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| Reference : Pathophysiological response of bovine diaphragm function to gastric distension |
| Scientific journals : Article | |||
| Life sciences : Veterinary medicine & animal health | |||
| http://hdl.handle.net/2268/72377 | |||
| Pathophysiological response of bovine diaphragm function to gastric distension | |
| English | |
Desmecht, Daniel  [Université de Liège - ULg > Département de morphologie et pathologie > Pathologie spéciale et autopsies >] | |
| Linden, Annick [Université de Liège - ULg > Département des maladies infectieuses et parasitaires > Santé et pathologies de la faune sauvage >] | |
| Lekeux, Pierre [Université de Liège - ULg > Département de sciences fonctionnelles > Physiologie - Doyen de la Faculté de Médecine vétérinaire >] | |
| 1995 | |
| Journal of Applied Physiology | |
| 78 | |
| 1537-1546 | |
| International | |
| 0021-8987 | |
| [en] Diaphragm ; Abdominal distension ; Stomach | |
| [en] Because of the anatomic association of an exceptionally bulky stomach with a striking compartmentation of the chest wall, leading to the most cranial insertion of the diaphragm among mammals, gastric overdistension in the bovine species offers a unique pathophysiological condition for the diaphragm. The purpose of the present study was to determine whether increased intragastric pressure (Pga) (1, 2, 3, 4, and 5 kPa) leads to perturbations of respiratory and diaphragm function in calves. Changes in diaphragmatic strength and inspiratory action followed a biphasic pattern: 1) transdiaphragmatic pressure (Pdi) in response to constant bilateral maximal phrenic nerve stimulation at 30 Hz increased with moderate gastric distension and then fell abruptly as Pga continued to rise and 2) the magnitude of the ratio of the fall in pleural pressure to total Pdi was maintained up to a Pga amounting to 2 kPa but declined at higher pressures. We conclude that gastric distension in the bovine species provokes physiologically significant alterations of the diaphragm excitation-to-pressure generation coupling as well as of its capacity to convert Pdi into useful inspiratory pleural pressure. We suggest that these perturbations resulted from the combination of 1) altered tension-generating capacity due to compromised perfusion, 2) altered diaphragm geometry capable of altering tension-to-pressure generation coupling, and 3) modified coupling of the diaphragm with the chest wall that reduced its ability to drive inspiration | |
| Researchers ; Professionals | |
| http://hdl.handle.net/2268/72377 |
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