Myocardial protection by non-invasive limb preconditioning: the role of nuclear factor kappa-B / 中国应用生理学杂志

<p><b>AIM</b>To investigate a possible role for the transcription factor nuclear factor kappa-B (NF-kappaB) in preconditioning of the heart to ischemia by remote, early protection.</p><p><b>METHODS</b>48 Wistar rats were randomly divided into three experimental groups. In group I/R, the rats underwent 30 min occlusion of the left anterior descending coronary artery, and 120 min reperfusion. In group PL, the rats underwent four cycles of 5 min occlusion and reperfusion of both hind limbs using a tourniquet before the experiment was continued as in Group I/R. In Group P(L-D), we administered NF-kappaB specific inhibitor, ProDTC 125 mg/kg peritoneally, 15 min before IPG. Infarct size as a percentage of the area at risk was determined by triphenyltetrazolium chloride staining. And another 8 rats in each group were killed and myocardium were stored in liquid nitrogen for the measurement of NF-kappaB mRNA.</p><p><b>RESULTS</b>The myocardial infarct size (IS) was decreased significantly in Group PL compared with group I/R, and the IS/AAR was 34.5% +/- 7.6% and 58.5% +/- 8.5%, respectively ( P < 0.05). The IS/AAR was 54.4% +/- 8.9% in group P(L-D), and there was no significant difference compared with group I/R (P > 0.05). The NF-kappaBmRNA was weaker in P(L) group than that in I/R Group,but is stronger than that in P(L-D) group (P < 0.05). There was almost no expression of NF-kappaB mRNA in P(L-D) group.</p><p><b>CONCLUSION</b>Noninvasive limb IPC is effective in protecting the myocardium from ischemia reperfusion injury. NF-kappaB plays an important role in the mechanism of this acute remote preconditioning.</p>

Mechanism of the protective effects of noninvasive limbs preconditioning on myocardial ischemia-reperfusion injury / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>This study aimed at assessing the effect of noninvasive limb preconditioning on myocardial infarct size, and determining whether nitric oxide and neurogenic pathway play an important role in the mechanism of acute remote ischemic preconditioning (IPC).</p><p><b>METHODS</b>Forty Wistar rats were randomly divided into four experimental groups. In Group I, the rats underwent 30-minute occlusion of the left anterior descending coronary artery, and 120-minute reperfusion. In Group PL, the rats underwent four cycles of 5-minute occlusion and reperfusion of both hind limbs using a tourniquet before the experiment was continued as in Group I. In Group PL-N and Group PL-H, we administered L-nitro-arginine methyl ester (L-NAME) 10 mg/kg or hexamethonium chloride 20 mg/kg intravenously, 10 minutes before IPC. Infarct size as a percentage of the area at risk was determined by triphenyltetrazolium chloride staining.</p><p><b>RESULTS</b>There were no statistically significant differences in mean arterial pressure and heart rate among these groups at any time point during the experiment (P>0.05). The myocardial infarct size (IS) was decreased significantly in Group PL and Group PL-H compared with Group I, and the IS/AAR was 34.5%+/-7.6%, 35.9%+/-8.6% and 58.5%+/-8.5%, respectively (P< 0.05). The IS/AAR was 49.1%+/- 6.5% in Group PL-N, and there was no significant difference compared with Group I (P>0.05).</p><p><b>CONCLUSIONS</b>Noninvasive limb IPC is effective in protecting the myocardium from ischemia reperfusion injury. Nitric oxide plays an important role in the mechanism of acute remote IPC, in which the neurogenic pathway is not involved.</p>

Effect of breathing pure oxygen on the development of atelectasis in healthy adults / 中华麻醉学杂志

Objective To investigate the development of absorption atelectasis in healthy adult volunteers breathing 100% oxygen.Methods Six healthy volunteers aged 31-36 yrs weighing 60-80 kg were recruited into this study.Chest computed tomograph(CT)of the layer of interventricular septum was performed at the end of normal expiration(FRC)at 6 time points:(1)the baseline(T_1);(2)after 5 min maximal expiration(close to residual volume)(T_2);(3)immediately after 10 maximal inspiration and expiration(T_3);(4)after breathing 100% O_2 through face mask at tidal volume for 30 min(T_4);(5)after breathing 100% O_2 at maximal expiration for 5 min(T_5)and(6)breathing room air deeply 10 times(T_6).The area of atelectasis and poorly ventilated lung were expressed as percentage of the total lungs.Results There was no atelectasis or poorly ventilated lung at T_1. At T_2 the poorly ventilated lung accounted for 22.9%?5.0%,but there was no atelectasis.There was no atelectasis and poorly ventilated lung at T_3 and T_4.At T_5 atelectasis accounted for 4.5%?1.1% which was reduced to 0.9%?0.4% at T_6.Conclusion Breathing 100% oxygen at reduced lung volume can result in atelectasis.