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PubMed1991

Enhancement of the murine primary antibody response by phenylephrine in vitro.

Phenylephrine was found to enhance the primary (immunoglobulin M) antibody response of murine splenocytes to sheep erythrocytes when added to splenocyte cultures at the time of in vitro immunization. The enhancement was seen at all times during the developing antibody response. One day after the peak response the enhancement was 78% above the control response, and was completely blocked by equimolar concentrations of the alpha adrenoceptor antagonist phentolamine. The alpha-1 adrenoceptor antagonist prazosin dose dependently antagonized the enhancement associated with phenylephrine one day after the peak response. These results suggest that phenylephrine prolongs the in vitro IgM antibody response by way of alpha-1 adrenoceptor activation. The adrenoceptors responsible for this pharmacologic response could not be demonstrated using direct radioligand binding techniques.

Animals↗

PubMed2005

Pulmonary edema following phenylephrine intranasal spray administration during the induction of general anesthesia in a child.

Topical phenylephrine, an agent used to facilitate nasotracheal intubation and prevent nasal mucosal bleeding, can cause severe hypertension in some patients, secondary to its stimulation of alpha-adrenergic receptors. Moreover, a high incidence of pulmonary edema is found in patients whose phenylephrine administration is followed by treatment with beta-blocking agents. We report a case of acute pulmonary edema in a pediatric patient who developed severe hypertension after the inadvertent administration of a large dose of topical nasal phenylephrine, followed by beta-adrenergic antagonists (esmolol).

Administration, Intranasal↗

PubMed1997

[Effects of EDRF on the vasoconstrictor action of phenylephrine in rat aorta].

The influence of endothelium-derived relaxing factor (EDRF) on the vasoconstrictor effect of phenylephrine on rings of rat aorta was studied in this paper. Rings of rat aorta, with or without endothelium, were suspended in organ chambers for the measurement of contractive force and contractive speed. All experiments were performed in the presence of indomethacin (10 mumol/L) to prevent the production of vasoactive prostanoids. When the preparations with intact endothelium were treated with methylene blue (10 mumol/L), an inhibitor of the target enzyme of EDRF, or NG-nitro-L-arginine (30 mumol/L), an inhibitor of EDRF formation, dose-contractive force curves of phenylephrine shifted to left: the EC30 value decreased 5-fold and the maximal response ratios were 1.6 +/- 0.4 and 1.6 +/- 0.5 (n = 8) respectively. These results were similar to those observed after mechanical removal of the endothelium: a 3-fold decrease in the EC30 value and the maximal response ratio was 1.0 +/- 0.2 (n = 8), The latter results may be related to a little EDRF produced by vascular smooth muscle. Our results suggest that the vasoconstrictive effect induced by phenylephrine may also be regulated by EDRF production from vascular endothelium and smooth muscle.

Animals↗

PubMedDate not supplied

[Phenylephrine synchromizes rhythm of protein synthesis in hepatocyte culture].

Published data indicate that 1-3 microM adrenomimetic phenylephrine increases the concentration of calcium ions in the cytoplasm of cultured hepatocytes. We studied low-density cultures exhibiting no protein synthesis rhythm in the fresh medium and demonstrated that a 2 min action of 2 microM phenylephrine induces protein synthesis rhythm, i.e., synchronizes the synthesis oscillations in hepatocytes. A similar effect was observed for a selective inhibitor of the reticulum calcium pump, di-tert-butyl-benzohydroquinone, that increases the cytoplasm concentration of calcium ions by a receptor-independent mechanism. A calcium antagonist imipramine obviated the synchronization effect of phenylephrine. We propose that short-term changes in the cytoplasm concentration of calcium ions covering the whole cell population are among intracellular mechanisms of protein synthesis synchronization in hepatocytes in vitro.

Adrenergic alpha-Agonists↗

PubMed2001

Assessment of baroreflex sensitivity in patients with preserved and impaired left ventricular function by means of the Valsalva manoeuvre and the phenylephrine test.

