不同剂量甲泼尼龙治疗小儿严重脓毒症的疗效分析

目的探讨不同剂量甲泼尼龙治疗小儿严重脓毒症的临床疗效。方法将2014年1月至2016年8月我院共收治148例小儿严重脓毒症患儿的临床资料进行回顾性分析,采用随机数字表法将患儿分为三组,对照组和甲泼尼龙大剂量组、甲泼尼龙小剂量组,比较分析三组患儿治疗前后CPR、PCT水平,计算APACHEⅡ评分,随访三组患儿的病死率。结果甲泼尼龙小剂量组治疗3 d后的CPR、PCT水平与对照组治疗3 d后比较,有明显下降,经比较,P<0.05,差异具有统计学意义。甲泼尼龙小剂量组治疗后的APACHEⅡ评分、病死率均明显小于对照组,经比较,P<0.05,差异具有统计学意义。结论在小儿严重脓毒症的治疗中应用小剂量甲泼尼龙,可以明显降低患儿的CPR、PCT水平,降低APACHEⅡ评分和病死率,说明小剂量甲泼尼龙对小儿严重脓毒症患儿的治疗具有重要的辅助作用,值得临床推广应用。     

大剂量和小剂量甲泼尼龙治疗重症手足口病的效果对比

目的：探讨大剂量和小剂量甲泼尼龙在重症手足口病患儿中治疗效果。方法选取2014年3月～2016年2月我院收治重症手足口病患儿78例为研究对象,根据患儿就诊奇偶顺序随机分为研究组和对照组,两组患者均给予常规治疗,同时研究组患儿给予大剂量甲泼尼龙（10～15mg／（kg? d））治疗,对照组患儿给予小剂量甲泼尼龙（2mg／（kg? d））治疗,比较两组患儿症状缓解时间及不良反应发生情况。结果研究组患儿发热、易惊、机械通气、高血压及心率增快等症状缓解时间均短于对照组,比较有统计学意义（P＜0．05）。研究组患儿肺出血、肺水肿不良反应发生率均低于对照组,比较有统计学意义（P＜0．05）。结论大剂量甲泼尼龙在重症手足口病患儿中治疗可更有效缓解患儿临床症状,且一定程度上降低不良反应发生率。     

注射用甲泼尼龙琥珀酸钠致严重过敏性休克1例

目的为临床甲泼尼龙琥珀酸注射液的使用提供经验参考。方法报告 2018年 10月 15日陆军军医大学大坪医院1例使用甲泼尼龙琥珀酸注射液致严重过敏性休克的病例,结合该药的临床药理作用,对该病例进行临床个体分析。结果该病人为声带息肉手术后使用甲泼尼龙琥珀酸抗水肿、抗炎治疗,治疗过程中出现严重过敏性休克反应,经简易呼吸器辅助呼吸、扩容、补充电解质、吸氧、监测生命体征等治疗后病人休克纠正,生命体征逐渐平稳,康复出院。结论在使用甲泼尼龙琥珀酸时应提高警惕,仔细观察病人不良反应,尤其有多种药物过敏史的病人;一旦发生过敏反应时及时抢救,确保病人用药安全。     

重组人干扰素α-2b联合大剂量甲泼尼龙冲击治疗90例小儿重症手足口病的临床研究

目的:探讨小儿重症手足口病采用重组人干扰素α-2b联合大剂量甲泼尼龙冲击治疗的临床疗效。方法:随机将2015年1月～2018年1月收治的90例重症手足口病患儿分为两组,甲组采用小剂量甲泼尼龙冲击治疗,乙组采用大剂量甲泼尼龙冲击联合重组人干扰素α-2b治疗,比较两组治疗效果。结果:乙组发热、易惊、机械通气、高血压与心率加快等症状缓解时间明显短于甲组,治疗后的IL-6、IL-10、TNF-α水平与不良反应发生率明显低于甲组,差异有统计学意义(P<0.05)。结论:重症手足口病患儿采用重组人干扰素α-2b联合大剂量甲泼尼龙冲击治疗,能有效减轻炎性反应,缓解临床症状,减少用药后的不良反应。     

甲泼尼龙治疗重型颅脑损伤的临床体会

目的用大剂量甲泼尼龙对急性重型颅脑损伤治疗的疗效体会作一综述。方法对急性颅脑损伤后的6h之内,使用甲泼尼龙24h静脉冲击的治疗方案进行临床研究。结果大剂量甲泼尼龙冲击治疗组的恢复良好率较对照组高,死亡率降低。结论大剂量甲泼尼龙冲击治疗对急性重型颅脑损伤的治疗有助于提高疗效和降低死亡率。     

