厄贝沙坦片联合盐酸贝尼地平片治疗高血压肾病的临床疗效

目的：探讨厄贝沙坦片联合盐酸贝尼地平片治疗高血压肾病的临床疗效。方法选取2011年1月—2014年1月魏县人民医院收治的高血压肾病患者132例,采用随机数字表法将患者分为厄贝沙坦组（49例）,贝尼地平组（43例）,联合治疗组（40例）。厄贝沙坦组患者予以厄贝沙坦片治疗;贝尼地平组患者予以盐酸贝尼地平片治疗;联合治疗组患者予以厄贝沙坦片联合盐酸贝尼地平片治疗。观察3组患者治疗前后血压、肾功能〔24h 尿蛋白定量、血肌酐（Scr）、血尿素氮（BUN）、内生肌酐清除率（Ccr）〕及不良反应发生情况。结果治疗前3组患者收缩压、舒张压、24h 尿蛋白定量、Scr、BUN、Ccr 比较,差异无统计学意义（P ﹥0.05）;治疗后3组患者收缩压、舒张压、24h 尿蛋白定量、Scr、BUN、Ccr 比较,差异有统计学意义（ P ﹤0.05）;联合治疗组患者收缩压、舒张压、24h 尿蛋白定量、Scr、BUN 低于厄贝沙坦组和贝尼地平组,Ccr 高于厄贝沙坦组和贝尼地平组,差异有统计学意义（P ﹤0.05）;3组患者不良反应发生率比较,差异无统计学意义（P ﹥0.05）。结论厄贝沙坦联合贝尼地平治疗高血压肾病的临床疗效显著,可改善患者临床症状,且不良反应小。     

Effect of klofenil on the hemodynamic and autonomic nervous system functions in patients with hypertensive disease

The degree of hemodynamic and vegetative changes is determined to a great extent by the time of clopheline intake. The maximal changes in the sympathetic activity at rest and during active orthostasis were revealed in the morning hours and in the second half of the day, the minimal ones--in the afternoon hours. The hemodynamic changes were most pronounced at 12 o'clock and minimal at 7 o'clock.     

Effect of benidipine hydrochloride, a long-acting T-type calcium channel blocker, on blood pressure and renal function in hypertensive patients with diabetes mellitus. Analysis after switching from cilnidipine to benidipine

BACKGROUND: Calcium channel blockers are commonly used to treat hypertension, and are known to generally act on the L-type calcium channel. Recent studies have shown, however, that some calcium channel blockers also block other calcium channel subtypes, including N- and T-type channels. Cilnidipine (CAS 132203-70-4) is an L- and N-type calcium channel blocker, and benidipine hydrochloride (benidipine, CAS 91599-74-5) is known to inhibit the T-type as well as L- and N-type calcium channels. In this study, effects of switching from cilnidipine to benidipine on blood pressure (BP) lowering and renal functions were investigated in order to clarify the physiological properties of the T-type calcium channel. METHODS AND RESULTS: Forty hypertensive patients with diabetes and poor BP control despite receiving cilnidipine were selected, and the changes in BP and urine protein (UP) scores were investigated retrospectively after switching from cilnidipine to benidipine for more than 3 months. BP (systolic/diastolic) significantly decreased from 155.8 +/- 13.7 mmHg/76.5 +/- 13.3 mmHg to 145.9 +/- 17.0 mmHg/71.4 +/- 13.7 mmHg after benidipine treatment, and this effect was stably maintained for one year. UP also significantly decreased from 1.29 to 0.67 in the mean score. The decrease in UP may be explained by a mechanism other than BP lowering effect. CONCLUSION: These results demonstrate that benidipine has a more potent antihypertensive effect than cilnidipine and also a renoprotective effect, indicating the high usefulness of benidipine in hypertensive patients with diabetes. T-type calcium channel blockade was suggested to be possibly involved in the enoprotective effect of benidipine.     

