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1.
目的 :探讨急性心肌梗死早期应用美托洛尔对QT离散度 (QTd)的影响。方法 :选择符合条件的 14 2例急性心肌梗死 (AMI)患者 ,男 95例 ,女 47例 ,平均年龄 5 7± 12 3岁 ,随机分为治疗组 78例 ,对照组 64例 ,两组病例性别、年龄等基本情况相似。在AMI常规治疗的基础上 ,治疗组给予美托洛尔 6 2 5~ 5 0mg口服 ,2次 /d ;对照组仅常规治疗。治疗前及治疗 1周后同步记录体表常规 12导联心电图 ,每一导联连续测量 3个Q -T间期 ,取其均值。最大QT间期 (QTmax)与最小QT间期 (QTmin)之差为QTd。结果 :治疗组在常规治疗基础上早期给予美托洛尔后 ,QTd、QTcd显著缩小 (P <0 0 1) ,QTmax无明显改变 (P >0 0 5 ) ,QTmin显著延长 (P <0 0 5 ) ,心率显著减慢 (P <0 0 1)。而对照组QTd、QTcd、QTmax、QTmin、HR均无明显变化 (P >0 0 5 )。结论 :AMI早期应用 β1 受体阻滞剂美托洛尔治疗 ,可显著延长正常心肌的复极过程 ,从而防治早期恶性心律失常 ,降低猝死率。 相似文献
2.
琥珀酸美托洛尔HPMC骨架片释放影响因素研究 总被引:3,自引:0,他引:3
以羟丙基甲基纤维素(HPMC)为骨架材料,乙基纤维素(EC)为阻滞剂,采用湿颗粒压片法制备琥珀酸美托洛尔亲水凝胶骨架片,考察HPMC用量、HPMC黏度、EC用量、制备方法、压片压力、释放介质及转速对琥珀酸美托洛尔(MS)骨架片体外释药的影响。结果表明,MS骨架片体外释药符合Higuchi方程,药物释放机制是骨架溶蚀和药物扩散的综合效应;HPMC用量与黏度、阻滞剂用量、制备方法、压片压力对释放速率均有显著性影响;释放介质的pH值及转速对释放速率无显著性影响。 相似文献
3.
目的 比较 2药对高血压左室肥厚患者的疗效及运动后对心率、血压的影响。方法 采用随机分组法将 80例高血压左室肥厚的病人分成两组 ,倍他乐克组和硝苯地平组 ,治疗前后查超声心动图 ,测定IVST、PWT及LVMI ,心率及血压。结果 ① 2药降压效果无明显差异。② 2组患者IVST、PWT、LVMI的下降幅度相同。③中度体力活动后 ,倍他乐克组心率增快 9± 2次 ,收缩压、舒张压上升均小于 3kPa(7 5mmHg) ,硝苯地平组心率增快 2 0± 4次 ,2组相比P <0 0 1,具有显著意义 ;收缩压、舒张压上升幅度均为 3 4± 1 2kPa(2 6±9mmHg) ,明显大于倍他乐克组。④结论 2药对高血压患者的左心室肥厚有相似的逆转作用 ,但倍他乐克可减少体力活动时血压及心率的上升 ,对心脏更具有保护作用。 相似文献
4.
H. Folgering 《Pflügers Archiv : European journal of physiology》1981,391(4):355-356
Summary In anesthetized cats, a carotid sinus nerve was stimulated electrically. After this stimulation the time course of the afterdischarge in the phrenic nerve activity was studied in the control situation, during infusion of isoprenalin and after administration of metoprolol. The time courses were identical in all situations.It is concluded that in spite of the fact that the beta-adrenergic drugs change the steady state phrenic nerve activity, the afterdischarge is unchanged and therefore probably mediated by a separate mechanism. A comparison is made with analogous findings in patients with a hyperventilation syndrome. 相似文献
5.
