Effect of Oxymatrine on cardiac function and left ventricular remodeling in rabbits after acute myocardial infarction / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To observe the effect of Oxymatrine on left cardiac function and ventricular remodeling in rabbits after acute myocardial infarction.</p><p><b>METHODS</b>Ligation of the left anterior descending artery was adopted to establish acute myocardial infarction model, forty eight rabbits were randomized into the sham operation group, model group and Oxymatrine group. Eight models were successfully established in each group. the sham operation group and model group were given conventional feed. Oxymatrine were gavage administration 0.5 ml/100 g, once a day, lasted for 4 weeks. Respectively in postoperative week, and three weeks, to observe the Oxymatrine on cardiac output (CO), left ventricular end systolic pressure (LVESP), left ventricular end-diastolic pressure (LVEDP), left indoor pressure change rate peak (dp/dtmax)), and left ventricular cavity internal diameter (D), ventricular weight index (VWI), ventricular weight (VW).</p><p><b>RESULTS</b>Left ventricular anterior wall was from red to deep purple, electrocardiogram showed II guide ST-segment camber up ≥ 0.25 mv. Postoperative week in Oxymatrine group compared with model group, LVESP increased significantly (P < 0.01), LVEDP decreased obviously (P < 0.01); After three weeks in Oxymatrine group compared with model group, VW, VWI decreased (P < 0.05), D significantly reduced (P < 0.01); LVESP increased significantly (P < 0.01), LVEDP decreased obviously (P <0.01); dp/dt(max), CO increased (P < 0.05).</p><p><b>CONCLUSION</b>After acute myocardial infarction in rabbit Oxymatrine can improve the left ventricular reconstruction parameters, increase cardiac output, and improve cardiac function.</p>

Electrophysiological effects of antiarrhythmic drugs on pacemaker cells in guinea pig left ventricular outflow tract / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore the electrophysiological effects of antiarrhythmic drugs on pacemaker cells of left ventricular outflow tract.</p><p><b>METHODS</b>By using conventional intracellular microelectrode technique to record action potentials, series antiarrhythmic drugs were used to investigate the electrophysiological features and regularities of spontaneous activity of left ventricular outflow tract.</p><p><b>RESULTS</b>(1) Perfusion with 1 micromol/L quinidine resulted in a significant decrease in rate of pacemaker firing (RPF, P < 0.05), velocity of diastolic depolarization (VDD, P < 0.05), amplitude of action potential (APA, P < 0.05), and maximal rate of depolarization (V(max), P < 0.05), and a marked prolonging in 50% and 90% of duration of action potential (APD50 and APD90, P < 0.05). (2) 1 micromol/L lidocaine decreased RPF, VDD, MDP, APA and V(max) significantly (P < 0.05), shortened APD50 and APD90 notably (P < 0.05). (3) 1 micromol/L propafenone led to a significant decrease in RPF (P < 0.01), VDD (P < 0.05), APA (P < 0.05), V(max) (P < 0.01), and a marked prolonging in APD50 (P < 0.01) and APD90 (P < 0.05). (4) Application of 5 micromol/L propranolol resulted in a significant decrease in RPF and VDD (P < 0.01), MDP and APA (P < 0.01), V(max) (P < 0.05) and a notable prolonging in APD50 and APD90 (P < 0.05). (5) Perfusion with 1 micromol/L amiodarone resulted in a significant decrease in RPF and VDD (P < 0.01), APA (P < 0.01), V(max) (P < 0.05), a marked prolonging in APD50 (P < 0.01) and APD90 (P < 0.05). (6) 1 micromol/L verapamil significantly decreased RPF and VDD (P < 0.01), MDP and APA (P < 0.05), V(max) (P < 0.05), notably prolonged APD50 and APD90 (P < 0.01). (7) 50 micromol/L adenosine significantly decreased RPF and VDD (P < 0.05), APA (P < 0.05), V(max) (P < 0.01), markedly shortened APD50 and APD90 (P < 0.05).</p><p><b>CONCLUSION</b>All kinds of antiarrhythmic drugs can decrease the autorhythmicity of guinea pig left ventricular outflow tract. By altering APD50 and APD90, they can affect effective refractory period (ERP) and having a significant effect on autorhythmicity of left ventricular outflow tract.</p>

Changes in aortic endothelium ultrastructure in male rats following castration, replacement with testosterone and administration of 5alpha-reductase inhibitor / 亚洲男科学杂志(英文版)