贝尼地平和培哚普利对老年高血压病伴蛋白尿患者肾功能的影响

目的比较新型钙通道阻滞剂贝尼地平与血管紧张素转换酶抑制剂培哚普利对老年高血压病伴蛋白尿患者肾脏保护作用的差别。方法将60例24h尿蛋白总量<1g的老年高血压病患者,随机分为贝尼地平组(A组)与培哚普利组(B组),分别给予贝尼地平与培哚普利治疗12月,比较A、B两组治疗前后收缩压(SBP),舒张压(DBP),24h尿蛋白(Pro)、血清肌酐(Scr)、肾小球滤过率(GFR)的差别。结果①治疗前A、B两组SBP、DBP、Pro、Scr、GFR无显著性差异(P>0.05);②A、B两组治疗后SBP、DBP、Scr较治疗前有显著下降,GFR均明显升高(P<0.05);③治疗后AB两组间SBP、DBP、Scr、GFR无明显差异(P>0.05)。结论贝尼地平与培哚普利比较,对老年高血压伴蛋白尿的患者,具有相似的肾脏保护作用。     

Effects of benidipine hydrochloride (Coniel) on blood pressure, heart rate and plasma norepinephrine concentration in spontaneously hypertensive rats]

We investigated the effects of benidipine hydrochloride (benidipine, Coniel) on blood pressure, heart rate and plasma norepinephrine (NE) concentration in spontaneously hypertensive rats and compared them with those of other calcium channel blockers. Benidipine (2 mg/kg, p.o.) was compared with the equihypotensive doses of nifedipine (5 mg/kg), cilnidipine (6 mg/kg) and amlodipine (3 mg/kg). All the 4 calcium channel blockers exhibited significant antihypertensive effects. Nifedipine and cilinidipine significantly increased heart rate, as compared with that in the control group, whereas benidipine or amlodipine did not significantly affect it. The area under the curves for hypotensive effect and tachycardic effect for 10 hr after the drug administration were compared among the 4 compounds. As a result, the tachycardic effect of benidipine was significantly lower than those of nifedipine, cilnidipine and amlodipine, while the hypotensive effects were similar among the 4 compounds. Nifedipine and amlodipine, significantly increased plasma NE concentration, cilnidipine tended to increase it. In contrast, benidipine did not significantly affect plasma NE concentration. These results suggest that the effects of benidipine on plasma NE concentration and heart rate are less prominent than those of the other calcium channel blockers.     

Effect of clonidine on sympathetic nervous activity in hydralazine-treated hypertensive patients

Summary Six patients with arterial hypertension were studied in hospital. They were given hydralazine iv in increasing doses, (2 mg, 3 mg, 5 mg, 6 mg, 10 mg) every 15 min, until the blood pressure was normal or side effects were encountered. Clonidine 150–600 µg/day was administered orally. Dose-blood pressure and heart rate-response curves to hydralazine and cold pressor test were performed when the patients were not taking drugs and after one week of clonidine administration; the urine noradrenaline excretion rate was also measured. The maximal iv dose of hydralazine reduced mean blood pressure from 133.7±7.54 (mean ± SEM) to 118.5±5.84 mm Hg (P<0.05) and increased heart rate from 77.3±2.88 to 102.2±4.36 beats/min (P<0.001). Clonidine decreased mean blood pressure from 133.7±7.54 to 116.8±7.75 mm Hg (P<0.001) and heart rate from 77.3±2.88 to 63.8±4.91 beats/min (P<0.001). During administration of maximal intravenous doses of hydralazine to patients treated with oral clonidine, mean blood pressure decreased from 116.8±7.75 to 98.4±3.61 mm Hg (P<0.001) and heart rate increased from 63.8±4.91 to 76.0±5.54 beats/min (P<0.001). The heart rate response to hydralazine was dose-related and the dose-response curve was shifted to the right by clonidine. The increase in mean blood pressure induced by the cold pressor test was significantly attenuated by clonidine (P<0.05). Clonidine decreased significantly the urine noradrenaline excretion rate from 43.78±9.31 to 13.66±3.65 µg/24 hr (P<0.05).     

