Conclusions: These results suggest that pulmonary edema in OZ following CX-5461 price orthopedic trauma is due to an elevated PGE2 and resultant increases in pulmonary permeability. “
“Please cite this paper as: Bruce AC and Peirce SM. Exogenous Thrombin Delivery Promotes Collateral Capillary
Arterialization and Tissue Reperfusion in the Murine Spinotrapezius Muscle Ischemia Model. Microcirculation 19: 143–154, 2012. Objective: We examined the effects of exogenously delivered thrombin on cell recruitment in skeletal muscle and the formation of new collateral arterioles in the microvasculature in response to ligation-induced ischemia. Methods: Thrombin or vehicle was locally applied to both
ligated and nonoperated Balb/c spinotrapezius muscles, which were harvested after three or seven days, imaged using confocal microscopy, and analyzed. Results: Thrombin treatment resulted in accelerated arterialization of collateral capillaries and accelerated tissue reperfusion in ischemic muscles. Uninjured muscle treated with thrombin displayed increased vascular cell adhesion molecule 1 expression on arteriole and venule endothelium, increased expression of smooth muscle α-actin on capillary-sized vessels, increased infiltration by CD11b+ leukocytes, and mast cell infiltration and degranulation. Conclusions: Exogenous delivery of thrombin enhances microvascular collateral development in response to ischemic
insult, and accelerates tissue reperfusion. Elicited responses from multiple cell types RAD001 molecular weight probably contribute to these effects. “
“Microcirculation (2010) 17, 1–10. doi: 10.1111/j.1549-8719.2009.00013.x Objective: Epoxyeicosatrienoic acids (EETs) are protective in both myocardial and brain ischemia, variously attributed to activation of KATP channels or blockade of adhesion molecule upregulation. In this study, we tested whether EETs would be protective in lung ischemia–reperfusion injury. Methods: The filtration coefficient (Kf), a measure of endothelial permeability, and expression of the adhesion molecules vascular cell SPTLC1 adhesion molecule (VCAM) and intercellular adhesion molecule (ICAM) were measured after 45 minutes ischemia and 30 minutes reperfusion in isolated rat lungs. Results: Kf increased significantly after ischemia–reperfusion alone vs time controls, an effect dependent upon extracellular Ca2+ although not on the EET-regulated channel TRPV4. Inhibition of endogenous EET degradation or administration of exogenous 11,12- or 14,-15-EET at reperfusion significantly limited the permeability response to ischemia–reperfusion. The beneficial effect of 11,12-EET was not prevented by blockade of KATP channels nor by blockade of TRPV4.