甲泼尼龙与地塞米松治疗过敏性休克的对比研究

目的 回顾性对比分析地塞米松(DX)和不同剂量甲泼尼龙琥珀酸钠(MP)治疗过敏性休克的临床缓解时间.方法 对36例过敏性休克患者进行回顾性分析,随机分为3组:DX组12例,先静脉推注地塞米松注射液10 mg,然后将地塞米松注射液10 mg加入0.9%氯化钠溶液250 ml静脉滴注维持;小剂量MP组12例,先静脉推注甲泼尼龙琥珀酸钠40 mg,然后将甲泼尼龙琥珀酸钠40 mg加入0.9%氯化钠溶液250 ml静脉滴注维持;大剂量MP组12例,先静脉推注甲泼尼龙琥珀酸钠80 mg,然后将甲泼尼龙琥珀酸钠120 mg加入0.9%氯化钠溶液中静脉滴注维持.其他治疗措施及方法相同.分析比较3组患者症状缓解所需时间.结果 经抗休克治疗后3组患者症状均得到有效缓解,3组患者症状缓解所需时间比较差异有统计学意义(P＜0.05),DX组平均缓解时间长于不同剂量MP组,而小剂量MP组患者症状平均缓解时间要长于大剂量MP组,3组平均缓解时间比较差异有统计学意义(P＜0.05).结论 过敏性休克患者早期使用大剂量甲泼尼龙琥珀酸钠治疗可迅速而有效的缓解临床症状.     

两种剂量甲泼尼龙治疗急性脊髓炎疗效与安全性比较的系统评价

目的:基于荟萃分析(Meta分析)方法,比较两种剂量甲泼尼龙治疗急性脊髓炎的有效性与安全性。方法:计算机检索PubMed、EMBase、the Cochrane Library、中国知网及维普数据库等数据库,收集两种剂量甲泼尼龙治疗急性脊髓炎的临床随机对照试验(大剂量组患者使用甲泼尼龙1次1000 mg,1日1次;小剂量组患者使用甲泼尼龙1次500 mg,1日1次),提取数据并进行方法学质量评价后,采用RevMan 5.3软件进行Meta分析。结果:共纳入8篇文献,涉及798例患者。Meta分析结果显示,治疗后,大剂量组患者的美国脊髓损伤协会评分(运动功能评分:WMD=-4.97,95%CI=-5.84^-4.10,P<0.00001;痛觉评分:WMD=-5.24,95%CI=-6.03^-4.46,P<0.00001;触觉评分:WMD=-6.92,95%CI=-7.85^-5.99,P<0.00001)明显高于小剂量组,差异有统计学意义;大剂量组患者的排尿恢复时间(WMD=-6.92,95%CI=3.24~7.52,P<0.00001)、自行下地行走时间(WMD=5.46,95%CI=3.73~7.18,P<0.00001)和肌力改善2级的时间(WMD=-0.02,95%CI=1.46~3.90,P<0.00001)明显短于小剂量组,差异均有统计学意义;大剂量组患者的临床总有效率明显高于小剂量组,差异有统计学意义(OR=2.68,95%CI=1.95~2.78,P<0.0001)。仅1篇文献报告治疗期间两组患者均未出现严重不良反应及并发症。结论:与小剂量(1次500 mg,1日1次)甲泼尼龙相比,大剂量(1次1000 mg,1日1次)甲泼尼龙在促进急性脊髓炎患者神经功能恢复、提高治疗效果和改善预后等方面更具优势,但仍需高质量的研究证据加以验证和支撑。     

不同剂量甲泼尼龙辅治小儿支原体肺炎对其肺功能改善及预后的影响研究

目的 探讨小剂量和大剂量甲泼尼龙辅助治疗小儿支原体肺炎的临床效果及其肺功能改善和预后影响情况.方法 选择2018年10月～2021年10月接诊的小儿支原体肺炎106例患儿为研究对象,按照随机数表法将其分为小剂量组(n=53)和大剂量组(n=53),两组均进行常规治疗,小剂量组在常规治疗基础上选择甲泼尼龙辅助治疗,剂量为...     