Effect of minoxidil on sympathetic nervous activity in clonidine-treated hypertensive patients

Summary The efficacy and safety of oral ciramadol, a synthetic partial agonist-antagonist analgesic, in rapid control of postoperative pain was compared with oral pentazocine in a double blind study in 46 patients. Ciramadol 20 mg and 60 mg and pentazocine 50 mg had a rapid analgesic effect, peaking within one hour. Although a similar pattern of activity was observed for ciramadol 20 mg and pentazocine 50 mg, ciramadol 60 mg provided significantly better and longer lasting pain relief (P<0.02). Side effects included sedation and sweating, which occurred with a similar frequency in the various treatment groups. Oral ciramadol appears to be a safe and highly effective analgesic.     

Effects of benidipine hydrochloride on 24-hour blood pressure and blood pressure response to mental stress in elderly patients with essential hypertension

OBJECTIVE: The effects of a new dihydropyridine calcium antagonist, benidipine hydrochloride, on 24-hour blood pressure and blood pressure response to mental arithmetic test were investigated. SUBJECTS: Ten elderly patients with essential hypertension (mean age: 65+/-4 years; 7 male and 3 female). METHOD: After a control period of 4 weeks, 4 mg benidipine was administered once daily in the morning for 12 weeks. Ambulatory blood pressure was monitored using a non-invasive automatic portable device with the cuff-oscillometric method at the end of both the control and treatment periods. RESULTS: Benidipine administration significantly decreased 24-hour blood pressure, while little change was noted in heart rate. Daytime blood pressure decreased significantly, from 148.2+/-11.5/90.8+/-8.8 to 133.8+/-9.2/82.5+/-10.8 mmHg. However, no significant decrease in nighttime diastolic blood pressure was noted, and the decrease in nighttime systolic blood pressure was small (from 129.8+/-9.9/77.1+/-7.6 to 121.8+/-10.1/74.7+/-9.1 mmHg). No significant changes were observed in diurnal variability of blood pressure and heart rate. The decrease in systolic blood pressure by benidipine administration showed a significant positive correlation with systolic blood pressure before treatment in the 24-hour and daytime periods. Single cosinor analysis showed that benidipine administration significantly decreased MESOR of both systolic and diastolic blood pressure, without an increase in amplitude. Both systolic and diastolic blood pressure during mental arithmetic test were significantly decreased after treatment with benidipine, and the increase in systolic blood pressure induced by mental arithmetic test was also significantly attenuated. CONCLUSIONS: These findings indicate that administration of benidipine once daily in the morning effectively decreases blood pressure and attenuates blood pressure response to mental stress. Neither reflex tachycardia, deterioration of diurnal blood pressure change, nor excessive lowering of nighttime blood pressure was observed after benidipine administration. It is suggested that benidipine is a potent and long-lasting calcium antagonist which may be useful for the treatment of elderly hypertensive patients with cardiovascular disease.     

Effect of propranolol on sympathetic nervous activity in hydrallazine-treated hypertensive patients.

1 The effect of propranolol was examined on a) blood pressure and heart rate responses due to i.v. hydrallazine b) modification of these cardiovascular parameters during cold pressor test c) urinary catecholamine excretion rate. 2 Intravenous hydrallazine reduced significantly mean blood pressure by 15.2 mm Hg and increased heart rate by 24.9 beats/min. Propranolol reduced significantly mean blood pressure by 19.0 mm Hg and heart rate by 14.1 beats/min. Hydrallazine plus propranolol caused a significant reduction of mean blood pressure (by 37.7 mm Hg) but this was not accompanied by a significant fall in heart rate (by 3.3 beats/min). 3 During the control period, cold pressor test increased mean blood pressure by 16.0 mm Hg. Heart rate was increased by 12.5 beats/min in four patients. However, there was a reduction in heart rate (5.5 beats/min) in two other patients. During the propranolol period, cold pressor test-induced increase of mean blood pressure was not reduced but propranolol blocked the increase of heart rate. 4 Urinary catecholamine excretion rate was increased during hydrallazine administration. This excretion was not modified by propranolol.     

