左旋精氨酸对兔肺缺血/再灌注损伤时细胞调忘的影响

Lung tissue is very sensitive to ischemia and reperfusion,and the injury mainly manifests as follows: increase in microvascular permeability and pulmonary capillary resistance,with formation of microthrombus and tissue edema,and disordered gas exchange~([1]). A number of studies showes that,apoptosis is involved in the pathophysiological mechanism of lung ischemia/reperfusion injury (LIRI)~([2-3]),and the intervention of apoptosis plays an obvious role in lung injury~([4]).

异氟醚保护离体大鼠肺缺血再灌注损伤

Objective To study the effects of isoflurane on ischemia-reperfusion (IR)-induced injury in isolated rat lungs. Methods This study was performed on an isolated buffer-perfused rat lung model. There were four groups: CON group ( n = 6): perfusion for 60 min without ischemia; IR group (n = 6): after perfusion for 30 min, then interruption of perfusion and ventilation for 45 min followed by reperfusion for 30 min; ISO1 group (n = 6 ): 1.38% isoflurane was administered for 30 min before 45 min ischemia, then followed by 30 min reperfusion; ISO2 group (n= 6): 1.38% isoflurane was administered during the period of reperfusion. The Myeloperoxidase (MPO) activity of lung, neutrophils counts, tumor necrosis factor-α(TNF-α), superoxide dismutase (SOD) activity, malondialdehyde (MDA) in perfusate, and the Wet-to-Dry lung weight ratios were measured. Results IR caused significant increases in the wet-to-dry lung weight ratios, the activity of lung MPO, the contents of MDA and TNF-α in perfusate, but decreasess in the SOD activity and neutrophils counts. Administration of isoflurane (both ISO1 and ISO2 groups) significantly protected against IR-induced injury the via inhibiting increases of MPO activity and contents of MDA and TNF-α in perfusate. Isoflurane significantly increased the SOD activity and neutrophils counts in perfusate. No difference was found between ISO1 and ISO2 groups. Conclusion Our results suggest that isoflurane protects the lungs against IR-induced injury in isolated rat lung model.

Objective: To determine the role of hemoglobin(HB) -induced heme oxygenase- 1 ( HO- 1 ) in injured lungscaused by limb ischemia-reperfusion (I/R) in rats.Methods: A rat model of ischemia in the hind limbswas made by clamping the infrarenal aorta with amicrovascular clip, and lung injury occurred afterreperfusion. To induce the expression of HO-1 in the lungs,Hb was administrated intraperitoneally at 16 hours beforereperfusion. Northern blotting and Western blotting wereused to detect the expression of HO-1 in the lungs, and thecarboxyhemoglobin (COHb) level in arterial blood wasassayed. The effect of hemoglobin (Hb) on the injuredlungs after limb I/R was determined by measuring thechanges of lung histology, polymorphonuclear (PMN)count, malondialdehyde (MDA) content and wet-to-dryweight ratio (W/D). Zinc protoporphyrin (ZnPP), aninhibitor of HO, was used to determine whether HO-1 wasinduced by Hb after lung injury.Results: Hb led to a significant increase in HO-1mRNA and protein expression in the lungs, accompanied bythe increase of COHb level in arterial blood. Comparedwith the sham controls, the lung PMN count, MDA contentand W/D significantly increased at 4 hours after limb I/R,which reversed by the pretreatment with Hb at 16 hoursbefore reperfusion. ZnPP blocked this protective role of Hbin the injured lungs.Conclusions: Hb can induce the lung HO-1expression, which plays an important role in the defenseagainst I/R-induced lung injury in rats.

Objective: To study the mechanism of rabbit lunginjury caused by explosive decompression.Methods: A total of 42 rabbits and 10 rats were served as the experimental animals. A slow recompressiondecompression test and an explosive decompression test were applied to the animals, respectively. And the effects of the given tests on the animals were discussed.Results: The slow recompression-decompression did not cause an obvious lung injury, but the explosive decompression did cause lung injuries in different degrees. The greater the decompression range was, the shorter the decompression duration was, and the heavier the lung injuries were.Conclusions: Explosive decompression can cause a similar lung injury as shock wave does. The primary mechanical causes of the lung injury might be a tensile strain or stress in the alveolar wall and the pulmonary surface's impacts on the inside wall of the chest.