Estimulação diafragmática elétrica transcutânea melhora as condições metabólicas dos músculos respiratórios de ratos

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Abstract

Objetivo: Avaliar o conteúdo de glicogênio dos músculos respiratórios e o registro eletrocardiográfico (ECG) de ratos submetidos à estimulação diafragmática elétrica transcutânea (EDET). Método: Ratos adultos Wistar foram divididos em 2 grupos (n=6): controle (C) e tratado com EDET (f=50Hz; T ON / T OFF= 2/2 seg.; T= 400ms, i= 5mA com acréscimo de 1mA a cada 3 min.; t= 20 minutos) durante 5 dias. Após o período experimental, a análise do ECG foi realizada seguida do sacrifício dos animais para a obtenção das amostras dos músculos peitoral, intercostal, diafragma e abdominal, que foram encaminhadas para a análise do conteúdo de glicogênio. A análise estatística foi feita através do teste de normalidade e teste tde Student (p<0,05). Resultados: A EDET promoveu elevação no conteúdo de glicogênio em 42,85% no diafragma (C: 0,21 ± 0,008 x EDET: 0,30 ± 0,04, p>0,05), 81,2% no intercostal (C: 0,32 ± 0,08 x EDET: 0,58 ± 0,17, p>0,05), 96,7% no peitoral (C: 0,30 ± 0,05 x EDET: 0,59 ± 0,06, p<0,05) e 104,5% no abdominal (C: 0,22 ± 0,01 x EDET: 0,45 ± 0,03, p<0,05) quando comparado ao C. Os resultados da análise do ECG mostraram que não houve alteração nos parâmetros analisados (freqüência cardíaca, intervalos QR, QT e QTc) no grupo que recebeu a EDET. Conclusão: Além do trabalho sugerir um protocolo de EDET em animais, os resultados mostraram sua eficácia na melhora das condições energéticas da musculatura respiratória sem interferir na dinâmica elétrica cardíaca.

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Steven Pohnert, Louise Zheng, W W Winder … (2001)

Skeletal muscle GLUT-4 transcription in response to treatment with 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), a known activator of AMP-activated protein kinase (AMPK), was studied in rats and mice. The increase in GLUT-4 mRNA levels in response to a single subcutaneous injection of AICAR, peaked at 13 h in white and red quadriceps muscles but not in the soleus muscle. The mRNA level of chloramphenicol acyltransferase reporter gene which is driven by 1,154 or 895 bp of the human GLUT-4 proximal promoter was increased in AICAR-treated transgenic mice, demonstrating the transcriptional upregulation of the GLUT-4 gene by AICAR. However, this induction of transcription was not apparent with 730 bp of the promoter. In addition, nuclear extracts from AICAR-treated mice bound to the consensus sequence of myocyte enhancer factor-2 (from -473 to -464) to a greater extent than from saline-injected mice. Thus AMP-activated protein kinase activation by AICAR increases GLUT-4 transcription by a mechanism that requires response elements within 895 bp of human GLUT-4 proximal promoter and that may be cooperatively mediated by myocyte enhancer factor-2.

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J Wojtaszewski, M. Michael, Y Higaki … (1999)

Physical exercise promotes glucose uptake into skeletal muscle and makes the working muscles more sensitive to insulin. To understand the role of insulin receptor (IR) signaling in these responses, we studied the effects of exercise and insulin on skeletal muscle glucose metabolism and insulin signaling in mice lacking insulin receptors specifically in muscle. Muscle-specific insulin receptor knockout (MIRKO) mice had normal resting 2-deoxy-glucose (2DG) uptake in soleus muscles but had no significant response to insulin. Despite this, MIRKO mice displayed normal exercise-stimulated 2DG uptake and a normal synergistic activation of muscle 2DG uptake with the combination of exercise plus insulin. Glycogen content and glycogen synthase activity in resting muscle were normal in MIRKO mice, and exercise, but not insulin, increased glycogen synthase activity. Insulin, exercise, and the combination of exercise plus insulin did not increase IR tyrosine phosphorylation or phosphatidylinositol 3-kinase activity in MIRKO muscle. In contrast, insulin alone produced a small activation of Akt and glycogen synthase kinase-3 in MIRKO mice, and prior exercise markedly enhanced this insulin effect. In conclusion, normal expression of muscle insulin receptors is not needed for the exercise-mediated increase in glucose uptake and glycogen synthase activity in vivo. The synergistic activation of glucose transport with exercise plus insulin is retained in MIRKO mice, suggesting a phenomenon mediated by nonmuscle cells or by downstream signaling events.

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Diaphragm Pacing by Electrical Stimulation of the Phrenic Nerve

William Glenn, Mildred L. Phelps (1985)

Sophisticated techniques for electrical stimulation of excitable tissue to treat neuromuscular disorders rationally have been developed over the past 3 decades. A historical review shows that electricity has been applied to the phrenic nerves to activate the diaphragm for some 200 years. Of the contemporary methods for stimulating the phrenic nerve in cases of ventilatory insufficiency, the authors prefer stimulation of the phrenic nerve in the thorax using a platinum ribbon electrode placed behind the nerve and an attached subcutaneously implanted radiofrequency (RF) receiver inductively coupled to an external RF transmitter. Instructions are given for implanting the electrode-receiver assembly, emphasizing atraumatic handling of the phrenic nerve and strict aseptic techniques. Diaphragm pacing is conducted with low frequency electrical stimulation at a slow repetition (respiratory) rate to condition the diaphragm muscle against fatigue and maintain it fatigue-free. Candidates for diaphragm pacing are those with ventilatory insufficiency due to malfunction of the respiratory control center or interruption of the upper motor neurons of the phrenic nerve. In the Yale series, there were 77 patients treated by diaphragm pacing; 63 (82%) started before 1981 and thus were available for follow-up for at least 5 years; 33 (52%) were paced for 5 to 10 years, and 15 (24%) were paced for 10 to 16. Long term stimulation of the phrenic nerves to pace the diaphragm is an effective method of ventilatory support in selected cases.