The purpose of the present study was to assess the agreement between measurements of baroreflex sensitivity (BRS) obtained by the Valsalva manoeuvre and by the phenylephrine test in patients with previous myocardial infarction and different degrees of left ventricular dysfunction. Patients with a previous myocardial infarction were enrolled consecutively into two groups according to their left ventricular ejection fraction (LVEF): 40% (n=52). All patients underwent BRS assessment by the phenylephrine technique (Phe-BRS) and by the Valsalva manoeuvre, with the latter using both the overshoot part of phase IV (Ov-VM-BRS) and the whole of phase IV (IV-VM-BRS). The linear association between methods was assessed by correlation analysis and the agreement was evaluated by computing the bias and the limits of agreement. IV-VM-BRS and Ov-VM-BRS could not be computed in 26% and 39% of patients respectively. For both indices a much higher percentage of non-computable Valsalva manoeuvre slopes was found in the group of patients with LVEF 40% the results were: r=0.91 (P<0.001), bias=0.1 ms/mmHg (P=0.84) and limits of agreement from -4.8 to 5 ms/mmHg. When comparing Phe-BRS and IV-VM-BRS, we found r=0.67 (P=0.001), bias=-1.5 ms/mmHg (P=0.06) and limits of agreement from -8.8 to 5.7 ms/mmHg in the group of patients with LVEF 40%. Dichotomizing Ov-VM-BRS, the best cut-off value to identify patients with a Phe-BRS of <3 ms/mmHg was found to be 7 ms/mmHg, giving 100% sensitivity and 69% specificity. In conclusion, estimation of BRS by the Valsalva manoeuvre in post-myocardial infarction patients is limited by a large number of non-measurable results. When computable, measurements are well correlated with those obtained by Phe-BRS, but, because of large limits of agreement, the two methods cannot be used interchangeably. If used as a screening test for risk stratification, the Valsalva manoeuvre could reduce by about one-third the need for phenylephrine injection.

Adult↗

PubMedDate not supplied

Determination of phenylephrine hydrochloride by flow injection analysis with chemiluminescence detection.

A new method is proposed for the determination of phenylephrine hydrochloride by flow injection analysis with direct chemiluminescence detection. The method is based on the oxidation of the drug by potassium permanganate in sulfuric acid medium at 80 degrees C. The calibration graph is linear over the range 0.03-8 ppm phenylephrine hydrochloride, with a relative standard deviation (n = 51, 0.5 ppm) of 1.1% and sample throughput of 134/h. The influence of 38 different foreign compounds was tested, and the method was applied to the determination of phenylephrine hydrochloride in 8 different pharmaceutical formulations.

Flow Injection Analysis↗

PubMed1992

The hemodynamic and fibrinolytic response to low dose epinephrine and phenylephrine infusions during total hip replacement under epidural anesthesia.

Lower rates of deep vein thrombosis have been noted following total hip replacement under epidural anesthesia in patients receiving exogenous epinephrine throughout surgery. To determine whether this is due to enhanced fibrinolysis or to circulatory effects of epinephrine, 30 patients scheduled for primary total hip replacement under epidural anesthesia were randomly assigned to receive intravenous infusions of either low dose epinephrine or phenylephrine intraoperatively. All patients received lumbar epidural anesthesia with induced hypotension and were monitored with radial artery and pulmonary artery catheters. Patients receiving low dose epinephrine infusion had maintenance of heart rate and cardiac index whereas both heart rate and cardiac index declined significantly throughout surgery in patients receiving phenylephrine (p = 0.0001 and p = 0.0001, respectively). Tissue plasminogen activator (t-PA) activity increased significantly during surgery (p < 0.005) and declined below baseline postoperatively (p < 0.005) in both groups. Low dose epinephrine was not associated with any additional augmentation of fibrinolytic activity perioperatively. There were no significant differences in changes in D-Dimer, t-PA antigen, alpha 2-plasmin inhibitor-plasmin complexes or thrombin-antithrombin III complexes perioperatively between groups receiving low dose epinephrine or phenylephrine. The reduction in deep vein thrombosis rate with low dose epinephrine is more likely mediated by a circulatory mechanism than by augmentation of fibrinolysis.

