The effects of phenylephrine on right ventricular performance in patients with pulmonary hypertension

Pulmonary hypertension causes right ventricular ischemia and failure as a result of increased afterload combined with reduced coronary blood flow. Increasing coronary driving pressure by raising aortic pressure with phenylephrine has been shown to reverse right ventricular ischemia from pulmonary hypertension in animals. Since vasodilators often fail to reduce afterload, we tested whether raising the coronary driving pressure would improve right ventricular function in man. Ten patients with pulmonary hypertension had hemodynamics and right ventricular coronary driving pressure measured before and 10 minutes after a steady state was reached with a phenylephrine infusion titrated to raise aortic pressure by 25 percent. Phenylephrine caused a significant (p less than .01) increase in mean aortic pressure (84 to 108 mm Hg) and right ventricular coronary driving pressure (46 to 69 mm Hg). In response, there was a significant (p less than .01) rise in mean pulmonary artery pressure (58 to 67 mm Hg), right ventricular end-diastolic pressure (10 to 16 mm Hg) and wedge pressure (5 to 9 mm Hg), and an insignificant fall in cardiac output (3.26 to 3.09 L/min) and pulmonary artery O2 saturation (57 to 49 percent). Although phenylephrine increased right ventricular coronary driving pressure, it worsened right ventricular function as manifest by a rise in end-diastolic pressure and fall in cardiac output. Any benefit of raising right ventricular coronary driving pressure may have been offset by alpha vasoconstriction of right ventricular coronary blood flow and/or pulmonary arterial vasoconstriction. Phenylephrine does not appear to be a useful therapy of right ventricular failure from pulmonary hypertension in patients who fail vasodilators.     

Norepinephrine and phenylephrine effects on right ventricular function in experimental canine pulmonary embolism

In a canine model of pulmonary embolism (PE) produced by infusion of autologous blood clots, mean arterial blood pressure (MAP) decreased to 73 +/- 4 mm Hg while cardiac output (CO) decreased to less than 50 percent of baseline. Intravenous infusion of phenylephrine (PHEN) and norepinephrine (NE) restored MAP to somewhat above baseline values. However, only NE restored CO to control levels. The right ventricular myocardial blood flow increased 15 percent in the PE group with PHEN and 229 percent with NE at equipressor concentrations. The right ventricular myocardial oxygen consumption (RVMVo2) was not significantly different between PE and PE + PHEN while PE + NE increased RVMVO2 by 144 percent to 20.2 +/- 1.8 ml/min/100 g. The RV output was not adequately restored with PE, but when RV contractility was augmented with NE, RV output was restored to baseline. Right ventricular minute work increased 100 percent with NE and was maintained with a 100 percent increase in oxygen consumption. Calculated pulmonary vascular resistance (PVR) was decreased during PE by 36 percent with PE + PHEN while PVR in NE-treated dogs decreased by 59 percent. In NE-treated animals, systemic vascular resistance (SVR) was restored to control levels while in PHEN-treated animals SVR increased about 75 percent from baseline. We conclude that the salutary effects of NE on RV output are due to both alpha and beta receptor stimulation, which increased contractility, RVMBF, and RVMVo2, and decreased both PVR and SVR. In the PHEN-treated dogs, our indices of minute-work, RVMBF, and RVMVo2 suggest that coronary autoregulation was intact; however, there was no apparent benefit to RV output. This study suggests that in the clinical setting of acute PE, the judicious use of NE, rather than PHEN, may be more beneficial in restoring RV function and systemic hemodynamics.     

卡托普利注射液对高血压急症的降压作用

目的：观察卡托普利注射液治疗高血压急症的急诊降压作用。方法：对34例高血压急症给予卡托普利注射液25mg加入5％葡萄糖20ml静注，观察注射后5、15、30、60和120min血压、心率、临床表现和不良反应。结果：用药后5minSBP和DBP即下降（P＜0．05），但以15、30、60、120min下降最明显（P＜0．01），心率略有下降（P＞0．05），总有效率91．2％。结论：卡托普利注射液降压效果明显，其急诊降压作用优于口服给药，且无明显副作用，特别适合老年人或长期高血压已产生耐受的患者，也适用于伴有急性左心衰竭或急性主动脉夹层分离的高血压急症。     

盐酸尼卡地平注射液对主动脉瓣返流的影响

目的 观察盐酸尼卡地平注射液对主动脉瓣返流的影响。方法 对主动脉返流的患者在应用盐酸尼卡地平注射液治疗前后 进行彩色多普勒超声心动图检查。结果在给患者静脉滴注盐酸尼卡地平注射液1小时后,主动脉返流束的长度、宽度、面积、返 流分数及返流频谱的下降斜率均显著减小或降低(P<0.05);主动脉瓣返流频谱的压差半降时间显著延长(P<0.05)。结论盐 酸尼卡地平注射液可以明显减轻主动脉瓣返流的程度。     

Effect of phenylephrine infusion on atrial electrophysiological properties.

