Effect of HTK on the microcirculation in the rat cremaster muscle during warm ischemia and reperfusion

✍ Scribed by Jacqueline Bastiaanse; Gary L. Anderson; Ralph J.P.M. Franken; Brigitte E.P.A. Van Der Heijden; Mirjam G.A. Oude Egbrink; Dick W. Slaaf; Moshe Kon

• Publisher: John Wiley and Sons
• Year: 2005
• Tongue: English
• Weight: 146 KB
• Volume: 25
• Category: Article
• ISSN: 0738-1085
• DOI: 10.1002/micr.20093

✦ Synopsis

Histidine-tryptophan-ketoglutarate (HTK) preserves rat muscle function during cold storage. We examined the effect of HTK perfusion on preservation of microvascular function during 4 h of warm ischemia and subsequent reperfusion (I/R) in the rat cremaster muscle. Leukocyteendothelium interactions, capillary perfusion, and arteriole diameters were quantified prior to HTK-perfusion and/or ischemia, and at 0, 1, and 2 h after restoration of blood flow. In all groups, the number of rolling leukocytes increased with time, whereas I/R induced a slight increase in leukocyte adhesion. After ischemia, capillary perfusion rapidly recovered to about 50% and returned to near normal (90%) after 2 h. HTK at 22°C did not affect the assessed microcirculation variables, whereas HTK at 4°C reduced leukocyte rolling, but not adhesion. Therefore, microvascular function of HTK-perfused muscles was not better preserved during warm I/R than that of nonperfused muscles. Contrary to other preservation solutions, HTK perfusion in itself was not detrimental to the microcirculation.