Behavioral and autonomic responses to intermittent social stress: differential protection by clonidine and metoprolol 总被引:2,自引:2,他引:0
The present study investigated physiological and pharmacological characteristics of socially stressed animals. Specifically, we examined (1) to what degree autonomic and behavioral stress reactions during intermittent confrontations between an intruder male adult Long-Evans rat with an aggressive resident undergo habituation, and (2) to what extent the defeat-experienced animal can be protected against these stress reactions with clonidine or metoprolol, two adrenergic agents with clinical anxiolytic effects. We developed an acute social stress situation that consisted of initially placing an experimental rat as an intruder into the homecage of a resident while the resident was not present, thereafter permitting brief physical agonistic interactions with the reintroduced resident until the intruder was forced into a submissive supine posture and emitted ultrasonic vocalizations (USV), and eventually exposing the intruder to the resident's threats for one hour, while being shielded from potentially injurious attacks (threat encounter). Over the course of the initial 4-weekly threat encounters the acute tachycardia but not the hyperthermic stress responses decreased in magnitude. Following the first three threat encounters core temperature (Tc) was significantly elevated for at least 3 h. The Tc was already elevated when the repeatedly defeated intruder was confronted with the olfactory cues of the resident's cage. This conditioned anticipatory hyperthermia developed in the course of the first three confrontations and was paralleled by a decrease in exploratory and motor behavior and by an increase in defensive behaviors and in both types of USV emitted in the low (20–30 kHz) and the high (31–70 kHz) frequency range. Clonidine (0.01–0.1 mg/kg, IP), an
2-adrenergic agonist and metoprolol, a -adrenergic blocker (1.0–10.0 mg/kg, IP), dose-dependently prevented the tachycardic response to stress. Only clonidine, but not metoprolol, also attenuated the rise in T0 during the 1-h agonistic interaction. Clonidine decreased those aspects of motor behavior (e.g. rearing, walking) that are of lesser cost for the individual but maintained high levels of defensive reactions and increased the duration of low USV. The high doses of clonidine (0.06, 0.1 mg/kg) attenuated the homeostatic regulation and sedated the intruder while exposed to threats during a social confrontation. The absence of attenuation of the high level of defensive behavior and the prolonged low USV suggest a stress intensification by the higher doses of clonidine. In conclusion, after the fourth encounter, the autonomic, behavioral and vocal response pattern prior to and during repeated weekly confrontations show no evidence for habituation for the following 6 weeks. Moreover, adrenergic therapeutic agents that are applied to treat symptoms of anxiety block the tachycardic response but may actually intensify defensive behavior and certain stress vocalizations. 相似文献
6.
M. Karita H. Sato Y. Koretsune K. Imai H. Ozaki H. Yokohama M. Hori T. Kamada H. Takeda M. Inoue 《European journal of clinical pharmacology》1995,48(6):467-471
The effects of a combination regimen of metoprolol and 1-adrenoceptor agonist denopamine on resting and exercise heart rate have been studied in 10 normal volunteers. Maximal ramp upright bicycle exercise was performed three times at 1-week intervals. Two hours before each exercise test, 5 mg metoprolol plus 20 mg denopamine, 5 mg metoprolol plus a denopamine placebo, or two placebos were orally administered in a double-blind fashion.During exercise after placebo administration, heart rate increased in parallel with the exercise intensity. Compared to the placebo values, resting heart rate was significantly decreased by an average of 10 beats · min–1 by 5 mg metoprolol, whereas it was not altered by the combination regimen. During exercise, however, both the combination regimen and metoprolol alone showed a significant negative chronotropic effect, decreasing peak exercise heart rate by an average of 14 and 21 beats · min–1, respectively. Peak oxygen uptake was also significantly decreased by both regimens.We conclude that concomitant administration of 5 mg metoprolol and 20 mg denopamine exerts an effective -adrenoceptor blocking action during exercise but a minimal effect at rest in normal subjects. The combination regimen appears to have a favourable pharmacological profile for -adrenoceptor blocker therapy in patients with chronic heart failure. 相似文献
7.
Jose Sänchez-Chapula 《Naunyn-Schmiedeberg's archives of pharmacology》1992,345(3):342-348
Summary The effects of the beta-adrenoceptor antagonist metoprolol on action potentials and membrane currents were studied in single guinea-pig ventricular myocytes. The experiments were carried out using the nystatin-method of whole-cell technique. This method was used in order to prevent the run-down of the calcium current. Metoprolol at concentrations of 10–100 mol/l shortened action potential in a dose-dependent way. The drug only decreased resting membrane potential at a concentration of 100 mol/1 in two out of five cells. Under voltage-clamp conditions, metoprolol blocked the high threshold calcium current at concentrations of 30 and 100 mol/l to 82 ± 4% and 73 ± 5% from control, respectively. The drug decreased the inward rectifying potassium current in a concentration-dependent manner. This effect was evident for inward current at voltages negative to the apparent reversal potential and for outward current at voltages between –30 and –80 mV. This blocking effect on the inward rectifying potassium current can explain the effect on resting membrane potential. At voltages positive to –30 mV metoprolol increased a time-independent outward current. This metoprolol-enhanced outward current was blocked by barium and cesium. This result suggests that the metoprolol-enhanced current is carried by potassium. The current component enhanced by metoprolol was not sensitive to glibenclamide and tetraethylammonium applied externally, which suggests that the adenosine triphosphate-sensitive channel is not the target of metoprolol. The activation of this time-independent outward current by metoprolol and the blocking effects on the calcium current seem to explain the shortening in action potential induced by the drug.