布地奈德雾化吸入联合甲泼尼龙治疗重症支气管哮喘

目的 评价雾化吸入布地奈德联合小剂量甲泼尼龙治疗重症支气管哮喘的效果.方法 将40 例重症支气管哮喘患者采用随机数字表法分为治疗组和对照组,每组20例.治疗组予以布地奈德雾化吸入联合甲泼尼龙;对照组以甲泼尼龙治疗,观察临床效果、动脉血气及并发症情况.结果 两组治疗前后组内动脉血气差异有统计学意义(P＜0.05),但两组间临床效果及治疗后动脉血气差异无统计学意义(P＞0.05),对照组并发症明显多于治疗组(P＜0.05).结论 雾化吸入布地奈德能减少全身甲泼尼龙用量,减少并发症.二者联合治疗重症支气管哮喘,能达到与单独使用大剂量甲泼尼龙相当的临床效果.     

甲泼尼龙琥珀酸钠致白细胞升高1例

研究在治疗“双肺间质性病变”时使用甲泼尼龙琥珀酸钠静脉注射给药后引起白细胞升高,停药后白细胞恢复正常。药师在工作时应给予患者个体化用药监测与用药教育。     

Prostacyclin can either increase or decrease heart rate depending on the basal state.

1 The influence of the basal heart rate on the change in rate induced by prostacyclin (PGI2) was investigated in beagles anaesthetized with chloralose. 2 In male dogs with a low basal heart rate (less than 100 beats/min) PGI2, in doses up to 0.5 microgram/kg intravenously, induced hypotension and tachycardia. 3 In contrast, PGI2-induced hypotension was accompanied by bradycardia when either the basal heart rate was increased (greater than 130 beats/min) with isoprenaline or nitroprusside, or the dose of PGI2 was increased. 4 Female beagles were less sensitive than males to the stimulation of a reflex bradycardia by PGI2. 5 The influence of prostaglandin E2 (PGE2) and bradykinin on heart rate was also found to depend upon the basal state in some dogs. 6 Bilateral vagotomy reversed the bradycardia provoked by PGI2, PGE2 and bradykinin. 7 Thus, PGI2-induced bradycardia in dependent on both the dose and the basal heart rate. Similarly the effects of PGE2 and bradykinin on heart rate also depend upon the basal state in some dogs. Moreover, there is a correlation between the ability of all three agonists to induce bradycardia, suggesting a common mechanism of action.     

153例利培酮致精神分裂症患者心动过缓分析

目的：探讨利培酮导致心动过缓的发生规律及特点，为安全合理用药提供参考。方法：利用医院信息系统检索具有临床意义的心动过缓病例，纳入使用利培酮的病例进行分析。结果：患者服用利培酮，多在4~6 mg的剂量范围内发生有临床意义的心动过缓。入院心率正常者和心动过缓者心率减慢平均值（入院心率-最低心率，求平均值）分别为29次/分、17次/分。153例心动过缓患者住院期间末次心电图示：85例心率<60次/分，54例心率正常，7例心律失常，2例心动过速，1例频发室性早搏，4例未知。结论：住院患者应用利培酮致心动过缓，对症处理仅1/3的患者心率恢复正常，因此应密切监测心电图，特别是具有心血管事件高危因素者。     

Concentration-response relations for apomorphine effects on heart rate in conscious rats

The pharmacokinetics of apomorphine in plasma and brain tissue have been studied in relation to the time courses of effects on heart rate in conscious rats. The kinetic behaviour was investigated after 2 mg kg-1 i.v. and 5 mg kg-1 s.c., respectively. Apomorphine showed a high total plasma clearance (165-207 ml min-1 kg-1) and, despite a relatively large volume of distribution (3.4-4.1 litre kg-1), a biological half-life of about 14 min was obtained irrespective of route of administration. The kinetics in whole brain were identical with those in plasma. Apomorphine produced biphasic effects on the heart rate during the time courses of subcutaneous single doses: a low dose (50 micrograms kg-1) induced pure bradycardia while the doses of 100 micrograms kg-1 and 5 mg kg-1 produced responses oscillating between bradycardia and tachycardia. When we evaluated the relation between apomorphine concentrations and effects on the heart frequency with a composed sigmoid Emax model, apomorphine exhibited a U-shaped steady-state plasma concentration-response curve. Bradycardia appeared after low concentrations, reached a maximum and then decreased with increasing concentrations. A further augmentation of apomorphine concentration resulted in the opposite effect, i.e. tachycardia. Separate concentration-response curves for bradycardia and tachycardia were calculated. The changes in biophase concentration that occur during the absorption and disposition may thus cause the fluctuations between contrasting effects seen during the time course of a single dose.     

