灯盏花素对离体大鼠胸主动脉环的作用

本实验采用雄性大鼠胸主动脉环，研究灯盏花素舒张血管的机制。结果表明：灯盏花素（１×１０＾－６～１０＾－３ｍｏｌ／Ｌ）对去甲肾上腺素（１×１０＾－６ｍｏｌ／Ｌ）的收缩反应呈剂量依赖性的松驰作用，与内皮无关；也不受普萘洛尔（１×１０＾－５ｍｏｌ／Ｌ）的影响。灯盏花素对拮抗去甲肾上腺素诱发的依外钙与依内钙的双相反应，而且对后者的抑制作用较强。结果提示，灯盏花素诱发血管舒张可能与受体操纵性钙通道和细胞内Ｃ     

蜂毒素对大鼠血小板内钙浓度的影响

应用Ｆｕｒａ－２作为荧光试剂，测定大鼠血小板细胞内Ｃａ~（２＋）浓度变化。蜂毒素１．５ｍｇ／Ｌ使血小板细胞内Ｃａ~（２＋）浓度增加；悬液中加入ＣａＣｌ＿２１ｍｍｏｌ／Ｌ，血小板细胞内Ｃａ~（２＋）继续增加。维拉帕米３．１２５ｍｇ／Ｌ作用５ｍｉｎ后，蜂毒素仍可使血小板内Ｃａ~（２＋）增加．但加入ＣａＣｌ２血小板Ｃａ~（２＋）的浓度不再增加。提示蜂毒素促进大鼠血小板细胞内Ｃａ~（２＋）的释放和细胞外Ｃａ~（２＋）进入细胞内。     

维拉帕米、福司考林和克罗马卡林对高K~ 及去甲肾上腺素预收缩血管舒张作用的比较

目的：比较３个作用机理不同的舒血管药在不同激动剂所致预收缩血管中的作用特点。方法：以高Ｋ＋及去甲肾上腺素预收缩家兔主动脉条，观察维拉帕米、福司考林和克罗马卡林的舒血管特点。结果：维拉帕米对高Ｋ＋收缩的舒张明显大于其对去甲肾上腺素预收缩血管的舒张作用，相反福司考林和克罗马卡林对去甲肾上腺素收缩的舒张远较其对高Ｋ＋收缩的舒张作用为大。克罗马卡林对高Ｋ＋预收缩血管的舒张作用比福司考林微弱得多。结论：维拉帕米、福司考林、克罗马卡林的舒血管效应各有其不同特点。为研究未知扩血管药的作用原理提供参考。     

The treatment of intractable supraventricular tachycardia after open heart surgery by a continuous infusion of verapamil and ventricular pacing

Four patients who developed intractable supraventricular tachycardia (SVT) after open heart surgery were treated using a new therapeutic method of creating a pharmacological atrioventricular block by the continuous infusion of verapamil with ventricular pacing. Both the initial dose and the effective dose, being the verapamil dose necessary to maintain pharmacological atrioventricular block to prevent the recurrence of SVT, were surveyed with clinical results. The verapamil-induced hemodynamic changes observed 4 h and 8 b after treatment, as indicated by systolic arterial blood pressure, mean arteral blood pressure, heart rate, cardiac index, and urine volume, were compared with the values I h before treatment. After an initial low dose infusion of 0.07 ± 0.02 mg/kg · h had been given, an effective and safe dose of 0.11 ± 0.05 mg/ g · h was determined. Good hemodynamic and clinical results were achieved in all four patients who are now leading an active life. These results therefore encourage us to apply this therapeutic method for treating patients with intractable and recurrent SVT after open heart surgery.     

气血注射液防治缺氧性肺动脉高压的研究

本实验观察中药气血注射液、西药钙通道阻断剂异搏定(Vp)及中西药合用对大鼠缺氧性肺动脉高压形成的影响。结果表明,气血注射液及Vp均可明显降低慢性缺氧引起的肺动脉压升高程度,且前者的效果显著优于后者;气血注射液还可显著改善缺氧造成的右心室收缩性能指标(IC)下降,并可使IC接近平原正常值。气血注射液的效果并不因合用Vp而加强。气血注射液、Vp及二者合用对大鼠颈动脉压、心率及左心功能均无明显影响。提示在缺氧过程中,增强心脏代偿能力可能滞延缺氧性肺动脉高压的发展进程。     

维拉帕米对牛眼小梁细胞增殖和吞噬功能的影响

目的　研究维拉帕米对牛眼小梁细胞 (BTMC)增殖和吞噬功能的影响。方法　采用MTT和3 H TDR实验检测 0 0 0 0 1、0 0 0 0 5、0 0 0 1、0 0 0 5、0 0 1、0 0 5、0 1mg/ml 7种质量浓度的维拉帕米对BTMC增殖功能的影响。以乳胶微粒为标记 ,定量检测等于和低于 0 0 1mg/ml维拉帕米对BTMC吞噬功能的影响。结果　低于 0 0 1mg/ml维拉帕米对BTMC增殖功能无抑制作用 (P >0 0 5 ) ,等于或高于 0 0 1mg/ml的维拉帕米可浓度依赖性地抑制BTMC增殖功能 (P <0 0 5 ) ,其IC50 分别为 0 0 3 2 3mg/ml(MTT)和 0 0 2 5 9mg/ml( 3 H TDR)。 0 0 0 1、0 0 0 5、0 0 1mg/ml维拉帕米可浓度依赖性地促进BTMC的吞噬功能 (P <0 0 5 )。结论　临床应用的 0 12 5 %维拉帕米滴眼剂在房水中的质量浓度为 ( 160 7± 2 72 )ng/ml ,该质量浓度范围不抑制BTMC增殖。选用等于和低于 0 0 1mg/ml作为后续实验的质量浓度。维拉帕米还可通过促进小梁细胞的吞噬功能 ,减少房水外流阻力 ,有望在发病学环节上治疗原发性开角型青光眼     

