Research Division, InCor, University of São Paulo Medical School, São Paulo, Brazil.
J Surg Res. 2010 Jun 1;161(1):54-61. doi: 10.1016/j.jss.2008.12.005. Epub 2009 Jan 3.
Acute mesenteric ischemia is a potentially fatal vascular emergency with mortality rates ranging between 60% and 80%. Several studies have extensively examined the hemodynamic and metabolic effects of superior mesenteric artery occlusion. On the other hand, the cardiocirculatory derangement and the tissue damage induced by intestinal outflow obstruction have not been investigated systematically. For these reasons we decided to assess the initial impact of venous mesenteric occlusion on intestinal blood flow distribution, and correlate these findings with other systemic and regional perfusion markers.
Fourteen mongrel dogs were subjected to 45 min of superior mesenteric artery (SMAO) or vein occlusion (SMVO), and observed for 120 min after reperfusion. Systemic hemodynamics were evaluated using Swan-Ganz and arterial catheters. Regional blood flow (ultrasonic flow probes), intestinal O(2)-derived variables, and mesenteric-arterial and tonometric-arterial pCO(2) gradients (D(mv-a)pCO(2) and D(t-a)pCO(2)) were also calculated.
SMVO was associated with hypotension and low cardiac output. A significant increase in the regional pCO(2) gradients was also observed in both groups during the ischemic period. After reperfusion, a progressive reduction in D(mv-a)pCO(2) occurred in the SMVO group; however, no improvement in D(t-a)pCO(2) was observed. The histopathologic injury scores were 2.7 +/- 0.5 and 4.8 +/- 0.2 for SMAO and SMVO, respectively.
SMV occlusion promoted early and significant hemodynamic and metabolic derangement at systemic and regional levels. Additionally, systemic pCO(2) gradient is not a reliable parameter to evaluate the local intestinal oxygenation. Finally, the D(t-a)pCO(2) correlates with histologic changes during intestinal congestion or ischemia. However, minor histologic changes cannot be detected using this methodology.
急性肠系膜缺血是一种潜在致命的血管急症,死亡率在 60%至 80%之间。几项研究广泛研究了肠系膜上动脉闭塞的血流动力学和代谢效应。另一方面,肠流出道阻塞引起的心循环紊乱和组织损伤尚未得到系统研究。基于这些原因,我们决定评估静脉性肠系膜闭塞对肠血流分布的初始影响,并将这些发现与其他全身和区域性灌注标志物相关联。
14 只杂种狗接受了 45 分钟的肠系膜上动脉(SMAO)或静脉闭塞(SMVO),并在再灌注后观察 120 分钟。使用 Swan-Ganz 和动脉导管评估全身血流动力学。使用超声探头评估局部血流(超声探头)、肠氧衍生变量以及肠系膜动脉和张力动脉 pCO2 梯度(D(mv-a)pCO2 和 D(t-a)pCO2)。
SMVO 与低血压和低心输出量相关。在缺血期,两组的局部 pCO2 梯度也显著增加。再灌注后,SMVO 组的 D(mv-a)pCO2 逐渐降低;然而,D(t-a)pCO2 没有改善。组织病理学损伤评分分别为 SMAO 和 SMVO 的 2.7 +/- 0.5 和 4.8 +/- 0.2。
SMV 闭塞在全身和局部水平上引起早期且显著的血流动力学和代谢紊乱。此外,全身 pCO2 梯度不是评估局部肠氧合的可靠参数。最后,D(t-a)pCO2 与肠充血或缺血期间的组织学变化相关。然而,这种方法无法检测到轻微的组织学变化。