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D Delbro

Publications and source records attributed to D Delbro.

57 records · Page 4Linked to original sources

Non-ganglionic cholinergic excitatory pathways in the sympathetic supply to the feline stomach. An efferent system or afferents with excitatory axon collaterals?

Experiments were performed on chloralosed, adrenalectomized cats, paralysed with gallamine and artificially ventilated. Gastric motility was recorded by the balloon method. Efferent stimulation of the cut greater splanchnic nerve, well proximal to the celiac ganglion, could either increase or decrease gastric tone. The excitatory responses called for higher stimulation intensities than the inhibitory ones but were as a rule observed at lower frequencies only (1-4 Hz). They could be abolished by atropine but were not prevented by bilateral vagotomy, hexamethonium nor guanethidine. The latter two drugs rather reversed inhibitory responses to excitatory ones which exhibited a hyperbolic frequency-response relationship with maximal effects already at 2-4 Hz. Heating of a nerve trunk selectively activates thin afferents of the delta group and C-class. Heating of the greater splanchnic nerve caused an increase in gastric motility which, like that caused by electric stimulation, was not prevented by hexamethonium nor guanethidine; nor was it eliminated by cutting the nerve centrally, nor by vagotomy, while it was abolished by atropine. These results suggest that the excitatory gastric responses to efferent splanchnic nerve stimulation are due to antidromic activation of thin afferent fibres. Their functional significance remains obscure but their peripheral arborizations may convey 'axon reflexes' influencing gastrointestinal motility.

Afferent Pathways↗

The interrelation between hypothalamically induced changes in sympathetic discharge to the gastrointestinal and cardiovascular systems.

In chloralose-anesthetized, adrenalectomized cats, the sympathetically conveyed effects of topical hypothalamic stimulations on gastric volume, blood pressure and heart rate were systematically explored. The vagal nerves were cut but could be kept active by graded efferent stimulation. In the absence of such vagal activity, hypothalamic stimulation had no appreciable influence on gastric volume, even though the stomach maintained considerable myogenic tone. When, however, a vagal excitatory activity was present, hypothalamic stimulation could markedly affect gastric tone, indicating that the sympathetic fibres exert their inhibitory influence on the stomach via its cholinergic intramural neurons. Hypothalamic stimulations that induced reductions in pressure or heart rate also usually caused an enhancement of gastric tone. Similarly, pressor responses were associated with decreases in gastric volume whereas stimulation-induced tachycardia was not linked to any particular type of gastric response. Thus, the hypothalamic sympathoinhibitory influences on the cardiovascular system seem closely connected to a supression of the sympathetic outflow to the stomach. There is, on the other hand, no regular association between hypothalamic sympathoexcitatory influences on the cardiovascular and gastrointestinal systems; in fact, there is in many areas even a suppression of sympathetic discharge to the stomach in association with cardiovascular stimulation.

Adrenalectomy↗

Role of cyclooxygenase-2 for fluid secretion by the inflamed gallbladder mucosa.

Inflammatory fluid secretion by the gallbladder mucosa in experimental cholecystitis is induced by activation of cyclooxygenase, which leads to an increase in prostaglandin formation. Cyclooxygenase exists as a constitutive (cyclooxygenase-l) and an inducible (cyclooxygenase-2) isoform. The aim of this study was to demonstrate the role of cyclooxygenase-2 in inflammatory fluid secretion of the feline gallbladder. Experiments were performed 10 weeks after a surgical procedure in which chronic cholecystitis was induced in cats by ligation of the cystic duct and implantation of a gallstone in the gallbladder. Gallbladder fluid transport was continuously monitored via a perfusion system. In inflammed gallbladders the continuous fluid secretion was reversed to absorption by intravenous injection of the selective cyclooxygenase-2 blocker, NS 398 (P <0.001). Increased levels of the inducible cyclooxygenase-2 were shown by immunoblotting in inflamed gallbladders. Selective pharmacologic blockage of cyclooxygenase-2 reduced the prostaglandin E2 release to the inflamed gallbladder lumen (P <0.01). These data suggest that cyclooxygenase-2 is involved in the inflammatory response during chronic cholecystitis. Selective cyclooxygenase-2 blockers may offer an alternative to traditional nonsterodial anti-inflammatory drugs with fewer side effects in patients with cholecystitis who are awaiting operation.

Animals↗