Long-term bradycardia caused by atrioventricular block can remodel the canine heart to detect the histamine H1 blocker terfenadine-induced torsades de pointes arrhythmias

Although a second-generation histamine H(1) blocker terfenadine induced torsades de pointes (TdP) arrhythmias in patients via the blockade of a rapid component of delayed rectifier K(+) current (I(Kr)), such action of terfenadine has not been detected in previous animal models. We analysed the potential of the canine persistent atrioventricular block heart, a new in vivo proarrhythmia model, to detect a torsadogenic effect of terfenadine of an oral dose of 3 or 30 mg kg(-1). The doses can provide therapeutic to supra-therapeutic plasma concentrations as an anti-histamine. In 2 weeks of bradycardiac heart model, there were no significant changes in any of the electrocardiogram parameters after the administration of both doses of terfenadine. In 4-6 weeks of bradycardiac heart model, the low dose of terfenadine hardly affected any of the electrocardiogram parameters except that it induced TdP in one out of six animals. The high dose significantly decreased the atrial rate and ventricular rate, prolonged the QT interval, and induced TdP in five out of six animals. Moreover, temporal variability of repolarization increased after the high-dose administration. These results suggest that long-term bradycardia caused by atrioventricular block can remodel the canine heart to detect terfenadine-induced TdP.     

Investigation into the cardioregulatory properties of the alpha 1-adrenoceptor blocker indoramin.

The cardioregulatory properties of the alpha 1-adrenoceptor blocker indoramin have been compared with those of prazosin in the anaesthetized rat. The effects of autonomic blockade on heart rate responses evoked by these two agents and their effects on blood pressure and heart rate after peripheral or central administration have been compared. Cumulative administration of indoramin (0.8-25.6 mg kg-1 i.v.) evoked significant decreases in arterial blood pressure and a concomitant bradycardia. Pithing or autonomic blockade, by pretreatment with a combination of practolol and bilateral vagotomy, prevented the bradycardia evoked by indoramin (0.8-3.2 mg kg-1 i.v.). Atropine sulphate pretreatment abolished the bradycardia until a cumulative dose of 25.6 mg kg-1(i.v.) of indoramin had been reached. Bilateral vagotomy, intravenous administration of atropine methylnitrate or practolol pretreatment attenuated the bradycardia. Prazosin (0.02-0.64 mg kg-1 i.v.) evoked a fall in arterial blood pressure of similar magnitude to that observed following indoramin. A bradycardia was evoked only at a relatively high dose (0.64 mg kg-1 i.v.). Intracisternal injection of indoramin or prazosin evoked bradycardia and hypotension at a dose which had no effect after intravenous injection (25 micrograms). Intracerebroventricular injection of indoramin (25 micrograms) had no significant effect on heart rate or blood pressure compared to control values, whereas prazosin (25 micrograms) evoked a significant tachycardia and hypotension. It is concluded that the bradycardia evoked by indoramin in the rat is not due to a direct action on the heart except possibly at high doses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transient bradycardia and subsequent sinus tachycardia produced by intravenous adenosine in healthy adult subjects.

Adenosine was administered in increasing intravenous bolus doses to nine healthy volunteers. A transient decrease in heart rate was observed which occurred about 20 s after injection. This was due to a reduction in sinus rate and/or transient block of conduction through the atrioventricular node, and lasted less than 10 s. An increase in sinus rate which followed any transient bradycardia was also observed. The maximum bradycardia and maximum tachycardia were each significantly related to the logarithm of adenosine dose.     

Central sympatho-inhibitory effects of intracisternal and intravenous administrations of noradrenaline in high doses

Intracisternal administration of noradrenaline (10, 20, 150 μg) decreased blood pressure, heart rate and spontaneous and evoked splanchnic nerve discharges in anaesthetized intact and ‘de-buffered’ cats.I.v. administration of lower dose of noradrenaline (4 μg/kg) increased blood pressure and reduced heart rate and splanchnic discharges; de-afferentation prevented the decrease in heart rate and in splanchnic discharges. Higher doses induced a delayed phase of hypotension, bradycardia and decreased spontaneous and evoked splanchnic discharges in intact and ‘de-buffered’ cats, indicating a central sympatho-inhibitory effect.     

