ABSTRACT
ObjectiveTo investigate the effect of Baicalin on the apoptosis of cardiomyocytes and the expression of Akt/Amp activated protein kinase (AMPK)/mammalian rapamycin target protein (mTOR) signaling pathway in rats with chronic myocardial failure.MethodsSixty male SD rats of SPF grade were randomly divided into normal group, model group, positive control group and experimental group, with 15 rats in each group. Rats in the positive control group were given 40mg/kg losartan once a day. Rats in the experimental group were given 50mg/kg Baicalin once a day. Rats in the normal group and the model group were given the same dose of saline once a day. Each group was given gavage for 4 weeks. HE staining was used to observe the pathomorphology of cardiomyocytes. The myocardial tissue index (CAI) was detected by in situ end labeling. The expressions of Bax and bcl-2 protein in myocardium were detected by immunohistochemistry. The cardiac function was detected by echocardiography. The expression of Akt, AMPK and mTOR mRNA was detected by RT-PCR.ResultsCompared with the normal group, the apoptosis indexes of the model group, the positive control group and the experimental group were increased (P0.05). Compared with the model group, the expression of Bcl-2 protein was increased and Bax protein was decreased in the positive control group and the experimental group (P0.05). Compared with the normal group, the LVEFs of the model group, the positive control group and the experimental group were decreased, while the LVD and LVS were increased (P0.05).ConclusionBaicalin can alleviate myocardial injury in rats with chronic myocardial failure, and its mechanism may be related to the upregulation of Akt/AMPK/mTOR signaling pathway.
ABSTRACT
ObjectiveTo investigate the effect of Baicalin on the apoptosis of cardiomyocytes and the expression of Akt/Amp activated protein kinase (AMPK)/mammalian rapamycin target protein (mTOR) signaling pathway in rats with chronic myocardial failure.MethodsSixty male SD rats of SPF grade were randomly divided into normal group, model group, positive control group and experimental group, with 15 rats in each group. Rats in the positive control group were given 40mg/kg losartan once a day. Rats in the experimental group were given 50mg/kg Baicalin once a day. Rats in the normal group and the model group were given the same dose of saline once a day. Each group was given gavage for 4 weeks. HE staining was used to observe the pathomorphology of cardiomyocytes. The myocardial tissue index (CAI) was detected by in situ end labeling. The expressions of Bax and bcl-2 protein in myocardium were detected by immunohistochemistry. The cardiac function was detected by echocardiography. The expression of Akt, AMPK and mTOR mRNA was detected by RT-PCR.ResultsCompared with the normal group, the apoptosis indexes of the model group, the positive control group and the experimental group were increased (P0.05). Compared with the model group, the expression of Bcl-2 protein was increased and Bax protein was decreased in the positive control group and the experimental group (P0.05). Compared with the normal group, the LVEFs of the model group, the positive control group and the experimental group were decreased, while the LVD and LVS were increased (P0.05).ConclusionBaicalin can alleviate myocardial injury in rats with chronic myocardial failure, and its mechanism may be related to the upregulation of Akt/AMPK/mTOR signaling pathway.
ABSTRACT
La insuficiencia respiratoria observada tras una injuria cerebral aguda es un fenómeno común que puede debersea múltiples causas, como broncoaspiración, neumonía, atelectasia, embolismo pulmonar y, raramente, edemapulmonar neurogénico. Esta última entidad se encuentra subdiagnosticada y sería un potencial contribuyente dela disfunción pulmonar temprana en pacientes con injurias cerebrales. La misma se ha asociado a convulsiones,accidentes cerebrovasculares, infecciones, traumatismos encéfalocraneanos, entre otros. Se origina por una lesióngrave del sistema nervioso central en ausencia de cardiopatías o neumopatías previas. La gravedad es directamenteproporcional a la lesión cerebral y se produciría por una disfunción del centro vasomotor hipotalámico. Se caracterizapor un incremento en el contenido de agua intersticial pulmonar. Los cambios hemodinámicos son sugestivosde disfunción cardíaca. El análisis temprano del fluido pulmonar revela un cociente de proteínas líquido/suerobajo, compatible con edema hidrostático. El tratamiento incluye oxígenoterapia, asistencia respiratoria mecánicay manejo hemodinámico. Presentamos a una paciente de 20 años, sin antecedentes patológicos, que ingresa portraumatismo encéfalocraneano moderado tras accidente en la vía pública y que posteriormente desarrolla una descompensacióncardiorrespiratoria interpretada como edema pulmonar neurogénico (EPN).
Respiratory distress observed following an acute brain injury is a common phenomenon which could suggest multiplecauses, such as bronchoaspiration, pneumonia, atelectasis, pulmonary embolism and, rarely, neurogenic pulmonary edema(NPE). NPE is usually under-diagnosed and could be a potential contributor to early pulmonary failure in patients whosuffer brain injuries. NPE has been associated, among others, to seizures, strokes, infections, and head trauma. It appearsas a result of a severe injury of the central nervous system (CNS), in absence of previous heart or lung diseases. Its severityis directly proportional to the brain injury and would be a consequence of a failure of the hypothalamic vasomotor center.It is characterized by an increase in the lung interstitial fluid content. The hemodynamic changes suggest heart failure. Theearly assessment of lung fluid reveals a low ratio of liquid/serum proteins compatible with hydrostatic edema. Treatmentinvolves oxygen therapy, mechanical ventilation and hemodynamic monitoring. We present a 20-year old female patient,with no pathologic history, who is admitted due to moderate head trauma after a street accident and who later developscardiopulmonary failure interpreted as a neurogenic pulmonary edema (NPE).
Subject(s)
Adult , Pulmonary Edema , Craniocerebral Trauma/complications , Heart Failure , Respiratory Insufficiency/complicationsABSTRACT
This study was conducted to assess the ability of two-dimensional tissue tracking (2DTT) to evaluate changes in left ventricular (LV) myocardial function associated with sustained high electrical pacing. Pacemakers were implanted at the right ventricular (RV) apex of five female Beagles, and sustained high electrical pacing of 250 beats per minute (bpm) was performed for three consecutive weeks. Conventional echocardiography and 2DTT were performed at baseline, and at every week for three weeks with pacing. The baseline parameters were then compared to those of weeks 1, 2, and 3. Three weeks of pacing resulted in significant reduction of radial and circumferential global strains (p < 0.001). Regional analysis revealed reduction of segmental strains in both radial and circumferential directions, as well as increased dyssynchrony after three weeks of pacing in the radial direction (p = 0.0007). The results of this study revealed the ability of 2DTT to measure radial and circumferential strains in dogs with sustained high-electrical pacing, and allowed assessment of global and regional myocardial function and the degree of dyssynchrony.