Intestinal secretion was produced in anesthetized cats and rats by exposing isolated intestinal segments to cholera enterotoxin. Giving, for example, tetrodotoxin, a nerve-conduction-blocking agent, or adding lidocaine, a local anesthetic agent, to the solution in the intestinal segments markedly inhibited the rate of choleraic secretion, and in most experiments a net absorption of fluid was observed. The results suggest that intramural nervous mechanisms are involved in the pathogenesis of choleraic secretion.
SUMMARY During a four hour observation period vasoactive intestinal polypeptide (VIP) is released in increasing amounts from the feline small intestine exposed to cholera toxin. As VIP is known to be located almost exclusively in the intestinal nerves, the present findings strongly suggest that cholera toxin activates the enteric nervous system. The findings of this and other studies performed in this laboratory lead to the proposal that the choleraic secretion is, at least in part, secondary to the activation of intramural nervous reflexes in the gut. The operative procedures were similar to those described by Jodal et al.8 After a tracheotomy the abdomen was opened by a midline incision and a 10-15 cm long segment from mid-jejunum was isolated with intact vascular supply. The remainder of the small intestine, the colon, the spleen, and the great omentum were extirpated.In all experiments the splanchnic nerves were cut bilaterally and in seven experiments the distal ends were mounted on ring electrodes. The stimulation characteristics in these experiments were 6 Hz, 6 V, 6 ms. The left adrenal gland was denervated and the right one excluded from the circulation by ligatures to minimise changes in the adrenal output of catecholamines while maintaining the necessary release of adrenal steroids. Atropine (0 5 mg/kg body weight) was given intravenously.After heparinisation (3 mg/kg body weight intravenously) the femoraq artery was cannulated and mean arterial blood pressure was recorded by means of a Statham pressure transducer (P23AE). In order to measure total venous outflow, the superior mesenteric vein draining the intestinal segment and its lymph nodes was cannulated and returned to the external jugular vein via an optical drop recorder, coupled to an ordinate writer recording on a Grass polygraph. The intestinal venous outflow pressure was kept constant at 8-10 mmHg throughout the experiments. Local intra-arterial injections were given by means of a catheter in a small branch of the superior mesenteric artery. RECORDING OF INTESTINAL NET WATER TRANSPORTIn most experiments the rate of intestinal net water 958 on 12 May 2018 by guest. Protected by copyright.
BackgroundThere is limited knowledge about the potential routes for H5N1 influenza virus transmission to and between humans, and it is not clear whether humans can be infected through inhalation of aerosolized H5N1 virus particles. Ferrets are often used as a animal model for humans in influenza pathogenicity and transmissibility studies. In this manuscript, a nose-only bioaerosol inhalation exposure system that was recently developed and validated was used in an inhalation exposure study of aerosolized A/Vietnam/1203/2004 (H5N1) virus in ferrets. The clinical spectrum of influenza resulting from exposure to A/Vietnam/1203/2004 (H5N1) through intranasal verses inhalation routes was analyzed.ResultsFerrets were successfully infected through intranasal instillation or through inhalation of small particle aerosols with four different doses of Influenza virus A/Vietnam/1203/2004 (H5N1). The animals developed severe influenza encephalomyelitis following intranasal or inhalation exposure to 101, 102, 103, or 104 infectious virus particles per ferret.ConclusionsAerosolized Influenza virus A/Vietnam/1203/2004 (H5N1) is highly infectious and lethal in ferrets. Clinical signs appeared earlier in animals infected through inhalation of aerosolized virus compared to those infected through intranasal instillation.
The intestinal secretion evoked by close intra-arterial infusion of 5-hydroxytryptamine (5-HT) in cats was inhibited by tetrodotoxin, a drug abolishing action potentials. Furthermore, the intestinal secretion produced by placing a 2-mM 5-HT solution in the intestinal lumen of rats was inhibited by hexamethonium, a ganglionic receptor-blocking agent. These observations strongly indicate that 5-HT-induced secretion is, at least in part, neurally mediated. It was also shown that 5-HT receptors are involved in the pathophysiology of choleraic secretion, since the secretion was inhibited by making the experimental animal tachyphylactic against 5-HT. No effects of 5-HT tachyphylaxis were noted on fluid transport in normal intestines. The results are discussed in relation to a new hypothesis for the pathophysiology of cholera secretion.
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