2. Intravenous injection of galanin (1-6-341 nmol/kg) evoked prolonged attenuation of cardiac vagal action: 409 + 8-2 % maximum inhibition with a half-time to recovery of 13-6 + 2-6 min. This effect of galanin was not significantly different from the action of sympathetic nerve stimulation. A slight depressor response (-14-4+ 1±9 mmHg) was seen in nine of sixteen cats.3. Intravenous injection of neuropeptide Y (NPY) (2-8-6-3 nmol/kg) evoked slight attenuation of cardiac vagal action: 11-9+4-5% maximum inhibition of cardiac vagal action on pulse interval, with a half-time to recovery of 4-1 + 1P7 min. Blood pressure increased by 68-6+557 mmHg.4. Following administration of guanethidine (1 mg/kg i.v.) the inhibitory effect of sympathetic nerve stimulation on cardiac vagal action was significantly reduced (P < 0O001). The responses to exogenous NPY and galanin on vagal action were unchanged after guanethidine.5. The prolonged attenuation of cardiac vagal action can be mimicked by exogenous galanin in the cat but not by exogenous NPY.
A diffuse lower motor neurone paralysis developed in a 6-month-old male Australian cattle dog pup 4 days after it had eaten the carcase of a rotting duck in Centennial Park, Sydney. Two other dogs which ate smaller portions of the same carcase were less severely affected. Clostridium botulinum type C was isolated from and C. botulinum type C toxin was detected in faeces from the severely affected dog. The serum contained 25 LD50 of toxin/ml. The high C. botulinum count and toxin level in the faeces declined progressively during the ensuing weeks, but 114 days after ingesting the carcase C. botulinum type C was still present in faeces and a low toxin titre persisted. Soil, mud and water samples in the area of the duck ponds in the park contained C. botulinum type C spores. Spores and high toxin titres were also found in the intestine of the carcases of 2 birds in the area.
In dogs anaesthetized with pentobarbitone, electrical stimulation of the parasympathetic nerve fibres to the nasal mucosa evoked frequency dependent increases in both nasal arterial blood flow and nasal secretion. Blood flow was measured using a transonic flow probe placed around the artery. Sympathetic nerve stimulation for 3 min at 10 Hz evoked significant and prolonged (> 30 min) attenuation of the vasodilator and secretory responses to subsequent parasympathetic stimulation. Intravenous and intranasal administration of the neuropeptide Y (NPY) analogue N‐acetyl [Leu28,Leu31] NPY 24–36, a selective NPY Y2 receptor agonist (20 nmol kg−1), significantly attenuated both vasodilator and secretory effects of subsequent parasympathetic nerve stimulation. When given intravenously, the inhibitory effect of this Y2 receptor agonist on vascular and secretory effects of parasympathetic nerve stimulation was rapid in onset (5 min) and lasted for more than 60 min. The modulatory effect of the Y2 receptor agonist was also seen with intranasal administration, but was slower in onset (15 min), and lasted less than 45 min. The effects of the intranasal pretreatment with the Y2 receptor agonist were significantly prolonged in the presence of the endopeptidase inhibitor phosphoramidon (10 nm). Atropine pretreatment did not significantly reduce the change in vascular conductance evoked by parasympathetic nerve stimulation. Subsequent pretreatment with the NPY Y2 receptor agonist N‐acetyl [Leu28,Leu31] NPY 24–36 reduced the stimulation induced increase in conductance by 30%. Nasal secretion was reduced by 70% following pretreatment with atropine and a further 30% by pretreatment with the NPY Y2 receptor agonist. Dose dependent vasodilator and secretory effects of local intra‐arterial infusion of acetylcholine and vasoactive intestinal peptide were not modified by the NPY Y2 agonist. Total protein and albumin concentration were measured in nasal lavage fluid collected after nerve stimulation. Atropine pretreatment increased the percentage of the total protein that was albumin in nasal lavage fluid. Neither sympathetic nerve stimulation nor Y2 receptor agonist pretreatment further modified the albumin exudation (a marker of vascular permeability) in nasal fluid lavage collected after parasympathetic nerve stimulation. We propose that sympathetic nerve stimulation releases NPY, which acts on Y2 receptors, probably located on parasympathetic nerve endings, to attenuate both vasodilatation and nasal secretion evoked by subsequent parasympathetic nerve stimulation. This effect is also observed after pretreatment with the Y2‐selective NPY analogue N‐acetyl [Leu28,Leu31] NPY 24–36.
SUMMARY1. Stimulation of cardiac sympathetic nerves caused prolonged inhibition of vagal effects on heart rate, an effect which has been proposed on the basis of previous studies to be due to neuropeptide Y or a neuropeptide Y-like substance, released from the sympathetic nerves.2. This prolonged vagal inhibitory effect was attenuated or abolished when the sympathetic stimulation responsible was given together with continuous vagal stimulation.3. Continuous vagal stimulation alone did not modify the ability of administered neuropeptide Y to cause inhibition of cardiac vagal action.4. The results are consistent with the cardiac vagal nerves releasing a transmitter (probably acetylcholine) which acts on cardiac sympathetic nerve endings, inhibiting them from releasing neuropeptide Y or a neuropeptide Y-like substance.
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