[Paradoxical cerebral embolization in atrial septal defect].
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Adult↗
Biomedical subjects
L Bojö
Publications and source records attributed to L Bojö.
Gastric reflex relaxation by colonic distension.
Previous studies in human volunteers have demonstrated an inhibition of gastric motility following painless rectal distension. In the present study we investigated, in anaesthetized rats, the effects of colonic distension on gastric tone and looked at certain aspects of the underlying nervous mechanisms. Changes in gastric volume were monitored continuously by a volumetric method. Colonic distension induced an immediate and pronounced gastric relaxation which lasted throughout the period of distension. The inhibition of gastric tone following colonic distension was abolished by hexamethonium or by bilateral cervical vagotomy. The selective adrenergic alpha 1 blocker, prazosin, the alpha 2 blocker, yohimbine, and the non-selective beta-blocker, propranolol, had no significant effect on gastric relaxation following colonic distension. Likewise, naloxone, an opioid receptor antagonist, did not significantly influence gastric reflex inhibition. It is concluded that colonic distension induced a non-adrenergic inhibition of gastric tone mediated through the vagal nerves. Ganglionic receptors are also suggested to form part of the inhibitory pathway.
Anesthesia↗
Pain-induced inhibition of gastric motility is mediated by adrenergic and vagal non-adrenergic reflexes in the rat.
Painful stimuli have been shown to inhibit gastric motility in animal experiments and delay gastric emptying in humans. The aim of the present study was to investigate in detail mechanisms involved in pain-induced gastric inhibition. Pain stimulation by exerting pressure on a testicle induced a prompt gastric relaxation which lasted throughout the period of stimulation. Pain-induced gastric relaxation was significantly reduced by the selective alpha-1 blocker, prazosin, and by the non-selective beta-blocker, propranolol. Similarly pain-induced inhibition of gastric tone was significantly reduced by bilateral cervical vagotomy. In contrast, gastric relaxation following pain stimulation was significantly potentiated by the selective adrenergic alpha-2 blocker, yohimbine. Combined administration of prazosin and propranolol followed by bilateral cervical vagotomy abolished gastric relaxation in response to pain stimulation. In conclusion, gastric relaxation in response to painful stimulation was found to be reflex-mediated via sympathetic neurons acting on alpha-1 and beta receptors and possibly also via vagal non-adrenergic fibres. Pain-induced inhibition of gastric tone was significantly increased by yohimbine. It is suggested that yohimbine by blocking presynaptic inhibitory receptors on adrenergic neurons facilitates the release of noradrenaline in response to pain stimulation.
Anesthesia↗
Effects of selective adrenergic agonists and antagonists on gastric tone in the rat.
The aim of the present in vivo study was to investigate in anaesthetized rats, the effects of selective adrenergic agonists and antagonists on basal gastric tone and phasic contractions by the use of a volumetric method. L-phenylephrine, an alpha-1 agonist, induced hypertension, bradycardia and a significant gastric relaxation. Clonidine, an alpha-2 agonist, caused hypotension, bradycardia and a significant gastric contraction and a reduction of the amplitude of phasic contractions. Salbutamol, a beta-2 agonist, induced a dose-dependent tachycardia and a significant inhibition of gastric tone whereas prenalterol, a beta-1 agonist, induced tachycardia without any significant influence on gastric basal tone. Yohimbine, an alpha-2 blocker, significantly decreased gastric basal tone and reversed the inhibition of phasic contractions induced by clonidine. Prazocine, a selective alpha-1 blocker, and propranolol, a non-selective beta-blocker, had no significant influence on gastric basal tone or phasic contractions. It is concluded that sympathetic inhibition of basal gastric tone in the rat is mediated by alpha-1 and beta-2 adrenergic receptors. Activation of alpha-2 adrenergic receptors significantly increased basal gastric tone and reduced the amplitude of phasic contractions. A blockade of alpha-2 receptors significantly decreased basal gastric tone and restored the amplitude of phasic contractions.
Adrenergic alpha-Agonists↗