beta-adrenoceptors localized on cholinergic interneurones of the enteric nervous system.
The administration of mesaton enhanced contractile activity of pyloric sphincter and diminished it in the duodenum in rabbits. The blockade of alpha-adrenoreceptors with dihydroergotoxin abolished the myoelectrical activity in the pyloric sphincter and sharply enhanced it in the duodenum. Both these effects could occur in the blockade and in the stimulation of alpha-adrenoreceptors of the ileum. The administration of mesaton against the background of the blockade of H-cholinoreceptors with bensohexonium never enhanced myoelectrical activity of the pyloric sphincter. The data obtained suggest different roles of alpha-adrenoreceptors in the pyloric sphincter, duodenum and ileum. The activating alpha-adrenoreceptors of the pyloric sphincter can be found on the neurons of the myenteric plexus.
Functional significance of beta-adrenoreceptors located at cholinergic interneurons of myenteric plexus was confirmed for motor responses to exogenous and endogenous acetylcholine, serotonin, histamine and bradykinin. A specific mechanism of the activation of small intestine's contractile apparatus by sympathoadrenal system seems to exist in the organism.
Blockade of H-cholinoreceptors, alpha- and beta-adrenoreceptors did not lead to disappearance of the colon and ileocecal sphincter contractile responses to i.a. administration of met-enkephalin (0.05-8.0 micrograms). The responses of the colon, as well as ileum and jejunum were augmented under blockade of alpha-adrenoreceptors whereas the responses of ileocecal sphincter decreased. The latters were augmented under blockade of beta-adrenoreceptors. Met-enkephalin infused into the vascular bed of an isolated portion of the intestine (0.01-5.0 micrograms/ml/min), potentiated the colon and ileocecal sphincter responses to acetylcholine (1.0-20.0 micrograms), the colon responses to stimulation of the n. vagus efferent fibers, and the ileocecal sphincter responses to serotonin (20-100 micrograms).
Experimental results, substantiating the idea of a specific mechanism for the activation of small-intestinal smooth muscle by the adrenergic system are summarized. This mechanism is realized via catecholamines affecting excitatory beta-adrenoreceptors located on cholinergic interneurones of the myenteric plexus. The excitatory beta-adrenoreceptors are shown to contribute to the realization of small-intestinal motor responses to acetylcholine, vagal stimulation and 5-hydroxytryptamine, histamine, bradykinin. The data obtained are an evidence of physiological significance of this specific adrenosensitive input of small-intestinal cholinergic neurones. The cholinergic neurones are shown to participate in producing small-intestinal responses to 5-hydroxytryptamine, histamine, bradykinin, the responses being, for this reason, dependent on the level of catecholamines, stimulating excitatory beta-adrenoreceptors. It is suggested that cholinergic neurones of the enteric nervous system are under double adrenergic control: a stimulating effect of catecholamines mediated by excitatory beta-adrenoreceptors is counteracted by an inhibitory effect of alpha-adrenoreceptor activation by sympathetic neuromediator noradrenaline.
Subcutaneous administration of serotonin (10 mg/kg) altered myoelectrical activity of the stomach, pylorus and duodenum in rabbits causing a discoordination of gastroduodenal motor activity. During activation of beta-Adrenoceptors serotonin induced discoordination superimposed on disturbance of normal coordination of the stomach, pylorus and duodenum induced with isopropylnoradrenaline. beta-Adrenoceptor blockade decreased the degree of serotonin-induced discoordination between motility of the stomach and duodenum as concerns the rhythmic component of their activity.