Effects of reboxetine on sleep and nocturnal cardiac autonomic activity in patients with dysthymia

Antidepressants may have sleep and autonomic side-effects. The acute and long-term effect of reboxetine (2 mg b.i.d.) on sleep and cardiac autonomic activity was compared with that of placebo in a single-blind study. Twelve patients affected by dysthymia underwent four polysomnographic studies at baseline (placebo); at night 3 (reboxetine; acute effect); at night 9 (reboxetine; intermediate-term effect); and at night 122 (reboxetine; chronic effect). After the first administration, reboxetine increased time awake after sleep onset, number of awakenings, percentage of stages 1 and 2 non-rapid eye movement (REM), and reduced the amount of stages 3-4 non-REM, but all these effects disappeared by continuing treatment. However, reboxetine caused a persistent suppression of REM sleep, which was accompanied by an increase of REM sleep latency. The spectral analysis of heart rate variability showed a trend towards an increase in sympathetic activity with both acute and intermediate reboxetine use. Long-term treatment with 4 mg reboxetine does not cause significant changes in cardiac autonomic function.     

Effects of a novel calcium antagonist, benidipine hydrochloride, on platelet responsiveness to mental stress in patients with essential hypertension.

The effects of a novel calcium antagonist, benidipine hydrochloride, on responses of platelets to mental stress were evaluated in nine patients with essential hypertension. Before and 12 weeks after the monotherapy with benidipine (2-4 mg/day), platelet aggregability and plasma beta-thromboglobulin were determined during rest and after a 10-min arithmetic stress. Before the treatment, arithmetic stress significantly increased platelet aggregability in response to adenosine diphosphate (ADP) and plasma beta-thromboglobulin level. Blood pressure, pulse rate, and plasma catecholamines also increased during arithmetic stress. The treatment with benidipine did not affect resting values of platelet functions, but attenuated significantly stress-induced alterations in primary aggregation to 1.0 microM ADP (34 +/- 4% to 40 +/- 3% before treatment vs. 32 +/- 2% to 34 +/- 3% after benidipine), ADP threshold for biphasic aggregation (2.2 +/- 0.4 to 1.8 +/- 0.3 microM before treatment vs. 2.2 +/- 0.3 to 2.2 +/- 0.4 microM after benidipine) and plasma beta-thromboglobulin level (74 +/- 16 to 104 +/- 15 ng/ml before treatment vs. 60 +/- 10 to 52 +/- 8 ng/ml after benidipine; p < 0.05 for Stress x Treatment interactions in all values). The pretreatment elevations in blood pressure and sympathetic activity with stress were not modified by benidipine treatment. In conclusion, the monotherapy with benidipine did not affect platelet function during the resting condition, but significantly suppressed the platelet activation induced by arithmetic stress in patients with essential hypertension.     

Effects of prazosin on hemodynamics and sympatho-adrenal activity in hypertensive patients

We studied peripheral and central hemodynamics and plasma catecholamine levels in 12 previously untreated patients with essential hypertension before and during treatment with the alpha 1-adrenoceptor antagonist prazosin (9.8 +/- 1.1 mg/day for 3-6 weeks following dose titration) as a single drug. Prazosin did not alter intra-arterially recorded blood pressures in the group as a whole, in spite of adequate plasma levels (12.6 +/- 1.2 ng/ml). There were no changes in cardiac output, blood volume, systemic or forearm vascular resistance, or forearm venous tone at rest during treatment. The blood pressure response to prazosin was correlated to pretreatment systemic and forearm vascular resistances. Arterial adrenaline levels were unchanged, but noradrenaline levels increased from 1.30 +/- 0.10 to 1.85 +/- 0.20 nM (p less than 0.05). Both noradrenaline and blood pressure responses to isometric hand-grip exercise were delayed and reduced during treatment. The hemodynamic and plasma catecholamine responses to a cold pressor test and tilting (50% head-up during 10 min) were similar before and during treatment. Our results may be related to development of tolerance to the alpha-adrenoceptor blocking effect of prazosin during long-term treatment. The elevation of arterial noradrenaline levels suggests that increased sympathetic activity also may have opposed the hypotensive response to prazosin.     