经桡动脉介入治疗局部应用维拉帕米防治桡动脉痉挛的有效性及安全性临床观察

目的：观察经桡动脉路径介入治疗时局部应用维拉帕米防治桡动脉痉孪的有效性及安全性。方法：80例经桡动脉路径介入治疗的患者，成功置入鞘管后注入维拉帕米5mg，记录维拉帕米注入前、注入后2，5，10，30min患者心率、血压、局部及全身情况变化。结果：80例患者均未发生桡动脉痉孪，均未发现心力衰竭和传导阻滞加重，均于维拉帕米注入后出现上肢烧灼和胀麻感，但很快消失（〈30s）。维拉帕米注入前、后心率及舒张压的差异均无显著性（P〉0．05）；注入前、后收缩压的差异有显著性（P〈0．05），但注入后不同时间点组间差异无显著性（P〉0．05）。结论：经桡动脉介入治疗时，局部应用维拉帕米可以有效防治桡动脉痉孪的发生，并且对心率、传导、舒张压和心功能无明显影响。     

Verapamil in Idiopathic Ventricular Tachycardia of Right Bundle Branch Block Morphology: Observations During Electrophysiologic and Exercise Testing

Electrophysiologic studies before and after administration of verapamil were performed in three young patients with recurrent sustained ventricular tachycardia (VT) of right bundle branch block morphology. VT was not provoked by maximal treadmill testing in any patient. Electrophysiologic findings at induction of VT suggested reentry in the first patient and triggered automaticity in the second. Findings were inconclusive in the third patient. Intravenous verapamil terminated the VT in all the three cases. Oral verapamil prevented laboratory induction of sustained VT in the latter two patients. However, VT could be provoked during exercise in both while on oral verapamil therapy. These findings suggest that different mechanisms may underlie ventricular tachycardia dependent upon slow-response tissue; the role of oral verapamil in the treatment of such VT needs further investigation.     

Dose-dependent Hemodynamic Effect of Digoxin Therapy in Severe Verapamil Toxicity

Calcium chloride (CaCl(2)) alone is an ineffective antidote in severe calcium channel antagonist overdoses. Digoxin has been evaluated as a therapy to increase the effectiveness of calcium in severe calcium channel antagonist overdoses. OBJECTIVE: To determine if there is a dose-dependent hemodynamic effect of digoxin in the setting of severe verapamil toxicity treated with high-dose CaCl(2). METHODS: Eight dogs were instrumented to measure systolic and diastolic blood pressure, cardiac output, pulmonary artery pressures, and left ventricular pressures. Verapamil toxicity (50% decrease in mean arterial pressure) was induced with verapamil 6 mg/kg/hr and maintained for 30 minutes by titrating the verapamil rate. Following verapamil toxicity, each dog received one dose of digoxin equivalent to 0, 1, 1.5, 2, 3, 4, 6, or 8 times the loading dose of digoxin (0.009 mg/kg). The verapamil rate was changed to 4 mg/kg/hr and continued for the next five hours. CaCl(2) boluses were given (0.5 g immediately following verapamil toxicity and 1 g at one, two, and three hours). Measurements were compared with the loading dose of digoxin using linear regression analysis. RESULTS: Digoxin resulted in a dose-dependent increase in systolic blood pressure at 4 hours (10.23 mm Hg/loading dose of digoxin, 95% CI = 2.74 to 17.73), 4 hours, 15 minutes (13.9 mm Hg/loading dose of digoxin, 95% CI = 8.75 to 19.01), and 5 hours (17.04 mm Hg/loading dose of digoxin, 95% CI = 1.76 to 32.32). Digoxin resulted in a dose-dependent increase in maximal ventricular pressure at the end of hour 3 (8.55 mm Hg/loading dose of digoxin, 95% CI = 3.41 to 13.69), 3 hours, 15 minutes (11.81 mm Hg/loading dose of digoxin, 95% CI = 4.89 to 18.73), hour 4 (8.26 mm Hg/loading dose of digoxin, 95% CI = 1.03 to 15.48), and 4 hours, 15 minutes (9.74 mm Hg/loading dose of digoxin, 95% CI = 4.47 to 15.00). The authors were unable to detect a dose-dependent increase in other parameters, including diastolic relaxation (diastolic change in pressure over time) and time to onset of death. No ventricular arrhythmias developed in any dogs. CONCLUSIONS: There is a dose-dependent effect of digoxin on systolic blood pressure and maximal ventricular pressure in the setting of severe verapamil toxicity treated with high-dose CaCl(2).