Effects of volsartan on transmural heterogeneous changes of transient outward potassium currents in hypertrophic cardiomyocytes in rabbits / 华中科技大学学报（医学）（英德文版）

The transmural heterogeneous changes of transient outward potassium currents (Ito) in rabbit hypertrophic cardiaomyocytes and the effects of long-term prophylactic treatment with volsartan were investigated. Rabbits were divided into hypertrophy group (left ventricular hypertrophy induced by partial ligation of abdominal aorta), vol-treated group (volsartan was administrated after the ligation), and control group (sham operated). Myocytes were isolated by a two-step enzymatical method. The sub-endocardial (Endo) and sub-epicardium (Epi) tissues were separated from midmyocardium (Mid) with a razor. Whole-cell patch-clamp technique was used to record potassium currents. The results showed that membrane capacitance was larger in hypertrophic cells than those in control and vol-treated cells (P<0.01 vs control cells, n=30). The densities of Ito in hypertrophic cells were reduced by sub-epicardium (Epi) (27.8 +/- 2.9) %, midmyocardium (Mid) (41.0+/-4.7) %, and sub-endocardium (Endo) (20.3 +/- 3.4) % compared with those in control cells. The decrease of Ito density was more pronounced in Mid than in Epi and Endo (P<0.01 vs Epi or Endo). There were no significant differences in Ito densities between vol-treated group and control group in three layers separately. In conclusion, volsartan can inhibit the transmural heterogeneous changes of Ito in left ventricular hypertrophic cardiomyocytes in rabbit.

The changes of potassium currents in rabbit ventricle with healed myocardial infarction / 华中科技大学学报（医学）（英德文版）

To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), the changes of action potential duration (APD), transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes in non-infarcted zone of HMI were investigated. Rabbits were randomly assigned into two groups: HMI group, in which animals were subjected to thoracotomy and ligation of the circumflex coronary and sham-operated group, in which rabbits underwent thoracotomy but no conorary ligation. 3 months after the operation, the whole myocyte patch clamp technique was used to record APD, Ito, IK, and IK1 of ventricular myocytes in non-infarcted zone. Our results showed that the membrane capacitance was larger in HMI group than in sham-operated group. Action potential duration was significantly lengthened in HMI group and early afterdepolarization (EAD) appeared in HMI group. The densities of Ito, I(K, tail), and IK1 were reduced significantly in HMI group, from 6.72 +/- 0.42 pA/pF, 1.54 +/- 0.13 pA/pF and 25.6 +/- 2.6 pA/pF in sham-operated group to 4.03 +/- 0.33 pA/pF, 1.14 +/- 0.11 pA/pF and 17.6 +/- 2.3 pA/pF, respectively. It is concluded that the reduced densities of Ito, I(K, tail) and IK1 in ventricular myocytes of non-infarcted zone in HMI were responsible for the prolongation of APD and the presentation of EAD which played important roles in the development of malignant arrhythmia in HMI.

Experimental study of adenovirus vector mediated-hVEGF165 gene on prevention of restenosis after angioplasty / 华中科技大学学报（医学）（英德文版）

This study evaluated the effects of adenovirus vector mediated human vascular endothelial growth factor-165 (hVEGF165) gene on prevention of restenosis after angioplasty. Rabbit models of bilateral carotid artery injury were established by balloon denudation. The recombinant adenoviruses containing hVEGF165 cDNA was directly injected into left side of the injured carotid arteries. On day 3 and week 3 after transfection the expression of VEGF was observed by RT-PCR and immunohistochemistry. The thrombokinesis, reendothelialization (rET) and intimal hyperplasia in carotid arteries were evaluated by computerized image analysis system 3 weeks after gene transfer. The changes in the VEGF gene-treated side were compared with the control side. Our results showed that 3 days and 3 weeks after hVEGF165 gene transfer the VEGF mRNA and antigen expression were detected in vivo. 3 weeks after the transfer, the carotid artery rET was markedly better in the VEGF gene-treated group compared with the control. The thrombokinesis, intima area/media area (I/M), maximal intimal and medial thicknesses (ITmax and MTmax) demonstrated a statistically significant decrease in arteries treated with VEGF gene as compared with the control group. It is concluded that VEGF gene transfer could be achieved by intra-arterial injection of recombinant adenoviruses. It might accelerate the restoration of endothelial integrity, inhibit thrombokinesis and attenuate intimal hyperplasia in the injured arteries after VEGF gene transfer. This procedure could be useful in preventing restenosis after angioplasty.