Long-term effects of benidipine on cerebral vasoreactivity in hypertensive rats

We tested the hypothesis that long-term application of a Ca2+ channel blocker would ameliorate the functional and morphological deterioration of the cerebral arteries during hypertension. Male spontaneously hypertensive rats (SHR) were fed a standard rat chow, containing a low (3 mg/kg/day) or high dose (6 mg/kg/day) of benidipine, a Ca2+ channel blocker, for 2 months. Using a cranial window, we examined responses of the basilar artery to acetylcholine, sodium nitroprusside, (-)-(3S,4R)-4-(N-acetyl-N-hydroxyamino)-6-cyano-3,4-dihydro-2,2-dimethyl-2H-1-benzopyran-3-ol (Y-26763; an opener of ATP-sensitive K+ channels), and (R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide (Y-27632; an inhibitor of Rho-associated kinase). Mean arterial pressure of the control group was 193+/-5 mm Hg (mean+/-S.E.M.), while that of the low-dose benidipine group was 183+/-5 mm Hg and that of the high-dose group was 159+/-4 mm Hg. Dilator responses of the basilar artery to acetylcholine and Y-26763 were impaired in SHR compared with those of normotensive Wistar-Kyoto (WKY) rats and treatment with benidipine enhanced the vasodilator responses to acetylcholine and Y-26763 in SHR. Y-27632-induced dilatation of the basilar artery was enhanced in SHR compared to that in WKY rats and the vasodilatation was reduced by benidipine in SHR. Sodium nitroprusside caused similar dilatation of the basilar artery, in both WKY rats and the SHR control group, and benidipine did not affect nitroprusside-induced dilatation of the artery in SHR. The wall of the basilar artery was significantly thicker in SHR than in WKY rats and benidipine treatment reduced the wall thickness of the artery in SHR. These findings suggest that chronic treatment with a Ca2+ channel blocker may enhance the dilator capacity and reduce contractility of the basilar artery during hypertension. Benidipine may also ameliorate the morphological changes of the basilar artery in hypertension.     

盐酸埃他卡林对高血压心脏重构的作用

目的　在自发性高血压大鼠 (spontaneouslyhyperten siverat,SHR)和脑卒中易感型自发性高血压大鼠 (stroke pronespontaneouslyhypertensiverat,SHRsp)上 ,评价盐酸埃他卡林 (iptakalimhydrochloride ,Ipt)对高血压心脏重构的实验治疗学作用。方法　SHR于第 12周龄进入实验 ,赖诺普利 (lisinopril,Lis) 12mg·kg-1,Ipt 3mg·kg-1灌胃每天 1次 ,连灌 4wk ;SHRsp于第 11周龄进入实验 ,实验设Ipt0 2 5、1和 4mg·kg-13个剂量组及溶剂对照组 ,灌胃给药每天 1次 ,持续给药 12wk ,观察药物对高血压心脏重构的影响。结果　实验期 4wk内 ,SHR对照组血压和心率进行性增高。Ipt能有效控制SHR的血压 ,降压效果确切 ,且可抑制SHR心率加快的趋势 ,但对SHR高血压心脏重构无明显作用。相同实验条件下 ,Lis也能有效控制SHR的血压 ,降压效果确切 ,对心率无明显影响 ;Lis治疗可减轻SHR高血压心脏重构。实验期 12wk内 ,SHRsp溶剂对照组血压持续性进行性增高。Ipt 3个剂量组均能降低SHRsp血压 ,Ipt 4mg·kg-1组在给药后第 4周开始出现心率减低。Ipt 3个剂量组的左心室和室间隔 (LV +S)重量及其与体重的比值[(LV +S) /BW ]低于溶剂对照组。 4组动物之间的右室重量(RV)均无差异。结论　Ipt能有效地控制SHR和SHRsp的血压 ,其对     

