Perry M A, Wadhwa S S
School of Physiology and Pharmacology, University of New South Wales, Sydney, Australia.
Am J Physiol. 1988 Mar;254(3 Pt 1):G366-72. doi: 10.1152/ajpgi.1988.254.3.G366.
Recent studies have shown that oxygen-derived free radicals are responsible for a major portion of ischemia-reperfusion injury in the stomach. The oxygen radicals are produced during reperfusion when oxygen delivery to the tissue increases. In the present study we investigate the effect on mucosal injury of regulating the rate of reintroduction of oxygen to the stomach after ischemia. Local gastric ischemia was achieved by reducing celiac artery pressure to 30 mm Hg for 1 h. Ischemic injury was assessed by measuring the loss of 51Cr-labeled red blood cells across the gastric mucosa. Mucosal blood loss was negligible before and during the ischemia period but increased to 0.178 ml.min.-1.100 g-1 during reperfusion. When blood flow to the stomach was gradually returned to normal after ischemia by increasing celiac artery pressure by 10 mmHg every 10 min, the mucosal blood loss was reduced to 0.013 ml.min.-1.100 g-1. If the stomach was vascularly perfused with low PO2 (34 mmHg) blood for 1 h after ischemia before being returned to normal arterial perfusion, the mucosal blood loss was also reduced to 0.063 ml.min.-1.100 g-1. When the stomach was made hypoxemic for 1 h rather than ischemic by perfusing the vasculature with low PO2 (29 mmHg) blood then reperfused with normoxic blood, there was very little mucosal bleeding (0.014 ml.min.-1.100 g-1). The data indicate that gastric mucosal bleeding after ischemia is reduced if the tissue is returned slowly to a normal PO2. These findings support the concept that reperfusion injury is due largely to the production of oxygen radicals.(ABSTRACT TRUNCATED AT 250 WORDS)
最近的研究表明，氧衍生的自由基是胃缺血再灌注损伤的主要原因。当组织的氧输送增加时，再灌注期间会产生氧自由基。在本研究中，我们调查了缺血后调节胃氧再引入速率对粘膜损伤的影响。通过将腹腔动脉压力降至30 mmHg持续1小时来实现局部胃缺血。通过测量51Cr标记的红细胞穿过胃粘膜的损失来评估缺血性损伤。缺血期之前和期间粘膜失血量可忽略不计，但在再灌注期间增加至0.178 ml·min⁻¹·100 g⁻¹。当缺血后通过每10分钟将腹腔动脉压力提高10 mmHg使胃血流逐渐恢复正常时，粘膜失血量降至0.013 ml·min⁻¹·100 g⁻¹。如果在恢复正常动脉灌注之前，缺血后用低PO₂（34 mmHg）血液对胃进行血管灌注1小时，粘膜失血量也降至0.063 ml·min⁻¹·100 g⁻¹。当通过用低PO₂（29 mmHg）血液灌注血管使胃缺氧1小时而非缺血，然后用常氧血液再灌注时，几乎没有粘膜出血（0.014 ml·min⁻¹·100 g⁻¹）。数据表明，如果组织缓慢恢复到正常PO₂，缺血后胃粘膜出血会减少。这些发现支持了再灌注损伤主要归因于氧自由基产生的概念。（摘要截断于250字）
