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Objective: To observe the effect of combination of nitric oxide (NO) inhalation and inverse ratio ventilation (IRV) on oxygenation and hemodynamics in endotoxin-induced acute respiratory distress syndrome (ARDS) in sheep., Methods: Sheep ARDS model was induced by an intravenous infusion of low dose endotoxin, and then animals were randomly divided into two groups. (1) NO group (n=6), inhalation of 40x10(-6) nitric oxide. (2) Combination group (n=6), receiving mechanical ventilation with IRV (inspiratory-to-expiratory ratio of 2:1) and inhalation of 40x10(-6) NO. The dynamic changes in gas exchange and hemodynamics were measured with the aid of Swan-Ganz catheter and arterial blood gas analysis before and after the onset of, ARDS and 30 minutes after treatment., Results: The combination of IRV and 40x10(-6) NO inhalation rapidly reduced mean pulmonary arterial pressure (MPAP), increased PaO(2), decreased P((A-a))O(2), and Qs/Qt without inducing significant change in systemic hemodynamics, and it was a more effective method of correcting hypoxemia than inhalation of nitric oxide alone. NO inhalation did not change the airway pressure of the model, but the combined treatment resulted in reduction of peak inspiratory pressure and increase of mean airway pressure., Conclusion: The combined use of IRV and NO inhalation has an additive effect on improving oxygenation in endotoxin-induced acute respiratory distress syndrome in sheep.

Objective: To observe the in situ expression of TNF mRNA and protein in myocardial cell, so as to explore the possible mechanism of early myocardial injury in scalded rats with endotoxemia., Methods: One hundred and seventy eight Wistar rats inflicted with 20% TBSA III degree napalm burn compound with endotoxemia and multiple organ injury were employed as the model and were randomly divided into four groups as follow. (1) burn and infusion group (BI): the rats were burned and infused with endotoxin. (2) simple burn group (S): the rats were burned only. (3) simple endotoxin infusion group (EI): the rats were only infused with endotoxin. (4) normal control (C). The observation time points were designed to be 0.5, 1, 3, 6, 12, 24 and 48 postburn hours (PBH). The morphological and functional changes in rat myocardium, the change in serum TNFalpha, the cellular location and distribution of TNFalpha mRNA and proteins were observed by light microscope (LM), electronic microscope (EM), ELISA, immunohistochemistry and in situ hybridization staining., Results: There exhibited a series of pathomorphological changes in the myocardium at early postburn stage in rats of BI group, such as wavy degeneration of myocardial fibers, the formation of contractile bands, fragmentation of myocardial fibers and focal cytoplasmic lysis, etc. The left ventricular systolic pressure (LVSP) and the maximum change rate of intraventricular pressure (plus minus dp/dtmax) decreased significantly (P < 0.01). Serum TNFalpha level increased obviously at 1 PBH (P < 0.01) and peaked at 3 similar 6 PBH. It was found that TNFalpha mRNA was principally located in myocardial cells and in a part of inflammatory cells. But these milder pathomorphological changes in myocardial injury were found in rats of S and EI groups. In addition, there appeared elapsed TNFalpha peak values and relative weaker expression of myocardial TNFalpha mRNA., Conclusion: TNFalpha mRNA and protein could be expressed in myocardium in burned rats with endotoxemia which might be one of the origins of TNF in participating in the development of early postburn myocardial structural and functional injury.

To investigate the effects of endotoxin (ETX) on coronary circulation, we infused endotoxin (4ng/ml) intravenously in a small dose (0.3ng/kg.min-1) which did not reduce the blood pressure, nor did it disturb the coronary autoregulation, and the flow kept constant during the ETX infusion. But when the left coronary artery descending branch (LAD) was narrowed and the LAD pressure was reduced to 4.67kPa, the ETX showed a vasodilator effect on the LAD (pre-ETX 65.2 +/- 29.2 ml/min, post-ETX 89.5 +/- 32.7 ml/min, P < 0.05). This effect suggested that the ETX in a small dose had a vasodilator effect on a narrowed coronary artery, even when it did not disturb the hemodynamics. The possible mechanisms were surveyed preliminarily.