Clinical study with azelnidipine in patients with essential hypertension. Antiarteriosclerotic and cardiac hypertrophy-inhibitory effects and influence on autonomic nervous activity

A dihydropyridine calcium (Ca) antagonist, azelnidipine (CAS 123524-52-7, Calblock), exhibits hypotensive effects for a prolonged duration, and has been reported to have a strong antiarteriosclerotic action due to its high affinity for vascular tissues and antioxidative action. It has also been reported that azelnidipine does not cause tachycardia associated with the baroreceptor reflex due to vasodilatation. In this study, the antiarteriosclerotic and cardiac hypertrophy-inhibitory effects, and the autonomic nervous activity in essential hypertension of azelnidipine were investigated. The study was performed using the following 2 protocols: 1) Pulse wave velocity (PWV), carotid arterial intima media thickness (IMT), echocardiography, high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), adiponectin, brain natriuretic peptide (BNP), and 8-isoprostane were measured after an initial treatment with azelnidipine. 2) The treatment was switched to azelnidipine in patients who had previously been under treatment with amlodipine for essential hypertension, and 123I-metaiodobenzylguanidine myocardial scintigraphy (123I-MIBG), measurements of plasma norepinephrine, atrial natriuretic peptide (ANP), and BNP, Holter electrocardiography, and heart rate variability analysis were performed. PWV, IMT, hs-CRP, IL-6, and TNF-alpha significantly decreased. The levels of 8-isoprostane, an antioxidative marker, were also significantly decreased, while adioponectin levels were significantly increased after the initial treatment with azelnidipine. After switching from amlodipine, azelnidipine exhibited a hypotensive effects comparable to amlodipine, and significantly decreased heart rate and the total number of extrasystoles. Noradrenaline levels and the LF/HF ratio were significantly decreased, and the washout rate was significantly reduced on 123I-MIBG myocardial scintigraphy. These findings suggest that azelnidipine inhibits the enhancement of sympathetic nervous activity and the progression of arteriosclerosis through its antioxidative effects.     

Effects of direct cedrol inhalation into the lower airway on autonomic nervous activity in totally laryngectomized subjects

Aims

Previous studies reported that Cedrol (odorant) inhalation (CI) induced changes in autonomic balance and baroreceptor sensitivity (BRS) in both healthy subjects and anosmic patients. This suggests that Cedrol may act on the lower airway, and that the pulmonary system may exert an inhibitory influence on the cardiovascular system.

Method

To test the above possibility, vaporized Cedrol (64.0 ± 7.7 10⁻⁹m) or blank air was directly inhaled through the lower airway from a hole in the trachea, but not through the upper airway, using totally laryngectomized subjects. During the experiment, ECG, systolic (SBP) and diastolic (DBP) blood pressures were measured. Sympathetic and parasympathetic nervous activity was estimated by spectral analyses of variability in these parameters (heart rate variability (HRV), SBP variability (SBPV) and DBP variability (DBPV)). BRS was computed from transfer gain between SBP and the R-R interval of the ECG.

Results

SBP and DBP significantly decreased during CI, although there were no significant differences in HR and respiratory rate. BRS significantly increased during CI. The low frequency components of SBPV and DBPV (indices for sympathetic activity) significantly decreased during CI, while high frequency components of HRV (an index for parasympathetic activity) significantly increased.

Conclusions

The present experiment using totally laryngectomized patients replicated the similar results in healthy subjects who inhaled Cedrol through the nose, suppression of sympathetic outflow and increase in parasympathetic outflow. These results demonstrated that Cedrol acts on the lower airway and pulmonary system, and suggest a new target for drug therapy of hypertension.

What is already known about this subject

• Relationships between smell sensation and autonomic changes have been studied extensively.
• However, the possibility that odorants may also act on the lung and lower airway remains unknown.

What this study adds

• The present results provide the first evidence that the lung and lower airway exert an inhibitory influence on the cardiovascular system in response to Cedrol (odorant) in the air under physiological conditions.