The changes of potassium currents in rabbit ventricle with healed myocardial infarction / 华中科技大学学报（医学）（英德文版）

To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), the changes of action potential duration (APD), transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes in non-infarcted zone of HMI were investigated. Rabbits were randomly assigned into two groups: HMI group, in which animals were subjected to thoracotomy and ligation of the circumflex coronary and sham-operated group, in which rabbits underwent thoracotomy but no conorary ligation. 3 months after the operation, the whole myocyte patch clamp technique was used to record APD, Ito, IK, and IK1 of ventricular myocytes in non-infarcted zone. Our results showed that the membrane capacitance was larger in HMI group than in sham-operated group. Action potential duration was significantly lengthened in HMI group and early afterdepolarization (EAD) appeared in HMI group. The densities of Ito, I(K, tail), and IK1 were reduced significantly in HMI group, from 6.72 +/- 0.42 pA/pF, 1.54 +/- 0.13 pA/pF and 25.6 +/- 2.6 pA/pF in sham-operated group to 4.03 +/- 0.33 pA/pF, 1.14 +/- 0.11 pA/pF and 17.6 +/- 2.3 pA/pF, respectively. It is concluded that the reduced densities of Ito, I(K, tail) and IK1 in ventricular myocytes of non-infarcted zone in HMI were responsible for the prolongation of APD and the presentation of EAD which played important roles in the development of malignant arrhythmia in HMI.

Effect of autonomic nervous system on the transmural dispersion of ventricular repolarization in intact canine / 华中科技大学学报（医学）（英德文版）

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall in 12 open-chest dogs. MAPD90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD90 of Epi, Mid and Endo before autonomic nervous stimulation were 278 +/- 11 ms, 316 +/- 16 ms and 270 +/- 12 ms respectively, the MAPD90 of Mid was significantly longer than that of Epi or Endo (P<0.01). MAPD90 of Epi, Mid and Endo were shortened by 19 +/- 4 ms, 45 +/- 6 ms, 18 +/- 3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44 +/- 4 ms to 15 +/- 3 ms (P<0.01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41%) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.

Effect of autonomic nervous system on the transmural dispersion of ventricular repolarization in intact canine / 华中科技大学学报（医学）（英德文版）

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall in 12 open-chest dogs. MAPD90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD90 of Epi, Mid and Endo before autonomic nervous stimulation were 278 +/- 11 ms, 316 +/- 16 ms and 270 +/- 12 ms respectively, the MAPD90 of Mid was significantly longer than that of Epi or Endo (P<0.01). MAPD90 of Epi, Mid and Endo were shortened by 19 +/- 4 ms, 45 +/- 6 ms, 18 +/- 3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44 +/- 4 ms to 15 +/- 3 ms (P<0.01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41%) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.

Long-term effects of imidapril on calcium and potassium currents in rabbit left ventricular hypertrophic myocytes / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the long-term effects of imidapril (IMI) on action potential and calcium and potassium currents in rabbit left ventricular hypertrophic myocytes.</p><p><b>METHODS</b>Rabbits were randomly divided into three groups: IMI-treated, hypertrophic and sham-operated control groups. Cardiac hypertrophy was induced in hypertrophy group by partial ligation of the abdominal aorta. In the IMI-treated group, the rabbits were administered IMI (1.5 mg x kg(-1) x d(-1)) for 8 weeks after surgery. In the sham-operated control group, the animals underwent an abdominal laparotomy without further procedure. Whole-cell patch clamp technique was used to record ionic currents.</p><p><b>RESULTS</b>Membrane capacitance was larger in hypertrophic cells than in sham-operated cells or IMI-treated cells. Action potential duration was lengthened in hypertrophic cells and was remarkably shortened by IMI. The density of ICa, L was reduced from 12.8 +/- 0.7 pA/pF in the sham-operated cells, to 7.7 +/- 0.8 pA/pF in hypertrophic cells, while it resembled the control cells after IMI treatment (11.9 +/- 1.0 pA/pF). After IMI treatment, the density of I(Ks,tail) was enhanced from 2.5 +/- 0.1 pA/pF in hypertrophic cells to 4.7 +/- 0.6 pA/pF (n = 7, P < 0.01), which was similar to the sham-operated cells. The densities of Ito and IK1 were significantly increased in IMI-treated cells, from 3.8 +/- 0.4 pA/pF and 3.7 +/- 0.5 pA/pF in the hypertrophic cells to 6.4 +/- 0.8 pA/pF and 6.5 +/- 0.3 pA/pF, respectively, but the IKr densities were not different in the three groups.</p><p><b>CONCLUSION</b>IMI could reverse the increase in membrane capacitance in hypertrophic cells, shorten action potential duration, and increase the densities of ICa, L, IKs, Ito and IK1 in hypertrophic cells.</p>

