ABSTRACT
Objective To observe the changes of serum aldosterone(ALD)in children with patent ductus arteriosus(PDA)at before and after interventional therapy,and explore its relationship with cardiac remodeling and its clinical significance.Methods Serum ALD level taken in supine position,left heart chambers sizes and heart f unction in children with PDA were measured and compared before,24 hours part intervention and at 1 month and 3 months after.The relationship between ALD and the left heart chambers sizes and the heart function were analyzed.Results Serum ALD levels were significantly lower 24 hours,1 month and 3 months than the pre-procedure levels [(348.44± 54.27)pmol/L vs.(311.35±50.34)pmol/L vs.(258.14±50.56)pmol/L vs.(199.09±48.12)pmol/L,F=18.98,P＜0.05].The lef t atrial diameter indexes[(42.33±6.44)mm/m2 vs.(36.22±5.33)mm/m2 vs.(35.54±5.36)mm/m2 vs.(34.26±4.32)mm/m2,F=12.18,P ＜ 0.05] and the lef t ventricular end diastolic diameter indexes [(69.34±7.43)mm/m2 vs.(67.43±6.33)mm/m2 vs.(66.35±6.56)mm/m2 vs.(60.54±5.34)mm/m2,F=11.71,P＜0.05] were also lower at 24 hours,1 month and 3 months after intervention than pre-procedure measurements.The left ventricular end systolic diameter indexes measured at 24 hours,1 mouth and 3 mouths after intervention were all lower as compared to pre-procedure condition[(39.43±8.32)mm/m2 vs.(38.47±7.45)mm/m2 vs.(36.85±5.43)mm/m2 vs.(35.63±5.34)mm/m2,F=13.13,P ＜ 0.05].There was relevance between the serum ALD level and the left heart chamber size indexes(P ＜ 0.05).Conclusions Early interventional therapy for PDA can reverse the activation of aldosterone secretion and cardiac remodeling.
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The aim of this study is to clarify whether edaravone postconditioning had protective effect against renal ischemia/reperfusion injury and to compare the protective effect between ischemic postconditioning and edaravone postconditioning. Rats were subjected to 45 min ischemia followed by 24 h reperfusion. The rats were randomly assigned to seven groups: a sham-operated control group, an ischemia/reperfusion group, an ischemic postconditioning group, a normal saline vehicle postconditioning group and an edaravone postconditioning (1, 3, and 6 mg x kg(-1)) group. Renal function was assessed by serum creatinine and BUN concentration, while histological damage of renal tissue was assessed with HE staining. MDA content and SOD activity of renal tissue were determined. TUNEL staining was performed to analyze the apoptosis of the tubular epithelial cells, the protein level of Bcl-2 and Bax in renal tissue was examined by Western blotting. Compared to the ischemia/reperfusion group, edaravone postconditioning significantly decreased serum creatinine and BUN concentration, and ameliorated histological damage of renal tissue. MDA was less after 24 h reperfusion in the edaravone postconditioning group than that in the ischemia/reperfusion group, consistent with an increase in SOD activity. In addition, edaravone postconditioning decreased TUNEL-positive cells and Bax expression, and increased Bcl-2 expression. Results detected in the edaravone postconditioning group showed no significant difference from the ischemic postconditioning group. Edaravone administered during the last 3 min of ischemia, prior to reperfusion induces a pharmacological postconditioning in vivo against renal ischemia/reperfusion injury in rats. This protection is similar to that observed with ischemic postconditioning.
