Aortic surgery results in ischemia/reperfusion of the lower body. This may liberate inflammatory mediators that activate neutrophils, and may result in lung microvascular changes with increased permeability and respiratory failure. We studied circulating inflammatory mediators and the pulmonary leak index (PLI) of 67Ga, a measure of transvascular transferrin transport and permeability, in patients scheduled for elective aortic and peripheral vascular surgery, before and after surgery. Aortic surgery patients in Groups 1 (n = 10)and 2 (n = 7) were studied before and at a median of 2.5 and 21.0 h after surgery, respectively. A control Group 3 (n = 6) was studied before and at a median of 2.9 h after peripheral vascular surgery. The PLI (median) increased from a median of 9.1 (range, 6.6 to 14.7) before to a median of 23.4 (range, 18.7 to 86.4) × 10−3/min after surgery in Group 1 but not in the other groups (p < 0.001). The postoperative increase in circulating neutrophils and elastase-α1-antitrypsin, a marker of neutrophil activation, was similar among the groups. Plasma levels of activated complement 3a and tumor necrosis factor (TNF-α) did not change in any of the groups. In contrast, plasma levels of interleukin-8 (IL-8) increased in Group 1 from < 3 (range, < 3 to 37) before to 324 (range, 36 to 868) pg/ml after surgery, but did not change in the other groups (p < 0.005). The decrease in plasma levels of angiotensin converting enzyme (ACE) was greater in Group 1 than in the other groups (p < 0.05). Ischemia/reperfusion of the lower body associated with aortic surgery probably activates neutrophils through a non-complement- and non-TNF-α-mediated pathway and transiently releases IL-8. This in turn may further activate neutrophils and promote their sequestration in the lungs, thereby resulting in transient changes in the pulmonary microvasculature, involving an increase in permeability and decrease in ACE release. None of the aortic surgery patients developed adult respiratory distress syndrome (ARDS) related to surgery during follow-up in the intensive care unit, although some had transient radiographic evidence of pulmonary edema. Nevertheless, our data may help to explain the development of ARDS after major vascular surgery.
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Raijmakers et al. (1995) studied this question.
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