     

原发性高血压病血压昼夜节律变化与自主神经功能关系

目的 探讨高血压病人血压昼夜节律与心率变异性关系，观察自主神经功能改变对血压影响。方法 随机选择22例原发性高血压昼夜节律存在者（H1组）与性别、年龄配对的22例昼夜节律消失者（H2组）作为研究对象，应用动态心电图与动态血压监测仪同步记录24h心率变异性和血压变化。结果 在H2组中SDNN，VLF，LF，HF均显著性低于H1组（P＜0．05）。HF尤其在夜间下降更明显（P＜0．01）。在H2组内白昼与夜间SDNN,rMSSD，HF，LF／HF比值均无显著性差异。结论 24h血压波动情况与自主神经调节有关，说明高血压病血压昼夜节律消失者自主神经损更严重，从而继发心、脑、肾脏器功能损害。     

RP-HPLC法测定盐酸贝尼地平片的含量及有关物质

目的：建立高效液相色谱法测定盐酸贝尼地平片含量的方法。方法：应用HPLC法,色谱柱为Hypersil ODS C18（4.6mm×200mm,5μm）,检测波长为237nm,柱温为室温,流速为1.0ml/min,进样量为20μl,流动相为甲醇∶水（82∶18,v/v）。结果：盐酸贝尼地平浓度在1.25～50mg·L-1的范围内线性关系良好（R2=0.9998,n=6）,平均加样回收率为99.43%,RSD＝0.18%。结论：本方法简便、准确、快速、重复性好,可用于盐酸贝尼地平片的含量测定。     

The effects of transdermal scopolamine on autonomic nervous activity during sleep

We studied the effect of transdermally applied scopolamine (scopolamine-TTS) on autonomic nervous activity during sleep. The double-blind, randomized, crossover study was carried out in six healthy male volunteers by applying 1.5 mg scopolamine-TTS or placebo patch on the retroauricular skin and by monitoring heart rate, cardiac ballistogram, respiration and body movements by using electrocardiogram and static charge sensitive bed.Scopolamine did not decrease the time the subjects desired to sleep (516 min after TTS, 511 min after placebo) or the number of body movements of 3–5 s duration the subjects spontaneously performed during sleep (47 after TTS, 58 after placebo). No adverse effects of scopolamine were reported spontaneously. Scopolamine-TTS slowed the mean heart rate during quiet sleep from 53.2 to 44.9 beats · min^–1, and increased the duration of bradycardia in response to body movements (MIB-reflex) from 12.5 to 14.7 s with a significant difference between scopolamine and placebo effects. The bradycardias were not associated with disturbances in cardiorespiratory or central nervous system functions. The cardiac vagomimetic action of scopolamine-TTS could be explained by low plasma drug concentrations (175 pg/ml) primarily blocking only neuronal inhibitory prejunctional muscarinic receptors which regulate acetylcholine release from the autonomic ganglia and parasympathetic nerve-endings.Because of the central role of acetylcholine in the physiological regulation of sleep, the effect of scopolamine-TTS on sleep merits further investigations.     

右侧星状神经节阻滞对糖尿病患者自主神经功能的影响

目的 研究右侧星状神经节阻滞对糖尿病患者自主神经功能的影响.方法 50例糖尿病患者接受了右侧星状神经节阻滞.记录并分析右侧星状神经节阻滞前后的平均动脉压(MAP)、心率(HR)及心率变异性(HRV),包括低频功率(LF),高频功率(HF)及LF/HF比值变化.结果 与阻滞前比较,阻滞后HR下降[(84.6±6.5)次/分vs.(72.3±4.4)次/分](P<0.05),血压无明显变化.阻滞前后LF[(110.2±17.5)vs.(76.1±18.4)]和LF/HF比值[(2.42±1.41)vs.(1.52±1.32)],阻滞后显著小于阻滞前(P<0.01),HF无明显改变(P>0.05).结论 右侧星状神经节阻滞通过调节交感-迷走神经活性,可使糖尿病患者自主神经系统功能的失衡状况得到改善.