Cardiovascular and respiratory effects of beta-endorphin in anesthetized and conscious rats

This study deals with the effects of beta-endorphin on blood pressure, heart rate, and respiratory frequency in anesthetized and conscious rats after both peripheral and central administration. Intravenous injection of beta-endorphin (40 and 160 micrograms/kg) in urethane-anesthetized rats resulted in a prolonged decrease in blood pressure, which, after the higher dose, was accompanied by bradycardia. In the pentobarbitone-anesthetized animals the same doses of beta-endorphin caused a small rise in blood pressure without affecting heart rate. No effect on respiratory frequency was observed. In urethane-anesthetized rats with hemorrhagic shock intravenous naloxone elicited a small pressor effect. Intracerebroventricular injection (i.c.v.) of beta-endorphin (40 micrograms/rat) in urethane-anesthetized rats resulted in severe respiratory depression and death. With lower doses there was a decrease in all parameters studied without ensuing death. Respiratory depression was even more pronounced in pentobarbitone-anesthetized rats, occurring with much lower doses of the peptide than in the urethane-anesthetized animals. beta-endorphin in the dose of 0.6 micrograms/rat still reduced respiratory frequency as well as heart rate without affecting blood pressure. Naloxone pretreatment antagonized the respiratory depression and death, while the decrease in heart rate was diminished. In conscious rats 10 microgram/rat, i.c.v., of beta-endorphin resulted in a decrease in heart rate and blood pressure without affecting respiratory frequency. It is concluded that beta-endorphin, or related opioid peptides, may be involved in cardiovascular and respiratory regulation. The effects of beta-endorphin, however, are markedly modified by the anesthetic agent used.     

Centrally mediated cardiovascular effects of nicergoline in the dog compared to those of clonidine

The intracisternal administration of nicergoline (5 micrograms/kg) or clonidine (4 micrograms/kg) in chloralose-anesthetized dogs induced significant decreases in blood pressure and heart rate. The same dose of nicergoline induced similar effects on atropine-pretreated dogs. Guanethidine pretreatment (30 mg/kg i.v. the day before) prevented the hypotension but not the bradycardia induced by clonidine. Guanethidine prevented both the hypotension and the bradycardia induced by nicergoline. Thus, nicergoline, unlike clonidine, does not increase cardiac parasympathetic activity. When administered by the same route at the same doses, nicergoline did not change the slope and reduced the amplitude whereas clonidine increased both the slope and the amplitude of the heart period vs. blood pressure curve obtained by intravenous administration of phenylephrine. Taken together, these results suggest that nicergoline and clonidine probably act on different structures within the central nervous system.     

THE CARDIOVASCULAR EFFECTS OF CENTRALLY ADMINISTERED 5-HYDROXYTRYPTAMINE IN THE CONSCIOUS NORMOTENSIVE AND HYPERTENSIVE RAT

• 1 The cardiovascular effects of centrally administered 5-hydroxytryptamine (5-HT) have been analysed in conscious normotensive and hypertensive rats.
• 2 In conscious normotensive rats, 5-HT, (1–30 μg) administered intracerebroventricularly (i.c.v.) produced profound and immediate dose-related decreases in heart rate and small increases in blood pressure. The initial pressor responses were followed by secondary secondary depressor responses at high doses of 5-HT.
• 3 Similar effects were produced by 5-HT i.c.v. in conscious DOCA-salt and spontaneously hypertensive rats, although the magnitude of the pressor responses was substantially greater in hypertensive than normotensive rats.
• 4 Pretreatment with either N-methylatropine or atenolol intra-arterially reduced the 5-HT-induced bradycardia in normotensive rats; the reduction was enhanced when both antagonists were given in combination.
• 5 The 5-HT₂ antagonist, cyproheptadine (10 μg i.c.v.) increased basal blood pressure and heart rate in normotensive rats. Subsequent administration of 5-HT i.c.v. produced biphasic effects on heart rate consisting of an initial tachycardia followed by a marked bradycardia.
• 6 Methysergide (10 μg i.c.v.) pretreatment did not alter resting heart rate, but attenuated the 5-HT induced bradycardia. A higher dose of methysergide, (30 μg i.c.v.), decreased resting blood pressure and heart rate.
• 7 This study has demonstrated, therefore, that the 5-HT induced bradycardia is produced by not only a centrally mediated decrease in sympathetic tone, but also an increase in vagal drive to the heart. The bradycardia is antagonised by centrally administered methysergide, but not by cyproheptadine, which suggests that it is probably mediated through a ‘5-HT₁-like’ receptor mechanism.