Aged↗

PubMed1992

Calcium antagonists block angiotensin II-mediated vasoconstriction in humans: comparison with their effect on phenylephrine-induced vasoconstriction.

Calcium antagonists are known to decrease peripheral vascular resistance in vivo in humans. The mechanism of this vascular relaxation has not been clearly elucidated. Vascular tone is maintained by several endogenous neurohumoral systems including sympathetic nervous system activity and angiotensin II. We compared and contrasted the capacity of calcium antagonist drugs to prevent angiotensin II and phenylephrine-induced alpha-1 adrenergic vasoconstriction using brachial artery infusion and measurement of forearm blood flow by strain gauge plethysmography. In a dose-dependent manner, calcium antagonists blocked angiotensin II-induced vasoconstriction. The rank order of this blockade was nifedipine greater than verapamil greater than diltiazem. Nifedipine and verapamil, but not diltiazem blocked alpha-1 adrenergic (phenylephrine-induced) vasoconstriction. At 7.64 and 19.1 micrograms/min infusion rates for nifedipine and verapamil, respectively, they abolished the angiotensin II effect; however, the phenylephrine effect was incompletely blocked. Calcium antagonist-induced vascular relaxation in vivo in humans is in part explained by their capacity to block angiotensin II-mediated vasoconstriction. In addition, two calcium antagonists (nifedipine and verapamil) may inhibit alpha-1 adrenergic vasoconstriction.

Adult↗

PubMedDate not supplied

[Testosterone inhibits the contractile responses to phenylephrine associated with the release of intracellular calcium in rat aorta].

Using endothelium-denuded rat aortic rings incubated in Ca2+ -free solution, we assessed the ability of testosterone to influence the contractile effect of phenylephrine, and the increase in resting tone (IRT) associated with Ca2+ ability to cross the plasma membrane. The addition of testosterone [10(-5)-10(-4) 5 min before phenylephrine [10(-6) M], inhibited both phenylephrine-induced contraction and IRT. These changes were not affected by cycloheximide (10(-5) M; a protein synthesis inhibitor of), flutamide (10(-5) M; an androgenic receptor antagonist), or by adding aminoglutethimide (10(-5) M; an aromatase inhibitor). Testosterone also blocked the contractile response to serotonin [10(-5) M] but not to caffeine [10(-2) M]. On the other hand, testosterone inhibited the contractile responses to cyclopiazonic acid (10(-6) M; a selective Ca2+ -ATPase inhibitor) or ryanodine (10(-5 M; an activator of sarcoplasmic reticulum Ca2+ -release channels) associated with capacitative Ca2+ influx through non-L-type Ca2+ channels. These data suggest that by acting on the cellular membrane, testosterone interferes with the signal transduction pathway of G(q-11) protein-coupled receptors, and inhibits capacitative Ca2+ influx through both L-type and non-L-type Ca2+ channels. These effects are non-genomic, non-mediated by the intracellular androgen receptor, and not due to the conversion of testosterone to estrogens.

Animals↗

PubMedDate not supplied

The effect of repeated treatment with antidepressant drugs or electroconvulsive shock on the phenylephrine-induced elevation of the plasma corticosterone concentration in rats.