Results of invasive electrophysiologic evaluation in 268 patients with unexplained syncope / 华中科技大学学报（医学）（英德文版）

In order to assess the diagnostic value of invasive electrophysiologic study (EPS) in the patients with unexplained syncope, the electrophysiologic findings of 268 patients with unexplained syncope despite a complete clinical evaluation were analyzed. Results showed positive EPS finding was 38% in total patients and 50% in the patients aged > 70 years. With increasing age, the diagnostic yield of EPS also increased. No significant differences of complication rate were found among the different age groups. It was concluded that EPS have high diagnostic value in the patients with unexplained syncope. Its complications are few and mild. EPS may be recommended in elderly patients with unexplained syncope.

Results of invasive electrophysiologic evaluation in 268 patients with unexplained syncope / 华中科技大学学报（医学）（英德文版）

In order to assess the diagnostic value of invasive electrophysiologic study (EPS) in the patients with unexplained syncope, the electrophysiologic findings of 268 patients with unexplained syncope despite a complete clinical evaluation were analyzed. Results showed positive EPS finding was 38% in total patients and 50% in the patients aged > 70 years. With increasing age, the diagnostic yield of EPS also increased. No significant differences of complication rate were found among the different age groups. It was concluded that EPS have high diagnostic value in the patients with unexplained syncope. Its complications are few and mild. EPS may be recommended in elderly patients with unexplained syncope.

Experimental study of the effect of autonomic nervous system on the transmural dispersion of ventricular repolarization under acute myocardial ischemia in vivo / 华中科技大学学报（医学）（英德文版）

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization (TDR) under acute myocardial ischemia in intact canine was investigated. Using the monophasic action potential (MAP) recording technique, MAPs of the epicardium (Epi), mid-myocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall under acute myocardial ischemia in 12 open-chest dogs. MAPD90 and TDR among three myocardial layers as well as the incidence of the early afterdepolarization (EAD) before autonomic nervous stimulation and during autonomic nervous stimulation were compared. It was found that 10 min after acute myocardial ischemia, TDR was increased from 55 +/- 8 ms to 86 +/- 15 ms during sympathetic stimulation (P 0.05). The EAD was elicited in the Mid of 2 dogs (16%) 10 min after acute myocardial ischemia, but the EAD were elicited in the Mid of 7 dogs (58%) during sympathetic stimulation (P < 0.01). It was concluded that: (1) Sympathetic stimulation can increase the transmural dispersion of repolarization and induce early afterdepolarizations in the Mid under acute myocardial ischemia, which provide the opportunity for the ventricular arrhythmia developing; (2) Parasympathetic stimulation has no significant effect on the transmural dispersion of repolarization under myocardial ischemia.

