RESUMO
Seventeen cases of postburn multiple organ failure (MOF) were studied prospectively.It was found that MOF mainly occurred in those patients with a burn area over 70% TBSA.Mortality rate of the cases of MOF was directly proportional to the number of organs involved.The incidence of pulmonary failure was the highest and the highest mortality was attributed to renal failure;MOF in the early stage after burns was mainly induced by burn shock and that in the late stage by burn wound infection.Endogenous infection seemed to be one of the important causes to precipitate the outbreak of postburn MOF.The morphological changes of the functionally failed organs were as follows:There were various degrees of cellular degeneration and necrosis.Or- ganelle changes such as swelling and vacuolization of mitochondria,enlargement of endoplasmic reticulum,gap formation of capillary endothelium etc were seen.Extravascular organ water volume of the functionally failed organs was increased.Stasis and/or hyperemia were found in the heart,the lungs,the liver and the GI,tract,but ischemia in the kidneys.The changes of the.enzyme spectrum of the myocardium,PaO2,RI,IB/DB,and DB were parallel to those of pathomorphology and extravascular organ water volume and they could reflect the severity of organ damages firly well.
RESUMO
The role of lipid peroxidation in the precipitation of umg damage after smoke inhalation was investigated in 16 dogs. Superoxide dismutase(SOD) activity and plasma MDA in arterial blood, and ethane in the exhaled air were determined to demonstrate oxygen free radicals and lipid peroxidation. PaO2 and extravascular lung water (EVLW) were determined to evaluate lung damage.It was found that in the early postinjury period, the experimental animals suffered from pulmonary edema and acute pulmonary dysfunction. MDA in arterial plasma and exhaled ethane markedly increased (P
RESUMO
This study observed the relationship between active oxygen radicals and early lung injury after smoke inhalation injury in awake goats (N = I5) with chronic lung lymph fistular. We measured superoxide dismutase (SOD) to demonstrate the active oxygen radicals; Lung lymph flow (QL), lung lymph/plasma total protein and albumin ratio (L/P) , lung lymph total protein clearance (CL) , lung transvascu-lar protein flux, extravascuiar lung water (EVLW) , as well as PaO2 as parameters indicating lung injury.The result demonstrated that during the earlier postinjury period the injuried animals were suffering from hypoxemia, matabolic acidosis and respiratory alkalosis. EVLW and QL increased sharply during the first hour. Interstitial and alveolar edema were seen under microscope. 'These results indicated that the animals develop lung edema and acute respiratory failure. Changs of QL and EVLW were similar to L/P, CL and lung transvascular protein flux; the correlation between L/P and EVLW was significant. These data showed that the pulmonary edema was mainly a permeability one. Changes of active oxygen radicals of lung lymph fluid and arterial blood were earlier than that of venous blood; and active oxygen radicals of arterial blood was slightly higher than that of venous blood. The active oxygen radicals in pulmonary tissue and fluid of lung lavage and the lung lymph SOD clearance increased immidiatly in postinjury. These data suggested that active oxygen radicals were increased and produced in lungs. The active oxygen radicals changed with EVLW, QL, L/P and lung transvascular protein fluxi the correlation between EVLW and active oxygen radicals in pulmonary tissue, fluid of lung lavage, lung lymph SOD clearance and lung transvascular protein flux were all significant. These observations showed that early after smoke inhalation injury active oxygen radicals played a possible role in the development and progression of lung injury and pulmonary edema.