Subject(s)
Animals , Male , Rats , Antipyrine , Therapeutic Uses , Apoptosis , Blood Urea Nitrogen , Creatinine , Blood , Free Radical Scavengers , Therapeutic Uses , Ischemic Postconditioning , Kidney , Pathology , Malondialdehyde , Metabolism , Proto-Oncogene Proteins c-bcl-2 , Metabolism , Random Allocation , Rats, Sprague-Dawley , Reperfusion Injury , Metabolism , Pathology , Superoxide Dismutase , Metabolism , bcl-2-Associated X Protein , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanism of ATP-sensitive potassium channel (K(ATP)) activator cromakalim (CRK) on action potentials and transient inward current (I(ti)) in isolated guinea pig papillary and ventricular myocytes and to explore the mechanisms of effects of I(ti) and K(ATP) treatment in idiopathic ventricular tachycardia.</p><p><b>METHODS</b>The whole-cell patch clamp recording technique was used to detect the action potentials and I(ti) and K(ATP) current alterations during the stimulated and triggered activity. Myocytes were isolated from guinea pig ventricle by enzyme digestion. The experiment was divided into four groups: (1) Control; (2) Control + Ouabain; (3) Control + CRK; (4) Control + Ouabain + CRK. (5) Control + Ouabain + CRK + glibenclamide (GLB). The action potential of guinea pig papillary muscles was measured by using standard microelectrode. The parameters in the experiment included the amplitude (APA), resting potentials (RP), action potentials duration (APD), as well as maximum rise of the action potential (Vmax).</p><p><b>RESULTS</b>(1) When the guinea pig ventricular papillary myocytes were pretreated with Ouabain 0.5 micromol/L, APD prolonged significantly, especially APD(20), APD(50), APD(90). Delayed after depolorazion (DAD) and triggered activity were elicited. I(ti) currents and DAD as well as triggered activity increased. I(ti) current was (126.9 +/- 10.8) pA, lagT (1173.0 +/- 70.9) ms (n = 10, P < 0.01). (2) When guinea pig ventricular myocytes were pretreated with CRK (10 micromol/L), APD was shortened and the amplitude of DAD was lowered. The coupling time in CRK group was significantly prolonged compared with Ouabain group (n = 10, P < 0.01). (3) CRK 50 micromol/L pretreatment of the ventricular myocytes led to an increase of K(ATP) up to (342 +/- 89) pA, which was statistically significant as compared with the control group (P < 0.01). ATP-sensitive potassium channel blocker glibenclamide (10 micromol/L) could antagonize the effects of CRK on APD and I(ti) currents.</p><p><b>CONCLUSION</b>CRK might reduce the toxic effect of Ouabain on cardiomyocytes, shorten APD, terminate DAD and trigger excitation, and have protective effect on cardiomyocytes. The effects of CRK, may be associated with the inhibiting I(ti) current and increasing K(ATP).</p>
Subject(s)
Animals , Action Potentials , Cromakalim , Pharmacology , Guinea Pigs , Heart Ventricles , Myocytes, Cardiac , Physiology , Patch-Clamp Techniques , Potassium Channels, Inwardly RectifyingABSTRACT
Backgroud and Objective Proline-rich tyrosine kinase2(Pyk2) is a Ca~(2+) sensitive,non-receptor tyrosine protein kinase.Previous reports showed Pyk2 involved in development of left ventrieular hypertrophy. The present paper aimed to study the effects of valsartan on ventricular hypertrophy and its effect on the expression of Pyk2 in myocardium in renovascular hypertensive rats(RHR).Methods Two-kidney and one-clip(2K1C) renal hypertensive model was established in Sprague-Dawley rats by chronic partial occlusion of left renal artery,and ran- domized to receive valsartan (30 mg/kg?d) or without treatment for 4 or 8 weeks.Left ventricular mass to body mass ratio was measured.Pyk2 protein expression and phosphorylation was detected by Western blotting.Results Blood pressure,left ventricular mass to body mass ratio,Pyk2 activity in myocardium of RHR were increased gradu- ally.Valsartan reduced BP and prevent myocardial hypertrophy(P
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<p><b>AIM</b>To investigate the effects of melatonin (MT) on histology and behavioral tests during global cerebral ischemia-reperfusion in gerbils.</p><p><b>METHODS</b>Global cerebral ischemia was induced by occluding the bilateral common carotid arteries for 10 min in gerbils. Three doses of MT were administrated intraperitoneally 30 min prior to the onset of ischemia. Locomotor activity was measured by using the open field method 3 and 7 days after the ischemic episode. T maze test was carried out 4, 5 and 6 days after ischemia to assess the working memory of gerbils. Neuronal damage was assessed in CA1 pyramidal layer of gerbil hippocampus and evaluated 7 days after ischemia.</p><p><b>RESULTS</b>MT significantly reversed the locomotor activity increases, ameliorated learning and working memory deficit, and reduced the extent of CA1 hippocampal pyramidal cells injury after transient global cerebral ischemia in the Mongolian gerbil.</p><p><b>CONCLUSION</b>MT provides significantly protective effect against both histological and behavioral consequences of global cerebral ischemia-reperfusion injury in gerbils.</p>