The selective alpha 1-adrenoceptor agonist phenylephrine, administered intracerebroventricularly in doses of 20-80 micrograms/10 microliters, increased the plasma corticosterone level in rats in a dose-dependent manner. Repeated treatment with amitriptyline (10 mg/kg po, twice daily for 14 consecutive days) or electroconvulsive shock (ECS) (once daily for 10 consecutive days) neither modified the basal corticosterone concentration nor affected the increase in the hormone level induced by phenylephrine (40 micrograms/10 microliters) injected 24 h after the last treatment with amitriptyline or ECS. Repeated treatment with imipramine (10 mg/kg po, twice daily for 14 consecutive days) did not affect the basal corticosterone concentration, but enhanced the corticosterone response to phenylephrine. These results indicate that repeated treatment with imipramine, but not with amitriptyline or ECS, increases responsiveness of the alpha 1-adrenoceptors involved in the hormonal response.

Amitriptyline↗

PubMed1991

Bethanechol and phenylephrine responses in canine inferior vena cava and abdominal aorta.

Both canine inferior vena cava and abdominal aorta showed a concentration dependent increase of contraction in response to phenylephrine; however, inferior vena cava contracted in response to bethanechol but abdominal aorta did not respond to bethanechol. When the inferior vena cava was preconstricted with 1 x 10(-3)M bethanechol, low concentrations of phenylephrine (1 x 10(-7)M to 1 x 10(-6)M) induced relaxation, but relaxation by phenylephrine of abdominal aorta pretreated with 1 x 10(-3)M bethanechol did not occur.

Animals↗

PubMed2006

Single dose of 1% tropicamide and 10% phenylephrine for pupil dilation.

OBJECTIVE: To compare the efficacy of pupil dilation between a single dose and three doses of 1% tropicamide and 10% phenylephrine for binocular indirect ophthalmoscopy. MATERIAL AND METHOD: A prospective randomized double-blind clinical controlled trial was conducted. All patients underwent the binocular indirect ophthalmoscopy and met the inclusion criteria were randomized into two groups using block randomization. Group A received a single dose of 1% tropicamide and 10% phenylephrine eye drops, and Group B received three doses of the same drugs. The primary outcome was the horizontal pupil diameter measured by slit-lamp biomicroscope (Haag-Streit model 900) before and at 10, 15, 20, 25 and 30 minutes after eye drop instillation. The clinical equivalence of the efficacy of pupil dilation between the two groups was defined as the difference of less than or equal to 1 mm (-1 mm to + 1 mm). RESULTS: Eighty patients (160 eyes) were randomized into 40 patients (80 eyes) in group A and 40 patients (80 eyes) in group B. The mean pupil sizes at baseline of group A were 3.51 +/- 0.63 mm in the right eye and 3.39 +/- 0.67 mm in the left eye. Those in group B were 3.61 +/- 0.67 mm in the right eye and 3.66 +/- 0.72 mm in the left eye. The mean pupil diameters at 30 minutes of group A were 7.34 +/- 0.51 mm in the right eye and 7.41 +/- 0.56 mm in the left eye, whereas those of group B were 7.49 +/- 0.45 mm in the right eye and 7.51 +/- 0.40 mm in the left eye. The mean difference of the pupil size between the two groups was 0.15 mm (p = 0.175) in the right eye and 0.l0 mm (p = 0.362) in the left eye. The 95% confidence intervals of the difference in pupil size were -0.36 to 0.07 mm in the right eye and -0.32 to 0.12 mm in the left eye. CONCLUSION: The 95% confidence interval of the difference in pupil size lay entirely within the range of equivalence. The single dose of 1% tropicamide and 10% phenylephrine was clinically equivalent to the three doses of the same drugs.

Adult↗

PubMed1991

The hemodynamic effects of intravenous norepinephrine versus epinephrine and phenylephrine in patients with ischemic heart disease.

The hemodynamic effects of an intravenous bolus of norepinephrine 10 micrograms, phenylephrine 100 micrograms and epinephrine 10 micrograms were investigated in 30 patients scheduled for coronary artery bypass grafting. The hemodynamic changes following norepinephrine were similar to those achieved by phenylephrine. Both drugs increased the mean blood pressure and systemic vascular resistance without any significant change of cardiac output. In contrast, epinephrine increased the mean arterial pressure and cardiac output without a significant change of systemic vascular resistance. The results suggest that intravenous norepinephrine acts similar to phenylephrine as an alpha-adrenergic agonist, while epinephrine acts predominantly as a beta-adrenergic agonist.