OBJECTIVE: To determine the effect of changes in autonomic tone induced by phenylephrine infusion on atrial refractoriness and conduction. DESIGN: Left and right atrial electrophysiological properties were measured before and after a constant phenylephrine infusion designed to increase sinus cycle length by 25%. SUBJECTS: 20 patients, aged 53 (SD 6) years, undergoing electrophysiological study for investigation of idiopathic paroxysmal atrial fibrillation (seven patients) or for routine follow up after successful catheter ablation of supraventricular tachycardia (13 patients). MAIN OUTCOME MEASURES: Changes in left and right atrial effective refractory periods, atrial activation times, and frequency of induction of atrial fibrillation. RESULTS: Phenylephrine (mean dose 69 (SD 18) mg/min) increased mean blood pressure by 22 (12) mm Hg (range 7 to 44) and lengthened sinus cycle length by 223 (94) ms (20 to 430). Left atrial effective refractory period lengthened following phenylephrine infusion from 250 (25) to 264 (21) ms (P < 0.001) but there was no significant change in right atrial effective refractory period: 200 (20) v 206 (29), P = 0.11. There was a significant relation between the effect of phenylephrine on sinus cycle length and on right atrial refractoriness (r = 0.6, P = 0.005) with shortening of right atrial refractoriness in patients with the greatest prolongation in sinus cycle length. During phenylephrine infusion, the right atrial stimulus to left atrial activation time at the basic pacing cycle length of 600 ms was unchanged, at 130 (18) v 131 (17) ms, but activation delay with a premature extrastimulus increased: 212 (28) v 227 (38) ms, P = 0.002. Atrial fibrillation was induced by two of 58 refractory period measurements at baseline and by 12 of 61 measurements during phenylephrine infusion (P < 0.01). Phenylephrine increased the difference between left and right atrial refractory periods by 22.8 (19.4) ms in the five patients with induced atrial fibrillation after phenylephrine compared to 0.9 (16.2) ms in the 13 patients without induced atrial fibrillation after phenylephrine infusion (P = 0.02). CONCLUSIONS: Phenylephrine infusion increased left atrial refractoriness and intra-atrial conduction delay following a premature right atrial extrastimulus. Induction of atrial fibrillation during phenylephrine infusion was associated with non-uniform changes in atrial refractoriness. These data support the concept that changes in autonomic tone may precipitate atrial fibrillation in susceptible individuals.     

The efficacy and adverse effects of topical phenylephrine for anal incontinence after low anterior resection in patients with rectal cancer

Background Anal incontinence is experienced by some patients with rectal cancer who received low anterior resection. This study was to examine the efficacy and adverse effects of the alpha-1 adrenergic agonist phenylephrine, which causes contraction of the internal anal sphincter and raises the resting pressure in these patients. Patients and methods Thirty-five patients with anal incontinence were treated with 30% phenylephrine or a placebo randomly allocated in a double-blind study. The efficacy of the drug was assessed by changes in the following standardized questionnaire scores: the fecal incontinence severity index (FISI), fecal incontinence quality of life (FIQL) scales, and a global efficacy question. Anal sphincter function was evaluated using anorectal manometry. Results Phenylephrine did not improve either the FISI score or any of the four FIQL scores. Five of 17 (29%) patients reported subjective improvement after phenylephrine compared with 4 of 12 (33%) using the placebo. The maximum resting anal pressure did not differ between baseline and after 4 weeks application of phenylephrine (30.0 to 27.3 mmHg). In the phenylephrine group, allergic dermatitis was developed in five patients and headache in two. Conclusion In the patients with anal incontinence after low anterior resection for rectal cancer, phenylephrine gel did not seem to be helpful in relieving symptoms with some adverse effects.     

Sympathoexcitation increases the QT/RR slope in healthy men: differential effects of hypoxia, dobutamine, and phenylephrine

Introduction: Dynamic ventricular repolarization assessed by QT/RR slopes studies the effects of modifications in cardiac repolarization independently of variations in RR interval (RR). The effects of changes in sympathetic and vagal activity on the QT/RR slope are controversial. We tested the hypothesis that sympathoexcitation is an important determinant of the QT/RR slope.
Methods and Results: We compared the effects of a reflex sympathetic activation in response to hypoxia, to the direct effects of the infusion of the beta-adrenergic agent dobutamine, on the QTa (apex) and QTe (end)/RR slopes. Dobutamine was titrated to obtain similar increases in cardiac output than with hypoxia. Cardiac vagal activity was estimated by rMSSD and pNN50. In a second group of healthy subjects, we assessed the effect of a reflex cardiac vagal activation in response to phenylephrine infusion on the same variables. We observed a similar increase in QTa and QTe slopes during hypoxia and dobutamine (both P < 0.017 vs. normoxia), despite divergent changes in cardiac vagal activity, as rMSSD and pNN50 decreased with hypoxia compared to normoxia (P < 0.001) but increased during dobutamine infusion compared to hypoxia (P < 0.017). In contrast, these slopes did not change during the rises in rMSSD and pNN50 elicited by phenylephrine (P > 0.7).
Conclusion: Beta-adrenergic stimulation induces comparable increases in the QT/RR slopes than hypoxia, but in the presence of a larger cardiac vagal activity. Vagal cardiac activation by phenylephrine does not change the QT slopes. This reveals that the sympathetic system is an important determinant of QT/RR dynamicity in healthy men.     

The effects of inadvertent intramuscular injection of BCG vaccine.

We report on a case of inadvertent intramuscular injection of BCG vaccine into an already tuberculin-sensitive individual which resulted in a severe and prolonged local reaction. There is no consensus on the best management of this complication, although in this case healing appeared to be hastened by anti-tuberculous chemotherapy.