Relationship between the U wave on electrocardiogram and the midmyocardium of the left ventricular wall / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the relationship between the U wave on electrocardiogram and the midmyocardium in rabbit left ventricle free wall in vivo.</p><p><b>METHODS</b>The monophasic action potentials in the epicardium, midmyocardium, and endocardium of the left ventricle free wall were recorded simultaneously in 16 rabbits. The rabbits were then given an intravenous injection of Sotalol (1, 1.5 and 2.0 mg/kg) in 30 minutes intervals, and measurements were taken.</p><p><b>RESULTS</b>In the basic condition, there were no U wave on electrocardiogram. The U wave appeared after the intravenous Sotalol at 1.5 mg/kg, and the U wave became greater with increased dosage of intravenous Sotalol (2 mg/kg). The repolarization duration of the midmyocardium was prolonged longer than that of the epicardium and endocardium by Sotalol, and the repolarization duration of the epicardium coincided with the apex of the T wave, The repolarization duration of the midmyocardium coincided with the end point of the U wave.</p><p><b>CONCLUSION</b>The U wave may originate from the delayed repolarization of the midmyocardium.</p>

Experimental study of the effect of autonomic nervous system on the transmural dispersion of ventricular repolarization under acute myocardial ischemia in vivo / 华中科技大学学报（医学）（英德文版）

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization (TDR) under acute myocardial ischemia in intact canine was investigated. Using the monophasic action potential (MAP) recording technique, MAPs of the epicardium (Epi), mid-myocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall under acute myocardial ischemia in 12 open-chest dogs. MAPD90 and TDR among three myocardial layers as well as the incidence of the early afterdepolarization (EAD) before autonomic nervous stimulation and during autonomic nervous stimulation were compared. It was found that 10 min after acute myocardial ischemia, TDR was increased from 55 +/- 8 ms to 86 +/- 15 ms during sympathetic stimulation (P < 0.01). The TDR (53 +/- 9 ms) during parasympathetic stimulation was not significantly different from that of the control (55 +/- 8 ms) (P > 0.05). The EAD was elicited in the Mid of 2 dogs (16%) 10 min after acute myocardial ischemia, but the EAD were elicited in the Mid of 7 dogs (58%) during sympathetic stimulation (P < 0.01). It was concluded that: (1) Sympathetic stimulation can increase the transmural dispersion of repolarization and induce early afterdepolarizations in the Mid under acute myocardial ischemia, which provide the opportunity for the ventricular arrhythmia developing; (2) Parasympathetic stimulation has no significant effect on the transmural dispersion of repolarization under myocardial ischemia.

Die Transmurale ERP-Dispersion von Epi-,Mid-und Endomyokard im gesunden und hypertrophierten Hundemyokard / 华中科技大学学报（医学）（英德文版）

Viele Studien haben das Vorliegen von M-Zellen im Midmyokard des Hundes in vitro beobachtet und weiterhin gefunden, da das Vorliegen von M-Zellen zur Differenz der Repolarisation und zur Dispersion der Refrakt?rzeit zwischen Midmyokard und Epi- und Endomyokard fuhren kann.Diese Dispersion hat enge Beziehungen mit der Entstehung der Arrhythmie. Aber die Beobachtungen in vitro waren nicht konkordant mit den Ergebnissen in vivo. Mittels direkten Messungen der ERP in drei Myokardschichten wurde erstmals im gesunden Hundemyokard und im hypertrophierten Hundemyokard in vivo untersucht. Die Untersuchung hat gezeigt, da die ERP von Endomyokard, Epimyokard und Midmyokard im gesunden Hundeherzen homogen sind. Die relevante transmurale Refrakt?rgradient, die die Induktion einer kreisenden Erregung begünstigt, besteht unter physiologischen Bedingungen nicht. Im Gegensatz dazu konnte eine deutliche Verl?ngerung der ERP in allen Myokardschichten von hypertrophierten Hundeherzen nachgewiesen werden. Weiterhin wurde gezeigt, d?eine transmurale ERP-Dispersion zwischen verschiedenen Myokardschichten im hypertrophierten Hundemyokard besteht. Es ist zu postulieren, d? diese transmurale ERP-Dispersion als Substrat für die Arrhythmie angesehen werden kann,weil diese Dispersion die lokalen kreisende Erregung zwischen Epikard und Midkard, oder zwischen Midkard und Endokard begünstigen kann. Nach den Ergebnissen l?t sich postulieren, d?eine transmurale ERP-Dispersion durch eine pl?tzliche Zyklusl?ngever?nderung, n?mlich durch eine Kurz-Lang- und eine Lang-Kurz-Sequenz verst?rkt werden kann.