Contractile responses of small intestine segments to isopropylnoradrenaline (INA) disappeared after the blockade of M- and N-cholinoreceptors, beta-adrenoreceptors and increased after the blockade of alpha-adrenoreceptors. Infusion of acetylcholine in subthreshold doses enhanced the small intestine contractile responses to the INA. The blockade of beta-adrenoreceptors with propranolol reduced contractile responses to exogenous (i. a. administration) and endogenous (electrical stimulation of the n. vagus' efferent fibers) acetylcholine, histamine and bradykinin. Stimulation of beta-adrenoreceptors with the INA enhanced contractile responses to exogenous acetylcholine and histamine and reduced the responses to bradykinin. The data obtained suggest the existence of activating beta-adrenoreceptors, apart from alpha- and beta-inhibitory adrenoreceptors, in the small intestine. Activating beta-adrenoreceptors are situated on cholinergic interneurons of the myenteric plexus and mediate the activating effect of endogenous catecholamines upon cholinergic neurons of small intestine.
The data obtained suggest that histamine evokes contractile responses of the cat jejunum and ileum acting mainly upon the preganglionic cholinergic neuron of the myenteral plexus. Alpha-receptors act as inhibitory, and beta-receptors as activating adreno-structures in respect to these responses.
In anesthetized cats with i. a. perfusion of isolated small intestine segments, the blockade of N-cholinoreceptors with benzohexonium of M-cholinoreceptors with atropine reduced jejunum and ileum contractility induced by bradykinin. After an alpha-adrenoreceptor blockade induced by phentolamine, an increase of responsiveness to bradykinin was evident whereas noradrenaline stimulation reduced the contractility. The blockade of beta-adrenoreceptors with propranolol as well as their stimulation with isopropylnoradrenaline also reduced small intestine contractility. The bradykinin-induced contractions of the small intestine segments seem to be due to the direct action of bradykinin on the smooth muscle cells and to the stimulating effect of acetylcholine released from the efferent cholinergic neurons. These effects can be modulated with catecholamine because of its influence on the excitatory presynaptic beta-adrenoreceptors and inhibitory postsynaptic alpha- and beta-adrenoreceptors.
In acute experiments on cats, an isolated loop of small intestine was vascularly perfused by means of the constant volume pump. The jejunum and ileum contractility was estimated by maximum isometric tension and total contractile activity. Neither N- nor M-cholinoreceptor blockade eliminates the contractile responses of jejunum and ileum to i.a. injection of metenkephalin. I.a. infusion of metenkephalin (10(-8)--10(-6) g/ml/min) potentiated contractile responses to acetylcholine, inhibited those to serotonin, potentiated or inhibited responses to electrical stimulation of vagal efferents. The data suggest metenkephalin to be able to modulate the contractile activity of intestinal smooth muscle, affecting the cholinergic excitatory and noncholinergic, nonadrenergic inhibitory mechanisms.
Isopropylnoradrenaline (1-2 micrograms/ml-1) induced contractile responses of the jejunum and ileum. The contractions could occur practically simultaneously with the onset of responses of arterial vessels or their latency period (reaching up to 33 sec). Blockade of M-cholinoreceptors with atropine (0.2-0.4 mg/kg) prevented both response types whereas blockade of alpha-adrenoreceptors with phentolamine (1 mg/kg) augmented them. Preliminary infusion of acetylcholine in subthreshold concentration (10(-5)-10(-6) g/ml; 1 ml/min) into the small intestine vascular bed considerably augmented the responses to isopropylnoradrenaline. The data obtained corroborate existence of presynaptic activating beta-adrenoreceptors localized on a cholinergic neuron, in the small intestine.
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Acute experiments were performed on isolated segments of the cat small intestine vessels. The contractile activity of the jejunum and ileum was estimated by the maximal isometric tension. Blocking of the alpha-adrenoreceptors with phentolamine induced a reinforcement of the contractile reactions, whereas blocking of the beta-adrenoreceptors with propranolol led to inhibition of both jejunum and ileum contractile responses either to exogenous acetylcholine or electrical stimulation of vagal efferent fibers. The subthreshold activation of alpha-adrenoreceptors with noradrenaline induced mostly inhibition, whereas activation of beta-adrenoreceptors with isopropylnoradrenaline caused a potentiation of the contractile response to exogenous acetylcholine. The data obtained suggest existence of excitatory beta-adrenoreceptors with a presynaptic localization in the jejunum and ileum.