Adult↗

PubMed1978

Positive inotropic but no relaxant effects of phenylephrine in cat papillary muscle.

The effect of phenylephrine (30 micron) in the presence of propranolol (1 micron) on electrically induced isometric twitches and on KCl-contractures was studied in papillary muscles from reserpine-pretreated cats at 25 degrees C. Under these conditions phenylephrine has previously been shown to act solely via alpha-adrenoceptors and not to increase c-AMP. Phenylephrine increased force of contraction, time to peak tension and relaxation time. Contracture tension remained unaffected. These data indicate that the stimulation of cardiac alpha-adrenoceptors, in contrast to beta-adrenergic stimulation, does not lead to so-called relaxant effects. This qualitative difference between the two responses is probably due to the different capacity of both stimuli to increase c-AMP.

Animals↗

PubMed1990

Calcium dependence of phenylephrine-, endothelin-, and potassium chloride-stimulated atrial natriuretic factor secretion from long term primary neonatal rat atrial cardiocytes.

Since calcium is involved in both excitation-secretion and excitation-contraction coupling, it was of interest to evaluate its involvement in atrial natriuretic factor (ANF) release from atrial cardiocytes. In medium containing physiological levels of calcium (1.4 mM), the secretion of ANF from primary atrial cells was stimulated from 3- to 6-fold by a variety of agents including KCl, phenylephrine, and endothelium (ET). However, in medium containing 2 nM calcium, KCl was incapable of increasing ANF secretion above basal levels, while the stimulatory effects of phenylephrine and ET were only partially diminished. Nifedipine or verapamil could mimic the effects of the 2 nM calcium medium on KCl-, phenylephrine-, and ET-stimulated ANF secretion. Kinetic studies indicated that during the initial 5 min of ET-stimulated secretion the cells exhibited little requirement for extracellular calcium; however, the requirement was more apparent during the sustained secretion observed between 10 min and 2 h of secretagogue exposure. Additionally, the stimulation of ANF secretion by ET increased to a maximum of about 15-fold over basal by 10-min after ET application; subsequent to this time there was an apparent functional desensitization wherein the rate of secretion decreased by approximately 3-4-fold and remained at this level for the duration of secretagogue exposure up to 2 h. All forms of stimulated secretion could be inhibited through ionomycin-mediated depletion of intracellular calcium pools. Taken together, these results indicate that atrial cardiocytes require both extracellular and intracellular calcium to support maximal rates of stimulated ANF secretion, and that intracellular calcium pools may be used during the early phase of secretion, while the extracellular source of calcium may be important for the sustained phase of secretion.

Adrenocorticotropic Hormone↗

PubMed1989

[Anesthesia for Shy-Drager syndrome; effects of elastic bandage, phenylephrine, and IPPV].

A 57-year-old man with Shy-Drager syndrome underwent plastic surgery for decubitus on the buttocks under general anesthesia. Before induction of anesthesia, an elastic bandage was applied to the legs, and its effects were examined by raising the upper body. The fall in mean blood pressure decreased from 49% to 39%, and the symptoms of cerebral hypoxia disappeared. However, the induction of anesthesia with 5 mg diazepam, 0.05 mg fentanyl, and 100 mg thiamylal reduced blood pressure abruptly from 150/88 mmHg to 95/68 mmHg. Continuous infusion of phenylephrine was then started, and blood pressure became stable at around 150/90 mmHg. In this state, IPPV did not reduce the blood pressure in the supine position, and did not intensify its fall when the upper body was raised. Anesthesia was maintained with nitrous oxide 70% in oxygen, fentanyl and pancuronium. During the surgery, ventilation was controlled, and phenylephrine was infused at the rate of 5-15 micrograms.min-1 to maintain systolic blood pressure above 100 mmHg. Phenylephrine was infused during the two postoperative days, because blood pressure fell whenever the patient's posture was changed to prevent pressure on the operative site.