<p><b>AIM</b>To investigate the relationship between low androgen level and ultrastructure of vascular endothelium.</p><p><b>METHODS</b>Forty-eight male Sprague-Dawley rats were randomly divided into four groups: group A, normal rats with sham castration; group B, castrated rats; group C, castrated rats given testosterone (T) undecanoate; and group D, intact rats treated with 5alpha-reductase inhibitor. After 10 weeks of treatment or castration, rats in different groups were killed and serum T, free T (FT) and dihydrotestosterone (DHT) were measured. The aortic endothelia were scanned under electron microcopy and the Vascular Endothelium Structure Score (VESS) was computed.</p><p><b>RESULTS</b>Serum T and FT concentrations of rats in group B were significantly lower than those of the other three groups (P < 0.01); DHT concentrations of group D rats were significantly decreased (P < 0.01) when compared with those of groups A and C. Rats in groups B and D rats (with low androgen levels) had obvious damage to their endothelial surfaces, which appeared crimpled, rough, adhesive and ruptured, and had high destruction of VESS.</p><p><b>CONCLUSION</b>These results suggest that low concentrations of T and DHT are associated with ultrastructural damage of the aortic endothelia in male rats.</p>

Protective effect of rosiglitazone on myocardium in diabetic cardiomyopathy of rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the protective effect of PPARgamma ligands rosiglitazone on myocardium in diabetic cardiomyopathy of rats.</p><p><b>METHODS</b>The rat model of diabetes was induced by administration of streptozotocin (STZ) for 6 or 10 weeks. In the treatment group the STZ-induced diabetic rats were treated with rosiglitazone. The left ventricular muscle specimens were taken from treatment and control group; then were examined under transmission electron microscope.</p><p><b>RESULT</b>Cardiac myofibrils of diabetic rats in control group were obviously fewer and broken. There were fewer and smaller dissolved mitochondria with incomplete membrane and mixed cristae and karyopyknosis. Myocardium of diabetic rats treated with rosiglitazone was markedly improved although their blood glucose levels were still high.</p><p><b>CONCLUSION</b>Hyperglycemia can cause destruction of myocardial cell structure. Rosiglitazone has protective effect on myocardial cells of diabetic rats, which seems to be independent of blood glucose levels.</p>

Electrophysiological effects of neurotransmitters on pacemaker cells in guinea pig left ventricular outflow tract / 生理学报

This study was designed to explore the innervation of autonomic nervous system and the distribution of receptors on pacemaker cell membrane in guinea pig left ventricular outflow tract (aortic vestibule). By using conventional intracellular microelectrode technique to record action potentials, autonomic neurotransmitters and antagonists were used to investigate the electrophysiological features and regularities of spontaneous activity of left ventricular outflow tract cells. Electrophysiological parameters examined were: maximal diastolic potential (MDP), amplitude of action potential (APA), maximal rate of depolarization (V(max)), velocity of diastolic depolarization (VDD), rate of pacemaker firing (RPF), 50% and 90% of duration of action potential (APD(50) and APD(90)). The results are listed below: (1) Perfusion with 100 mumol/L isoprenaline (Iso) resulted in a significant increase in V(max) (P <0.05), VDD, RPF, and APA (P <0.01), a notable decrease in MDP (P<0.05), and also a marked shortening in APD(50) (P<0.01). Pretreatment with Iso (100 mumol/L), propranolol (5 mumol/L) significantly decreased RPF and VDD (P<0.01), decreased APA, MDP and V(max) (P<0.01) notably, prolonged APD(50) (P<0.01) and APD(90) (P<0.05) markedly. (2) Application of 100 mumol/L epinephrine (E) resulted in a significant increase in VDD (P<0.05), RPF (P<0.001), V(max) (P<0.05) and APA (P<0.001), and a notable shortening in APD(50) and APD(90) (P<0.05). (3) Perfusion with 100 mumol/L norepinephrine (NE) led to a significant increase in VDD, RPF, APA and V(max) (P<0.05), and a marked shortening in APD(50) (P<0.05). Pretreatment with NE (100 mumol/L), phentolamine (100 mumol/L) significantly decreased RPF and VDD, MDP and APA (P<0.01), decreased V(max) notably (P<0.05), prolonged APD(50) and APD(90) markedly (P<0.01). (4) During perfusion with 10 mmol/L acetylcholine (ACh), VDD and RPF slowed down notably (P<0.05), APA decreased significantly (P<0.001), V(max) slowed down notably (P<0.01), APD50 shortened markedly (P<0.05), Atropine (10 mmol/L) antagonized the effects of ACh (10 mumol/L) on APD(50) (P<0.05). These results suggest that there are probably alpha-adrenergic receptor (alpha-AR), beta-adrenergic receptor (beta-AR) and muscarinic receptor (MR) on pacemaker cell membrane of left ventricular outflow tract in guinea pig. The spontaneous activities of left ventricular outflow tract cells are likely regulated by sympathetic and parasympathetic nerves.