Alterações enzimáticas decorrentes de isquemia muscular esquelética em ratos / Enzymatic alterations due to skeletal muscle ischemia in rats

Os autores estudaram as alterações enzimáticas [transaminase oxalo-acética (TGO), creatinofosfoquinase (CPK) e desidrogenase lática (LDH)] decorrentes de isquemia muscular esquelética em ratos submetidos à isquemia de membro inferior por 0, 2, 4 e 6 horas. Vinte e oito ratos Wistar foram divididos em 4 grupos: Grupo I (controle); e Grupos II, III, e IV (isquemia por 2, 4 e 6 horas, respectivamente). Após o período de isquemia, foi coletado sangue do plexo retrocular para análise laboratorial. Os valores obtidos (média +/- desvio padrão) para TGO nos Grupos I, II, III e IV foram, respectivamente: 20,14 +/- 6,76; 59,71 +/- 28,91; 88,28 +/- 11,17 e 123 +/- 52,65 U/l. Para CPK, os valores foram: 67,85 +/- 62,76; 203 +/- 108,71; 237,71 +/- 95,06 e 291,71 +/- 173,19 U/l. Para LDH, obteve-se: 334,14 +/- 117,13; 414,42 +/- 222,47; 526 +/- 234,75 e 427,57 +/- 273,58 U/l. Para análise estatística, utilizou-se o método de ANOVA, seguido do teste t de Bonferroni (p<0,05). Os níveis de TGO foram significativamente superiores nos grupos III e IV quando comparados ao controle. Para CPK, houve distinção significativa entre os grupos IV e I. Os níveis de LDH não se demonstraram estatisticamente diferentes entre os grupos. Os autores concluem que em períodos de isquemia por 2, 4 e 6 horas, a dosagem de LDH não se mostra um parâmetro útil na avaliação de dano muscular esquético. A TGO e CPK tiveram alterações significativas a partir de 4 e 6 horas, respectivamente, mostrando-se úteis na avaliação de isquemia muscular em ratos.

Kallikrein-like amidase activity in renal ischemia and reperfusion

We assessed a kallikrein-like amidase activity probably related to the kallikrein-kinin system, as well as the participation of leukocyte infiltration in renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min of ischemia and to different periods of reperfusion. A control group consisted of sham-operated mice, under similar conditions, except for ischemia induction. Kallikrein-like amidase activity, Evans blue extravasation and myeloperoxidase activity were measured in kidney homogenates, previously perfused with 0.9 percent NaCl. Plasma creatinine concentration increased only in the 60-min ischemic group. After 20 min of ischemia and 1 or 24 h of reperfusion, no change in kallikrein-like amidase activity or Evans blue extravasation was observed. In the mice subjected to 20 min of ischemia, edema was evident at 1 h of reperfusion, but kidney water content returned to basal levels after 24 h of reperfusion. In the 60-min ischemic group, kallikrein-like amidase activity and Evans blue extravasation showed a similar significant increase along reperfusion time. Kallikrein-like amidase activity increased from 4 nmol PNA mg protein-1 min-1 in the basal condition to 15 nmol PNA mg protein-1 min-1 at 10 h of reperfusion. For dye extravasation the concentration measured was near 200 µg of Evans blue/g dry tissue in the basal condition and 1750 µg of Evans blue/g dry tissue at 10 h of reperfusion. No variation could be detected in the control group. A significant increase from 5 to 40 units of DAbs 655 nm g wet tissue-1 min-1 in the activity of the enzyme myeloperoxidase was observed in the 60-min ischemic group, when it was evaluated after 24 h of reperfusion. Histological analysis of the kidneys showed migration of polymorphonuclear leukocytes from the vascular bed to the interstitial tissue in the 60-min ischemic group after 24 h of reperfusion. We conclude that the duration of ischemia is critical for the development of damage during reperfusion and that the increase in renal cortex kallikrein-like amidase activity probably released from both the kidney and leukocytes may be responsible, at least in part, for the observed effects, probably through direct induction of increased vascular permeability.

The role of xanthine oxidase and the effects of antioxidants in ischemia reperfusion cell injury

During last years considerable interest has been devoted to understand the role of oxugen radicals in the inschemia induced cell injury associated with reperfusion. In the brain and in others tissues, free radicals play a role as modulators of vascular tone as well as a cytotoxic role as part of the ischemia associated pathology. This review discusses methods for free radical detection in brain and in other tissues, mechanisms of radical production in the course of the ischemia reperfusion process, and the efficacy of potential antioxidant agents in post ischemia therapy, especially with respect to allopurinol, an inhibitor of xanthine oxidase, and the role of taurine and its derivatives as antioxidants in different organs including the brain.

Isquemia miocárdica transitoria neonatal: informe clínico y revisión / Myocardic ischemia neonatal transitory: clinical report and review

Se presentan dos casos de isquemia miocárdiaca transitoria neonatal en pacientes del sexo femenino, sin evidencia de cardiopatía congénita o lesión de coronarias. Una con antecedente de hipoxia perinatal; la otra con poliglobulina significativa. Se analizan los hallazgos clínicos en ambos casos, hallazgos paraclínicos y especialmente la secuencia del perfil enzimático (STGO,CPK,LDH). Ambos casos evolucionaron satisfactoriamente, hasta su recuperación completa. Se estudia la terapéutica en cada una de las pacientes. Se procede a la revisión de la literatura