Abstract

To investigate the effects of carbachol (CAR) on pulmonary vascular permeability and pulmonary water content during oral fluid resuscitation of burn shock. Twelve male Beagle dogs with intubation of carotid artery and jugular vein for 24 hours were subjected to a 50% total body surface area (TBSA) full-thickness burn, then they were equally divided into oral resuscitation (OR) and OR plus CAR groups (OR+CAR). Dogs were given either a glucose-electrolyte solution (GES) in OR group or GES containing CAR (20 microg/kg) in OR+CAR group by gavage within 24 hours after burn. Dogs in each group were given intravenous fluid resuscitation after 24 post burn hour (PBH). The delivery rate and volume of GES was in accordance with that of Parkland formula. Respiratory rate (RR), arterial partial pressure of oxygen (PaO(2)), extravascular lung water index (ELWI) and pulmonary vascular permeability index (PVPI) were determined before burn (0 hour), and at 2, 4, 8, 24, 48 and 72 PBH. At 72 PBH or before death, dogs were sacrificed to collect lung tissue for evaluation of myeloperoxidase (MPO), malondialdehyde (MDA), and assessment of the tissue water content by dry to wet weight. Compared with those before burn, RR, ELWI and PVPI were greatly increased, and PaO(2) obviously decreased in two groups after burn (all P<0.01). At 72 PBH, PaO(2) returned to pre-burn level, while RR, ELWI and PVPI were still higher than pre-burn levels. RR, ELWI and PVPI at 4, 8 and 24 PBH, and PaO(2) at 8, 24, 48 PBH in OR+CAR group were respectively lower or higher than those in OR group (P<0.05 or P<0.01), but those measurements showed no statistical differences between two groups at 72 PBH (all P>0.05). MPO, MDA and lung water contents in OR+CAR group were significantly lower than those in OR group at 72 PBH [(2.64+/-0.38) U/mg vs.(4.12+/-0.46) U/mg, P<0.01; (3.60+/-0.54) micromol/mg vs.(5.14+/-0.62) micromol/mg, P<0.01; (77.40+/-0.56)% vs. (78.30+/-0.54)%, P<0.01]. The results indicate that CAR inhibits inflammatory response and oxidative damage in lung tissue, and alleviates pulmonary vascular permeability and lung edema during oral fluid resuscitation of burn shock.

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