Die Transmurale ERP-Dispersion von Epi-,Mid-und Endomyokard im gesunden und hypertrophierten Hundemyokard / 华中科技大学学报（医学）（英德文版）

Viele Studien haben das Vorliegen von M-Zellen im Midmyokard des Hundes in vitro beobachtet und weiterhin gefunden, da das Vorliegen von M-Zellen zur Differenz der Repolarisation und zur Dispersion der Refrakt?rzeit zwischen Midmyokard und Epi- und Endomyokard fuhren kann.Diese Dispersion hat enge Beziehungen mit der Entstehung der Arrhythmie. Aber die Beobachtungen in vitro waren nicht konkordant mit den Ergebnissen in vivo. Mittels direkten Messungen der ERP in drei Myokardschichten wurde erstmals im gesunden Hundemyokard und im hypertrophierten Hundemyokard in vivo untersucht. Die Untersuchung hat gezeigt, da die ERP von Endomyokard, Epimyokard und Midmyokard im gesunden Hundeherzen homogen sind. Die relevante transmurale Refrakt?rgradient, die die Induktion einer kreisenden Erregung begünstigt, besteht unter physiologischen Bedingungen nicht. Im Gegensatz dazu konnte eine deutliche Verl?ngerung der ERP in allen Myokardschichten von hypertrophierten Hundeherzen nachgewiesen werden. Weiterhin wurde gezeigt, d?eine transmurale ERP-Dispersion zwischen verschiedenen Myokardschichten im hypertrophierten Hundemyokard besteht. Es ist zu postulieren, d? diese transmurale ERP-Dispersion als Substrat für die Arrhythmie angesehen werden kann,weil diese Dispersion die lokalen kreisende Erregung zwischen Epikard und Midkard, oder zwischen Midkard und Endokard begünstigen kann. Nach den Ergebnissen l?t sich postulieren, d?eine transmurale ERP-Dispersion durch eine pl?tzliche Zyklusl?ngever?nderung, n?mlich durch eine Kurz-Lang- und eine Lang-Kurz-Sequenz verst?rkt werden kann.

Restrictive Effect of Puerarin on Myocardial Infarct Area in Dogs and Its Possible Mechanism / 华中科技大学学报（医学）（英德文版）

To evaluate the protective effect of puerarin on ischemic myocardium in dogs with acute myocardial infarction (AMI) and to reveal its possible mechanism, 10 dogs were randomly divided into puerarin group (group G) and control group (group C). AMI model was established in all dogs. Puerarin or saline was administered over a period of 21 days. Coronary angiography was performed before and after ligation of coronary artery. Eight hemorheological parameters were examined before and 22 days after the operation. The infarct area and vessel density of myocardium were assessed. The infarct area in group G was smaller than that in group C. Angiography 2 h and 22 d after ligation of coronary artery revealed significant augmentation of collateral vessels in group G as compared with control group. The platelet aggregation and the blood viscosity were increased during AMI when compared with control phase, and the increased indexes during AMI would be inhibited when puerarin were given. Capillaries and distribution vessel density in ischemic zone on day 22 showed statistically significant augmentation in group G as compared with control group. Puerarin might improve the opening and formation of coronary collateral circulation, and might inhibit the increase of platelet aggregation and the blood viscosity during AMI,and thereby improve microcirculation and restrict myocardial infarct area.

Restrictive Effect of Puerarin on Myocardial Infarct Area in Dogs and Its Possible Mechanism / 华中科技大学学报（医学）（英德文版）

To evaluate the protective effect of puerarin on ischemic myocardium in dogs with acute myocardial infarction (AMI) and to reveal its possible mechanism, 10 dogs were randomly divided into puerarin group (group G) and control group (group C). AMI model was established in all dogs. Puerarin or saline was administered over a period of 21 days. Coronary angiography was performed before and after ligation of coronary artery. Eight hemorheological parameters were examined before and 22 days after the operation. The infarct area and vessel density of myocardium were assessed. The infarct area in group G was smaller than that in group C. Angiography 2 h and 22 d after ligation of coronary artery revealed significant augmentation of collateral vessels in group G as compared with control group. The platelet aggregation and the blood viscosity were increased during AMI when compared with control phase, and the increased indexes during AMI would be inhibited when puerarin were given. Capillaries and distribution vessel density in ischemic zone on day 22 showed statistically significant augmentation in group G as compared with control group. Puerarin might improve the opening and formation of coronary collateral circulation, and might inhibit the increase of platelet aggregation and the blood viscosity during AMI,and thereby improve microcirculation and restrict myocardial infarct area.

