Subject(s)
Breast Neoplasms/diagnosis , Adult , Breast Neoplasms/epidemiology , Female , Humans , SwedenABSTRACT
Experiments were performed on anaesthetized dogs. Vagotomy was followed by an increase of gastric tone. The phasic responses of gastric tone to efferent vagal electrical stimulation were not separable in these experiments as they are in cats. Oesophageal distension, however, produced a marked gastric relaxatory response, which, as in cats, was non-cholinergic and non-adrenergic but abolished by vagotomy. This response is suggested to be equivalent to physiological receptive relaxation of the stomach, occurring during food intake.
Subject(s)
Gastrointestinal Motility , Muscle Contraction , Muscle Relaxation , Stomach/innervation , Vagus Nerve/physiology , Animals , Atropine/pharmacology , Dogs , Electric Stimulation , Esophagus/physiology , Gastrointestinal Motility/drug effects , Guanethidine/pharmacology , Muscle Contraction/drug effects , Muscle Relaxation/drug effects , Muscle Tonus/drug effects , VagotomyABSTRACT
Experiments were performed on 4 non-anaesthetized dogs with chronic gastric fistulae. Gastric tonus was studied by volume and inflow rate recording at low pressure heads. Gastric tonus was not affected by propranolol or phentolamine. It was markedly reduced by atropine, presumably by blocking excitatory cholinergic nervous activity. Guanethidine induced a marked increase of gastric tonus, presumably by inhibiting sympathetic modulating activity on intramural cholinergic ganglia. Feeding was accompanied by a marked gastric relaxation which was not blocked by any of the drugs mentioned. Vagotomy, however, entirely abolished the gastric relaxatory response to feeding. The findings suggest that gastric receptive relaxation accompanying feeding is mediated via specific relaxatory vagal nerve fibres, which are non-adrenergic and non-cholinergic.
Subject(s)
Gastrointestinal Motility , Muscle Contraction , Muscle Relaxation , Stomach/innervation , Vagus Nerve/physiology , Animals , Atropine/pharmacology , Dogs , Food , Gastrointestinal Motility/drug effects , Guanethidine/pharmacology , Muscle Contraction/drug effects , Muscle Relaxation/drug effects , Muscle Tonus/drug effects , Phentolamine/pharmacology , Pressure , Propranolol/pharmacology , VagotomyABSTRACT
Experiments were performed on 4 non-anaesthetized dogs with chronic gastric fistulae, Gastric tonus was studied by volume recording at low pressure head. 0.5 IE insulin/kg bodyweight intravenously was followed by an immediate gastric relaxation, obvious before any marked decrease of blood glucose or plasma potassium occurred, and furthermore not affected by administration of glucose or potassium. This initial relaxation was still present after vagotomy and might be due to transmembraneal metabolic changes upon insulin administration or to direct effect of insulin on gastric smooth smooth muscles. During hypoglycaemia, a second relaxatory phase occurred, and glucose given during this phase temporarily increased gastric tonus, indicating this relaxation to be due to hypoglycaemia. The hypoglycaemic relaxation was markedly reduced but not abolished by vagotomy, indicating also extravagal factors in this response.
Subject(s)
Gastrointestinal Motility/drug effects , Insulin/pharmacology , Muscle Contraction/drug effects , Muscle Relaxation/drug effects , Stomach/innervation , Vagus Nerve/physiology , Animals , Blood Glucose/analysis , Dogs , Glucose/pharmacology , Muscle Tonus/drug effects , Potassium/blood , Potassium/pharmacology , Pressure , VagotomySubject(s)
Gastrointestinal Motility , Muscle Contraction , Muscle Relaxation , Vagotomy , Vagus Nerve/physiology , Adaptation, Physiological , Animals , Atropine/pharmacology , Catecholamines/pharmacology , Dogs , Eating , Electric Stimulation , Esophagus/physiology , Gastrointestinal Motility/drug effects , Humans , Insulin/pharmacology , Muscle Contraction/drug effects , Muscle Relaxation/drug effects , Muscle Tonus/drug effects , Pylorus/physiology , Stomach/innervationABSTRACT
The dynamic gastric pressure response to expansion by direct intragastric air insufflation, 30-50 ml/s, was studied in healthy volunteers, non-operated ulcer disease patients, and in patients operated upon with antrectomy, antrectomy and vagotomy, or proximal selective vagotomy. Non-operated individuals accepted gastric expansion without considerable increase of pressure. Antrectomized patients showed a higher basal pressure and a moderate increase of pressure during expansion. Vagotomized patients, including the ones operated upon with proximal selective vagotomy, demonstrated a marked increase of pressure during expansion. The results indicate that vagal denervation of the corpus-fundus part of the stomach is followed by an impairment of gastric resrvoir function.
Subject(s)
Duodenal Ulcer/surgery , Gastrointestinal Motility , Stomach/physiology , Vagotomy , Cholecystectomy , Duodenal Ulcer/physiopathology , Gastrectomy , Humans , PressureABSTRACT
The effect of bradykinin on gastric and colonic motility was studied in anaesthetized cats with volume recording devices and compared with the effects of vagal nerve stimulation. When administered intrarterially bradykinin caused a profound and prolonged gastric relaxation. Stimultaneously there was a marked and likewise prolonged colonic contraction. The gastric relaxation closely mimicked the atropine resistant relaxation elicited by vagal nerve stimulation. These effects could not be blocked by antiadrenergic drugs and it is suggested that bradykinin and the unknown transmittor substance(s) released on vagal stimulation act in a similar way on the gastric smooth muscles and that a kinin mechanism may be involved in the vagal response. As regards the colonic motor response it was shown that bradykinin does not reproduce the vagal motility effects on colon smooth muscle but mimicks closely the atropine resistant expulsive contraction elicited by activation of the pelvic nerves.
