Effect of spinal cord stimulation on myocardial ischemia/infarction / 浙江大学学报·医学版

Fatal arrhythmias, heart failure, and sudden cardiac death after myocardial ischemia/infarction are serious threats to human health. In recent years, studies have shown that spinal cord stimulation (SCS) can balance autonomic activity, inhibit myocardial structural remodeling, improve blood flow to ischemic myocardium, effectively reduce the incidence of arrhythmia, heart failure and sudden cardiac death after myocardial ischemia/infarction, but its specific mechanism has not yet been fully elucidated. The effect of SCS on cardiac function may be achieved by inhibiting neural remodeling, or by ameliorating structural remodeling and electrical remodeling. This article reviews the progress on the role and mechanism of SCS in myocardial ischemia/infarction.

Application Value of Ablation Catheter for Pacemaker Atrial Lead Restoration in Patients With Atrial Lead Dislodgement After Pacemaker Implantation / 中国循环杂志

Objective: To explore the application value of ablation catheter for pacemaker atrial lead restoration in relevant patients. Methods: A total of 6 patients with atrial lead dislodgement after pacemaker implantation were selected for our study. The atrial lead restoration was conducted by using ablation catheter via femoral vein pathway. Results: The average operational time was (15.0 ± 3.7) min which was obviously less than traditional operational time. The position of electrode restoration was ideal with well immobilization. Conclusion: Ablation catheter is feasible for arial lead restoration in patients with atrial lead dislodgement after pacemaker implantation.

Vasodilating effect of capsaicin on rat mesenteric artery and its mechanism / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the vasodilating effect of capsaicin (CAP) on rat mesenteric artery and its mechanism.</p><p><b>METHODS</b>The third branch of the superior mesenteric artery in male Sprague-Dawley rat (250-350 g) was excised, the periadventitial fat and connective tissue were removed and the mesenteric artery was dissected into 2 mm rings. Each ring was placed in a 5 ml organ bath of DMT 610M system and the tension was recorded.</p><p><b>RESULTS</b>CAP (10(-9)-10(-5) mol/L) relaxed endothelium-intact and endothelium-denuded mesenteric artery pre-constricted by phenylephrine (10(-5) mol/L), and the vasodilation in endothelium-intact mesenteric artery was stronger than that in endothelium-denuded one. Pretreatment with either L-NAME (3 X10(-4) mol/L), an inhibitor of nitric oxide synthase(NOS), or CGRP8-37 (2 X 10(-6) mol/L), an antagonist of calcitonin gene-related peptide (CGRP), for 30 min significantly attenuated the relaxation of endothelium-intact mesenteric artery induced by CAP. CGRP (10(-10)-3 X10(-8) mol/L) relaxed endothelium-intact and endothelium-denuded mesenteric artery pre-constricted by phenylephrine, and the vasodilation in endothelium-intact mesenteric artery was stronger than that in endothelium-denuded one. Substance P did not relax the mesenteric artery pre-constricted by phenylephrine.</p><p><b>CONCLUSION</b>CAP has partial endothelium-dependent relaxation effect on rat mesenteric artery, which may be mediated by activating the endothelial NOS-NO pathway. The endothelium-independent relaxation in rat mesenteric artery induced by CAP may be mediated by CGRP.</p>

Effects of hydrogen peroxide on cell proliferation and expression of gelatinase A and its inhibitor in vascular smooth muscle cells / 中国病理生理杂志

AIM: To study the effects of hydrogen peroxied (H 2O 2) on cell proliferation and transcription of gelatinase A (MMP-2) and its inhibitor (TIMP-2) in vascular smooth muscle cells (VSMC). METHODS: Cell proliferation and toxicity by H 2O 2 were tested through MTT. The expression of MMP-2 mRNA and TIMP-2 mRNA in VSMC were evaluated by RT-PCR. RESULTS: The present study showed that H 2O 2 (more than 300 ?mol/L)was lethal to VSMC. 0 01-50 ?mol/L H 2O 2 promoted proliferation of VSMC in a time-dependant manner. A value (optical density) was reached to peak at 24 h after continuing stimulation of 10 ?mol/L H 2O 2. MMP-2/?-actin mRNA ratio significantly increased after stimulation with 1 ?mol/L?10 ?mol/L H 2O 2. TIMP-2/?-actin mRNA ratio was not significantly fluctuated at 12 h?24 h?36 h?48 h after continuing stimulation with 1 ?mol/L, 10 ?mol/L, and 50 ?mol/L H 2O 2.CONCLUSION: H 2O 2 at suitable concentrations stimulated proliferation of VSMC and induced transcription of MMP-2 gene in VSMC. There was no effect of H 2O 2 on transcription of TIMP-2 gene in VSMC. These results imply that H 2O 2 takes part in the pathological course of vascular remodeling through VSMC.

Effects of diltiazem on platelet activation and cytosolic calcium during percutaneous transluminal coronary angioplasty / 中国病理生理杂志

AIM: To evaluate effects of diltiazem on platelet hyperreactivity in situations associated with endothelial injury and their possible relationship to cytosolic calcium concentration. METHODS: Blood samples were collected at 7 time points from 35 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) who received combined diltiazem and aspirin/ticlopidine therapy or aspirin/ticlopidine therapy alone. Platelet expression of glycoprotein Ⅱb/Ⅲa and cytosolic calcium concentration were measured, respectively, by whole blood flow cytometry and fluorospectrophotometry. The effects of diltiazem of different concentrations on expression of glycoprotein Ⅱb/Ⅲa were also studied in vitro in blood samples from patients with chronic stable angina. RESULTS: Of the two treatments, aspirin/ticlopidine therapy did not prevent an acute increase of expression of glycoprotein Ⅱb/Ⅲa 5 minutes and 10 minutes after first inflation and 10 minutes after PTCA, whereas combined diltiazem and aspirin/ticlopidine therapy had a significant inhibitory effect. In the group receiving aspirin/ticlopidine therapy, there was a short-term elevation of platelet [Ca~(2+)]i immediately following PTCA which was significantly reduced by diltiazem treatment. Expression of glycoprotein Ⅱb/Ⅲa was significantly inhibited in vitro by diltiazem in the concentration of 200 ?g/L or higher, but not 50 ?g/L. CONCLUSIONS: Combined diltiazem and aspirin/ticlopidine therapy significantly inhibited platelet activation that continued in the presence of conventional aspirin/ticlopidine treatment. Antiplatelet effects of diltiazem were probably a consequence of reduction of platelet [Ca~(2+)]i and may only be achieved in higher than therapeutic concentrations. [