Anesthesia↗

PubMed1989

Myosin light chain phosphorylation in 32P-labeled rabbit aorta stimulated by phorbol 12,13-dibutyrate and phenylephrine.

The mechanism(s) of force development in vascular smooth muscle following pharmacological activation of protein kinase C by phorbol esters are not known. In this study, we examined the myosin light chain phosphorylation response following stimulation by phorbol 12,13-dibutyrate (PDB) or phenylephrine in rabbit aorta which had been incubated with 32PO4 in order to label ATP pools. Through tryptic phosphopeptide mapping of myosin light chain from intact tissue and comparison to controls using purified components, we inferred that Ca2+-dependent force stimulated by PDB was associated with small increases in serine-19 phosphorylation, consistent with a contractile mechanism involving indirect activation of myosin light chain kinase. Additional residues, consistent with the in vitro substrate specificity of protein kinase C, were also observed to be phosphorylated in response to PDB and represented proportionately a larger fraction of the total phosphorylated myosin light chain in Ca2+-depleted tissues. Stimulation by an alpha 1-adrenergic agonist (phenylephrine) resulted in phosphorylation of residues which were consistent with an activation mechanism involving myosin light chain kinase only. These results indicate that in rabbit aorta the contractile effects of PDB may be partially mediated by Ca2+-dependent activation of myosin light chain kinase. However, the data do not rule out a component of the PDB-stimulated contractile response which is independent of myosin light chain phosphorylation on the serine-19 residue. In addition, activation by a more physiological stimulus, phenylephrine, does not result in protein kinase C-mediated myosin light chain phosphorylation.

Amino Acids↗

PubMed1989

Characterization of cytosolic calcium oscillations induced by phenylephrine and vasopressin in single fura-2-loaded hepatocytes.

Changes of cytosolic free Ca2+ [( Ca2+]i) in response to receptor activation were studied at the single cell level by using digital imaging fluorescence microscopy of fura-2-loaded primary cultured hepatocytes. In response to phenylephrine and vasopressin, individual hepatocytes displayed dose-dependent oscillations of [Ca2+]i similar to those observed in aequorin-injected hepatocytes by Woods et al. (Woods, N. M., Cuthbertson, K. S. R., and Cobbold, P. H. (1986) Nature 329, 719-721). With increasing agonist concentration, the frequency of oscillations increased and the latent period decreased. For a given cell, peak [Ca2+]i was independent of applied agonist concentration. However, there was considerable variation from cell to cell in the absolute value of peak [Ca2+]i. There was also marked intercellular heterogeneity in the latency, frequency, and overall pattern of the Ca2+ responses. Such asynchronous responses can be explained in part by the apparent differential agonist sensitivity of individual cells for latency and frequency. At high doses, phenylephrine maintained an oscillatory pattern, whereas vasopressin produced a complex mixture of spiking and sustained [Ca2+]i responses. Vasopressin and phenylephrine also displayed differently shaped [Ca2+]i oscillations at submaximal doses, due primarily to a slower rate of decay with vasopressin. Despite the large cell-cell variation in the patterns of [Ca2+]i oscillations, successive readditions of the same agonist elicited identical cell-specific patterns of oscillation. In the absence of extracellular Ca2+ the frequency but not the magnitude of [Ca2+]i oscillations was decreased. Buffering of [Ca2+]i by increasing the fura-2 load of single hepatocytes also decreased the frequency of oscillations without affecting the peak Ca2+ level. These data provide further support for the importance of frequency modulation in agonist-induced Ca2+ responses and suggest that Ca2+ itself plays an important role in regulating the frequency of [Ca2+]i oscillations. Furthermore, the data demonstrate a broad heterogeneity in hepatocyte [Ca2+]i oscillations which may underlie the nonoscillatory responses of cell populations.

Animals↗