X Cui1, Z Sheng, Z Guo. 1. Burns Institute, 304th Hospital of the People's Liberation Army, Beijing.
Abstract
OBJECTIVE: To study the mechanisms of early gastro-intestinal ischemia developed in acute burn period and its relationships with hemodynamic and hemorrheologic changes. METHODS: Twelve pigs were randomly allocated into two groups: group C, a sham group that was subjected to all surgical procedures except burn; group B, 30% TBSA cutaneous thermal injury, and was resuscitated with Parkland formula one hour after burn. RESULTS: MAP remained stable after burn, but RAP, MPAP, PAWP and CI decreased significantly to the lowest level 4-8 hours after burn, and recovered after resuscitation 24 hours postburn. Intramucosal pH declined immediately (1 hour after burn) and remained abnormal throughout observation period. Portal venous blood flow demonstrated similar changes as pHi, and correlated well with intestinal pHi. Whole blood viscosity and plasma viscosity in portal venous blood elevated obviously after burn. CONCLUSIONS: 1. GI ischemia occurred early and recovered slowly during burn shock phase with conventional resuscitation regime. 2. GI ischemia correlated significantly with portal venous blood flow, but did not with systemic hemodynamic variables. 3. Hemorheologic changes in portal venous blood may exaggerate ischemia injuries.
OBJECTIVE: To study the mechanisms of early gastro-intestinal ischemia developed in acute burn period and its relationships with hemodynamic and hemorrheologic changes. METHODS: Twelve pigs were randomly allocated into two groups: group C, a sham group that was subjected to all surgical procedures except burn; group B, 30% TBSA cutaneous thermal injury, and was resuscitated with Parkland formula one hour after burn. RESULTS: MAP remained stable after burn, but RAP, MPAP, PAWP and CI decreased significantly to the lowest level 4-8 hours after burn, and recovered after resuscitation 24 hours postburn. Intramucosal pH declined immediately (1 hour after burn) and remained abnormal throughout observation period. Portal venous blood flow demonstrated similar changes as pHi, and correlated well with intestinal pHi. Whole blood viscosity and plasma viscosity in portal venous blood elevated obviously after burn. CONCLUSIONS: 1. GI ischemia occurred early and recovered slowly during burn shock phase with conventional resuscitation regime. 2. GI ischemia correlated significantly with portal venous blood flow, but did not with systemic hemodynamic variables. 3. Hemorheologic changes in portal venous blood may exaggerate ischemia injuries.