Send offprint requests to J. Sánchez-Chapula at the above address 相似文献
8.
P. T. Larsson G. Olsson B. Angelin E. Granström G. Hansson P. Hjemdahl 《European journal of clinical pharmacology》1992,42(4):413-421
Summary The possibility that -adrenoceptor blockers, especially 1-selective agents might inhibit platelet function is of considerable interest, as this might be of pathophysiological importance in cardiovascular diseases. Platelet function, however, is difficult to assess and in vivo related data are scarce.The effect of one week of treatment with metoprolol 200 mg/day on platelet aggregability during mental stress (colour word conflict test; CWT) and low and high dose adrenaline infusions has been evaluated in a double-blind, placebo-controlled, cross-over study in 10 healthy male volunteers. Platelet function in vivo was assessed using ex vivo filtragometry, and the urinary excretions of -thromboglobulin (HMW -TG) and 11-dehydro-TxB2 (a thromboxane metabolite). Conventional in vitro aggregometry and the urinary levels of 2,3-dinor-6-keto-PGF1 (a prostacyclin metabolite) were also studied.During the interventions there was increased platelet aggregability in vivo, as filtragometry readings were shortened by 41±11% during high dose adrenaline infusion, urinary HMW -TG levels increased and urinary 11-dehydro-TxB2 tended to increase. In contrast, platelet sensitivity to ADP in vitro was reduced. The urinary 2,3-dinor-6-keto-PGF1 levels were increased during the interventions.Despite the cardiovascular and biochemical signs of -adrenoceptor blockade at rest and during the interventions, metoprolol failed to influence platelet function in vivo, as measured by ex vivo filtragometry, or urinary HMW -TG or 11-dehydro-TxB2 levels. It tended rather to enhance the stress response measured by ex vivo filtragometry. Platelet aggregability in vitro and urinary 2,3-dinor-6-keto-PGF1 levels were not altered by metoprolol.Thus, metoprolol was not found to reduce platelet aggregability in healthy male volunteers either at rest or during sympatho-adrenal activation. The effect of treatment may still differ in patients; studies in patients with ischaemic heart disease are under way. 相似文献
9.
Rats were treated subchronically (14 days) or acutely (single dose) with the 1-selective adrenoceptor antagonist metoprolol or the 2-selective adrenoceptor antagonist ICI 118,551. Metoprolol (350 mg/kg/day for 14 days, orally) significantly reduced the 5-hydroxytryptophan (5-HTP) accumulation when measured 30 min after inhibition of L-amino acid decarboxylase by NSD 1015 (100 mg/kg IP) in the limbic forebrain, the corpus striatum, the cerebral cortex, the brain stem, and in the cerebellum. ICI 118,551 (0.5 mg/kg, twice daily for 14 days, SC) also significantly reduced the 5-HTP accumulation in the same brain regions except in the corpus striatum and the brain stem. Simultaneously assayed tryptophan levels were largely unaffected. Thus sustained -adrenoceptor blockade causes a decrease in the in vivo rate of tryptophan hydroxylation in various rat brain regions. The subchronic treatments with metoprolol or ICI 118,551 also significantly reduced the endogenous levels of 5-hydroxytryptamine (5-HT) in the various rat brain regions studied. Acute treatment with either metoprolol (2 mg/kg SC) or ICI 118,551 (0.5 mg/kg SC) did not affect the 5-HTP accumulation or the endogenous 5-HT levels in the brain regions studied. This inhibitory effect on brain 5-HT systems produced by sustained -adrenoceptor blockade may be of significance both for the long-term cardiovascular action and for occasional neuropsychiatric side effects during -blocking therapy. 相似文献
10.
目的:探讨美托洛尔降低急性心肌梗死(AMI)死亡率的可能机制。方法:60例AMI患者随机均分为治疗组和对照组,治疗组在对照组常规治疗的基础上应用美托洛尔,比较2组恶性心律失常和再发心肌梗死的发生情况以及QT离散度、左室重构指标的变化。结果:与对照组比较,治疗组恶性心律失常、再发心肌梗死的发生例数明显降低(P<0.01~0.05),QT离散度显著减少(P<0.01),左室重构变化更小(P<0.05)。结论:美托洛尔可能通过降低恶性心律失常及再发心肌梗死的发生、减少QT离散度、抑制左室重构等方面降低AMI的死亡率。 相似文献