Arachidonic acid cytochrome P450 epoxygenases protect vessel endothelial cells against apoptosis induced by tumor necrosis factor-? / 中国病理生理杂志

AIM: To investigate whether endogenous endothelium-derived hyperpolarizing factors(EHDFs) produced by CYP epoxygenases BM3?F87V,2C11OR or CYP2J2 transfection was able to protect endothelial cells against apoptosis induced by tumor necrosis factor alpha.METHODS: Three or four passages of cultured bovine aortic endothelial cells(BAECs) were transfected with epoxygenases or the empty vector(pCB6).Cell viability was detected by MTT assay.Apoptosis of transfected endothelial cells was evaluated by DNA ladder assay,flow cytometry and morphological observations under fluorescence microscopy.RESULTS: Overexpression of CYP epoxygenases BM3?F87V,2C11OR,CYP2J2 increased cell viability respectively observed by MTT assay.The percentage of cells undergoing apoptosis was decreased in 2C11OR-,BM3F87V-or 2J2-transfected cells compared to the vector as evaluated by DNA fragment assay,flow cytometry analysis and morphological observations under fluorescence microscopy.CONCLUSION: Overexpression of CYP epoxygenases BM3?F87V,2C11OR or 2J2 increases cell viability and protects endothelial cells against TNF-?-induced apoptosis.These findings suggest new targets to investigate the endothelium-associated disorders and provide novel therapeutic strategies to treat them by modulating cytochrome P450 epoxygenases.

Changes of transmural repolarization heterogeneity and ion currents in rabbits with left ventricular hypertrophy / 中国病理生理杂志

AIM: To investigate the changes of transmural repolarization heterogeneity and ion currents in rabbits with left ventricular hypertrophy. METHODS: Ventricular hypertrophy was induced by a partial constriction of the abdominal aorta in rabbits. Myocytes were isolated by a two steps enzymological method. The sub-endocardial (Endo) and sub-epicardium (Epi) tissues were separated from other region (midmyocardium, Mid) with a razor. Whole cell patch clamp technique was used to record the action potential and ion currents. RESULTS: The action potentials duration at 90% repolarization (APD 90 ) of Epi, Mid and Endo were all prolonged significantly in hypertrophy group compared to control group. This prolongation of APD 90 was more pronounced in Mid (26.0%?2.7%) than that in Epi (14.0%?1.6%) and Endo (10.0%?1.1%). The transmural repolarization heterogeneity was increased significantly in the hypertrophy group. The I Ks and I to density in Epi, Mid and Endo was decreased significantly in hypertrophy group compared to those in control group. This decrease in I Ks and I to density was more pronounced in Mid than in Epi and Endo. No significantly difference of I Ca,L and I Kr density between hypertrophy group and control group in three layers was observed. The I K1 density decreased significantly in hypertrophy group compared to control group, but the extent of the decrease had no differences among the three layers. CONCLUSIONS: The transmural repolarization heterogeneity increases significantly in rabbit hypertrophied ventricle. The decrease in transmural heterogeneity of I to and I Ks is the main causes. [

Changes of potassium currents in rabbit ventricle with healed myocardial infarction / 中国病理生理杂志

AIM: To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), and to investigate the changes of action potential duration (APD),transient outward potassium current (I to ), delayed rectifier potassium current (I K) and inward rectifier potassium current (I K1 ) of left ventricular myocytes in noninfarcted zone of HMI. METHODS: 12 rabbits were randomly assigned in two groups: HMI group (thoracotomy and ligation of the circumflex coronary); sham-operated group (thoracotomy but no conorary ligation). 3 months after operation, whole cell patch clamp technique was used to record APD, I to , I K and I K1 of ventricular myocytes in non-infarcted zone. RESULTS: Membrane capacitance was larger in HMI group than that in sham-operated group. Action potential duration was lengthened significantly in HMI group and early after depolarization (EAD) appeared in HMI group. The densities of I to , I K,tail and I K1 were reduced significantly in HMI group (P