Objetivo: Analisar as funções executivas de idosos com doença de Parkinson (DP – com e sem quadro demencial) e doença de Alzheimer (DA), e confrontar os escores dos participantes no que se refere às atividades funcionais da vida diária e à habilidade motora em situações de dupla tarefa. Métodos: Sob um desenho transversal, 54 idosos foram divididos em quatro grupos: G1, composto por 11 sujeitos com DP; G2, formado por 10 sujeitos com demência de Parkinson; G3, composto por 13 participantes com DA; e G4, formado por 20 idosos saudáveis. Os procedimentos metodológicos envolveram análise das funções cognitivas pré-frontais dos sujeitos, da realização das atividades da vida diária e da habilidade motora em situações de dupla tarefa. A análise dos dados envolveu a estatística descritiva (média e erro-padrão) e inferencial (teste ANOVA e pós-teste de Scheffé), admitindo significância de 5% (p < 0,05) e intervalo de confiança de 95%. Resultados: As funções cognitivas pré-frontais apresentaram diferença significativa entre os grupos, sobretudo nas comparações envolvendo G2 e G3, em relação a G1 e G4 (p = 0,001). Os grupos com déficit cognitivo apresentaram pior rendimento na realização das atividades da vida diária, com menor escore do G2, na qual há junção de déficit cognitivo e motor (p = 0,001). Em situações de dupla tarefa, G2 e G3 apresentaram maiores dificuldades que os demais grupos (p < 0,05). Conclusão: Distúrbios pré-frontais repercutem negativamente nas atividades funcionais e na habilidade psicomotora dos indivíduos. Quando não vinculado a quadro demencial, os pacientes com DP apresentaram escores cognitivos pré-frontais e independência funcional semelhantes aos de idosos saudáveis.

Ischemic postconditioning was able to minimize reperfusion injury of rats undergone mesenteric ischemia and reperfusion process. There was no difference in the effectiveness of the method comparing two cycles of two minutes with four cycles of 30 seconds by H&E histological evaluation of the ileum after 60-minute reperfusion.

INTRODUCTION Some publications have demonstrated the presence of lung reperfusion injury in mesenteric ischemia and reperfusion (I/R), but under to diverse methods. Postconditioning has been recognized as effective in preventing reperfusion injury in various organs and tissues. However, its effectiveness has not been evaluated in the prevention of lung reperfusion injury after mesenteric ischemia and reperfusion.OBJECTIVE To evaluate the presence of pulmonary reperfusion injury and the protective effect of ischemic postconditioning on lung parenchyma in rats submitted to mesenteric ischemia and reperfusion.METHODS Thirty Wistar rats were distributed into three groups: group A (10 rats), which was held mesenteric ischemia (30 minutes) and reperfusion (60 minutes); group B (10 rats), ischemia and reperfusion, interspersed by postconditioning with two alternating cycles of reperfusion and reocclusion, for two minutes each; and group C (10 rats), ischemia and reperfusion interleaved by postconditioning with four alternating cycles of reperfusion and reocclusion of 30 seconds each. Finally, it was resected the upper lung lobe for histological analysis.RESULTS There were mild lung lesions (grade 1) in all samples. There was no statistical difference between groups 1 and 2 (P>0.05).CONCLUSION The mesenteric ischemia and reperfusion in rats for thirty and sixty minutes, respectively, caused mild reperfusion injury in lung. Postconditioning was not able to minimize the remote reperfusion injury and there was no difference comparing two cycles of two minutes with four cycles of 30 seconds.

IntroductionIschemic postconditioning is a method that shows evidence of efficacy in minimizing reperfusion injury; however, its effectiveness in preventing injuries in distant organs is still unknown, especially in those who have undergone mesenteric ischemia and reperfusion.ObjectiveTo evaluate the effect of ischemic postconditioning in preventing reperfusion injury in the liver of rats submitted to mesenteric ischemia and reperfusion, comparing two different methods of ischemic postconditioning.Methods30 Wistar male rats were used, distributed into three groups: Group A: Ten rats submitted to intestinal ischemia for 30 minutes followed by reperfusion for 60 minutes; Group B: Ten rats subjected to ischemia and reperfusion; after ischemia, two cycles of reperfusion (two minutes each) interleaved with two cycles of ischemia (two minutes each); and Group C: Ten rats subjected to ischemia and reperfusion; after ischemia, four cycles of reperfusion (30 seconds each) interspersed with four cycles of ischemia (30 seconds each). After the experiment, the left lobe of the liver was resected for subsequent histological analysis, using the following classification: grade 1 - centrilobular congestion; grade 2 - centrilobular congestion with some degeneration of hepatocytes in one or two central veins; and grade 3 - multifocal centrilobular congestion and degeneration of portal hepatocytes.ResultsThe mean degree of liver damage found was 1.8 in group A, 1.7 in group B and 1.3 in group C. There was no statistically significant difference between the groups.ConclusionIschemic postconditioning was unable to minimize reperfusion injury in rats undergoing mesenteric ischemia and reperfusion.

Background: Sodium reabsorption depends on the Na/K/ATPase activity coupled to basolateral K⁺ recycling through K⁺ channels. ATP depletion reduces pump activity and increases K⁺ leak resulting in transport dysfunction. Kir4.1 is a pH-sensitive K⁺ channel expressed in the basolateral membrane of distal tubules. In this study, we evaluated whether Kir4.1 is also expressed in proximal tubules (PTs) and whether renal ischemia alters Kir4.1 mRNA expression levels. Methods: The presence of Kir4.1 mRNA was evaluated in PTs microdissected from collagenase-treated rat kidneys. Kir4.1 expression levels were estimated in the renal cortex by multiplex RT-PCR after 30 or 60 min of renal ischemia followed by 1, 24, 48 or 72 h of reperfusion. Results: The PCR product obtained from isolated tubules was sequenced and showed ∼98% homology with rat Kir4.1 cDNA. Ischemia/reperfusion for 30 min induced a time-dependent reduction in Kir4.1 mRNA expression in parallel with plasma creatinine, however recovery was delayed after 60 min of ischemia, remaining reduced after 72 h of reperfusion when plasma creatinine was already normalized. Conclusion: Kir4.1 mRNA expression was decreased by renal ischemia. The ischemia-induced cellular K⁺ loss may be minimized by Kir4.1 downregulation and may contribute to the mechanism by which cellular acidification induces cell protection against ATP depletion.