Abstract
We investigated kidney and lung alterations caused by intercellular adhesion molecule type 1 (ICAM-1) blockade after ischemia and reperfusion of hind limb skeletal muscles. Rats were submitted to ligature of the infrarenal aorta for 6 h. The animals were randomized into three groups of 6 rats each: group I, sacrificed after ischemia; group II, reperfusion for 24 h, and group III, reperfusion for 24 h after receiving monoclonal anti-ICAM-1 antibodies. At the end of the experiment, blood samples were collected for creatinine, lactate dehydrogenase, creatine phosphokinase, potassium, pH and leukocyte counts. Samples were taken from the muscles of the hind limbs and from the kidneys and lungs for histological analysis and measurement of the neutrophil infiltrate by myeloperoxidase staining. The groups did not differ significantly with regard to the laboratory tests. There were no major histological alterations in the kidneys. An intense neutrophil infiltrate in the lungs, similar in all groups, was detected. Myeloperoxidase determination showed that after reperfusion there was significantly less retention of polymorphonuclear neutrophils in the muscles (352 +/- 70 vs 1451 +/- 235 x 10(2) neutrophils/mg; P<0.01) and in the kidneys (526 +/- 89 vs 852 +/- 73 10(2) neutrophils/mg; P<0.01) of the animals that received anti-ICAM-1 before perfusion compared to the group that did not. The use of anti-ICAM-1 antibodies in this experimental model minimized neutrophil influx, thus reducing the inflammatory process, in the muscles and kidneys after ischemia and reperfusion of the hind limbs.
Highlights
During the first half of the 20th century, studies that associated extensive traumatic muscle lesions with a syndrome represented by dark urine, muscle pain, body weakness and acute renal insufficiency were published [1]
Many authors began to investigate the role of oxygen [4] and its toxic derivatives [5,6], polymorphonuclear neutrophils (PMN; 7-9) and the intercellular adhesion molecule type 1 (ICAM-1) in ischemia and reperfusion [10,11]
We evaluated the effect of ICAM-1 blockade with antibodies on the rat hind limb reperfusion syndrome especially on kidneys and lungs
Summary
During the first half of the 20th century, studies that associated extensive traumatic muscle lesions with a syndrome represented by dark urine (myoglobinuria), muscle pain, body weakness (hyperkalemia) and acute renal insufficiency were published [1]. This clinical condition was later called myonephropathic syndrome or reperfusion syndrome [2]. Despite advances in medical knowledge and technology, little progress has been made in the treatment of such patients This syndrome presents a high mortality rate, especially when associated with specific pathological conditions such as diabetes, senility, renal insufficiency and others [3]. Many authors began to investigate the role of oxygen [4] and its toxic derivatives [5,6], polymorphonuclear neutrophils (PMN; 7-9) and the intercellular adhesion molecule type 1 (ICAM-1) in ischemia and reperfusion [10,11]
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Schedule a callMore From: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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