RESUMO
Objective To establish an animal model for study on early oral fluid resuscitation of burn shock so as to provide experimental basis for oral fluid resuscitation of burn shock in wars, accidents or disasters. Methods Male Beagle dogs weighing 11-13 kg were used in the study and the carotis, jugular and duodenum were cannulated respectively for measurement of homodynamics, tissue perfusion and gastrointestinal function. Dogs were subjected to a 35% TBSA full thickness flame injury with 10-mi-nute anesthesia by intravenous injection of propofol 24 hours later, and then randomly and equally divided into two groups(8 dogs in each group) : no fluid resuscitation group (NR group) undergoing no treatment in the first 24 hours post burn and oral fluid resuscitation group ( OR group) undergoing gastric infusion of glucose electrolyte solution (GES) according to Parkland formula. From the second 24 hours post burn, animals in two groups were given delayed Ⅳ fluid resuscitation, and then intravenous nutritional support was initiated at the 72nd hour. The mean arterial pressures (MAP), cardiac output (CO), dp/dt max of left ventricular contractility (dp/dtmax) and plasma volume (PV) were monitored continuously. The pa-rameters of gastrointestinal tissue peffusion, the rates of gastric emptying and intestinal absorption of GES were determined, the morbidity was also recorded at the end of 5-day experiment. Results After 35% TBSA burn injury, MAP, CO,dp/dt max and PV dropped markedly and gastrointestinal tissue perfusion reduced obviously. CO and PV in OR group were significantly higher than those in NG group at 4, 8 and 24 hours after burn. Homodynamic parameters and gastrointestinal tissue perfusion in OR group were pro-moted to pre-injury level at 48 and 72 hours respectively, while homodynamic parameters in NR group did not return to pre-injury level till 72 hours, and gastrointestinal tissue perfusion kept lower than pre-injury till 120 hours post burn. Rates of gastric emptying and intestinal absorption of GES significantly reduced to the lowest level (42% and 37% of pre-injury) at about 4 hours post bum, but did not return to pre-in-jury level till eight hours post bum. Over five days, two out of eight dogs (25%) died in NG group but none in OR group. Conclusions The animal model can exactly simulate the actual circumstance, where oral resuscitation is superior to Ⅳ resuscitation in some aspects in treating early bum shock in wars, accidents and disasters, and provide practical and reliable method for measurement of homodynamic parameters, tissue perfusion, gastric emptying and intestinal absorptive function.
RESUMO
Objective To investigate the effect of carbachol on local gut inflammation during entetal resuscitation of rats with bum shock. Method Thirty-eight Wistar rats were subjected to 35%TBSA full thickness scald injury, and enteral fluid was infused into animal intestines via duodenal stomas 30 minutes post bum. The animals were randomly divided into four groups: no resuscitation (Control, n = 8), enteral resuscitation using either a glucose electrolyte solution (GES, n = 10) or GES plus carbachol (60 μg·kg-1,GES/CAR, n = 10), or carbachol alone (CAR, n = 10) .The volumeof GES infusion was based on the Parkland formula (4 ml· 1% TB-SA-1·Kg-1) - All animals were sacrificed 4 hours post bum, and specimens of jejunal tissue were collected to determine the levels of tumor necrosis factor (TNF)-α, nitric oxide (NO), nitric oxide synthase (NOS) and myeloperoxidase (MPO). Serum assays for plasma diamine oxidase (DAO) activities were also performed. Results There were no statistical differences in the intestinal levels of NOS, NO, TNF-α and MPO, and plasma OAO activities, between the GES group and the control group. Compared to the GES group, the GES/CAR group showed significantly lowered levels of intestinal NOS (1.276 ±0.391 vs. 1.818 ±0.436, P＜0.05), NO (0.925 ±0.402 vs. 1.561 ±0.190, P ＜ 0.05, TNF-α (0.87±0.13 vs. 1.94±0.47, P ＜0.01) and MPO (0.465 ±0.092 vs. 0.832±0.214, P＜0.05),and reduction in plasma DAO activites (0.732±0.192 vs. 1.381 ±0.564, P ＜0.05). The CAR group also showed significantly lowered levels of intestinal NOS, NO, TNF-α and MPO and reduced plasma DAO activites, compared to the GES group. Conclusions Theses results suggest that carbachol significantly inhibits the release of proinflammatory mediator and attenuates local inflammation in gut during enteral fluid resuscitation of rats in rats with bum shock. We postulate that carbachol may exert its and-inflammatory effects via the cholinergic anti-inflammatory pathway.