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PubMed1988

Phenylephrine-induced anterior chamber hypoxia.

The effect of topical phenylephrine 10% solution on anterior chamber oxygen tension (PO2) was studied in cats using an oxygen-sensitive electrode inserted into the midanterior chamber. A decrease in anterior chamber PO2 was usually observed within eight to 25 minutes and declined steadily thereafter. Within two hours, the drug caused a dramatic 60% reduction in anterior chamber oxygen tension (P less than or equal to .0005). We suggest that the mechanism for this phenylephrine-induced anterior chamber hypoxia is reduced blood flow, mediated by the direct vasoconstrictive effect of the drug and compression of the iris vasculature (induced by dilatation). The resulting decrease in the caliber of the iris arteries produced a parallel decrease in blood volume and flow which resulted in diminished PO2. Phenylephrine 10% may contribute to hypoxia and exacerbate the underlying pathology in those disorders where hypoxia plays an important causal role.

Animals↗

PubMed1988

Nasal airway response to infused phenylephrine in normals and in patients with allergic and non-allergic rhinitis.

To find whether patients with chronic rhinitis might be congested because of hyporesponsiveness to adrenergic vasoconstrictive influences, we measured nasal airway resistance (NAR) in normals and allergic and non-allergic rhinitics during intravenous infusion of graded doses of phenylephrine. All responded with decreases in NAR and first evidences of NAR fall appeared no later in those with rhinitis than in normals. Nasal congestion and response were asymmetrical; absolute NAR in the low resistance side was similar in all groups and there was little response to phenylephrine. In the high resistance side, NAR reached its minimum by the time the total infused dose was 1400 mcg, indicating maximum response to drug was achieved within the dose range studied. Minimum NAR achieved on the high resistance side was higher in rhinitics suggesting residual vascular engorgement resistant to phenylephrine or non-vascular mucosal swelling. Resistance to adrenergic vasoconstriction does not appear to be the primary contributor to mucosal swelling in chronic rhinitis.

Airway Resistance↗

PubMed1978

Does calcium mediate the increase in potassium permeability due to phenylephrine or angiotensin II in the liver?

Two agonists, phenylephrine and angiotensin II, which have been shown to alter K+ permeability in the liver were investigated as to the possible role of Ca++ in the K+ release response (measured as 86Rb efflux) in liver slices. Both phenylephrine and angiotensin II caused transient increases in 86Rb efflux from liver slices. For both agonists, the first in a series of responses was independent of extracellular Ca++, but Ca++ was required to obtain a subsequent response. This dependence on extracellular Ca++ for a second response was not receptor-specific suggesting that activation of either receptor elicited the release of the same cellular pool of Ca++. The cationophore, A-23187, only slightly increased 45Ca++ efflux and was without effect on 86Rb efflux. In contrast to the ionophore, phenylephrine stimulated a precipitous rise in 45Ca++ efflux. It is proposed that the liver may be similar to a number of other tissues in that Ca++ mediates changes in K+ permeability, but that the source is a bound Ca++ store, rather than the extracellular space.

Angiotensin II↗

PubMed1978

[The effect of low concentrations of pilocarpine with phenylephrine on intraocular pressure in glaucoma (author's transl)].

Orientating preliminary trials showed that the reducing action of pilocarpine on intraocular pressure is considerably enhanced by adding the alpha-receptor stimulant phenylephrine. Pilocarpine eyedrops 1% and pilocarpine drops 1% with phenylephrine 0.25% were compared in two double-blind crossover studies. Pressure reduction was more pronounced after administering the combination, the width of the pupil remaining unchanged. Attention is drawn to the advantages of pressure reduction without narrowing of the pupils in the treatment of all types of open-angle glaucoma. Miosis is of therapeutical advantage only in angle-closure glaucoma; hence, for reasons of safety, administration of phenylephrine should be avoided.

Clinical Trials as Topic↗

PubMed1985

Differential effects of phorbol ester on phenylephrine and vasopressin-induced Ca2+ mobilization in isolated hepatocytes.

Receptor-mediated breakdown of PtdIns(4,5)P2 produces two cellular signals, Ins(1,4,5)P3, which can release intracellular Ca2+, and diacylglycerol, which activates a Ca2+- and phospholipid-dependent protein kinase (protein kinase C). This study assesses the significance of protein kinase C in relation to phenylephrine- and vasopressin-induced Ca2+ mobilization in hepatocytes. Phorbol ester (4 beta-phorbol-12-myristate-13-acetate), which can directly activate protein kinase C, had no effect either on Ca2+ efflux from the cell (measured with arsenazo III) or on Ca2+ influx (measured with Quin-2), processes which are inhibited and stimulated, respectively, by both phenylephrine and vasopressin. No evidence of synergism between phorbol ester pretreatment of hepatocytes and the Ca2+ ionophore (ionomycin)-mediated effects on the increase of cytosolic free Ca2+ and phosphorylase activation could be obtained. These findings suggest that protein kinase C is not obligatorily involved in the regulation of hepatocyte Ca2+ fluxes. Pretreatment of hepatocytes with phorbol ester (PMA) or 1-oleoyl-2-acetylglycerol totally inhibited the effects of phenylephrine in elevating the cytosolic free Ca2+; half-maximal inhibitory effects occurred at PMA and 1-oleoyl-2-acetylglycerol concentrations of 1 ng/ml and 12 micrograms/ml, respectively. In contrast, pretreatment with PMA had a much smaller effect on Ca2+ mobilization induced by vasopressin. These observations suggest that protein kinase C may be involved in "down-regulation" of the alpha 1-receptor in hepatocytes and may thus exert a negative influence on the Ca2+-signalling pathway.

Aminoquinolines↗

PubMed1986

Prolongation of lidocaine spinal anesthesia with epinephrine and phenylephrine.

The effect of vasoconstrictors on the duration of lidocaine spinal anesthesia is controversial. We conducted a double-blind study of 28 neurologically normal ASA Class I or II patients to determine the effect of vasoconstrictors (epinephrine and phenylephrine) on the duration of lidocaine spinal anesthesia. The patients were randomized into three groups. All patients received 1.2 mg lidocaine per inch body height, mixed with 0.5 ml of test solution. Group 1 patients received lidocaine plus 0.5 ml normal saline; Group 2 patients received lidocaine plus 0.3 mg epinephrine; Group 3 patients received lidocaine plus 5 mg phenylephrine. Segmental sensory blockade was assessed by pinprick at 2-min intervals for the first 20 min and then every 5 min thereafter. Mean highest level was between T-2 and T-3 for all 3 groups. Time from injection to highest sensory level was similar in Groups 1 and 3, 11.6 +/- 3.57 and 12.0 +/- 5.10 min, respectively, but was significantly prolonged in Group 2, 18.1 +/- 4.33 min. Time for regression by two sensory dermatomes were significantly prolonged in both Groups 2 and 3, 102.9 +/- 18.1 and 105.7 +/- 33.1 min, respectively, compared to 78.1 +/- 12.6 min in Group 1. Times for regression to T-12 was also significantly prolonged in both Groups 2 and 3, 153.7 +/- 27.6 and 156.8 +/- 26.7 min, respectively, compared to 117.71 +/- 10.0 min in Group 1. In the doses used in the present study, both epinephrine and phenylephrine significantly prolong the duration of lidocaine spinal anesthesia.

Adolescent↗

PubMed1985

[Effect of adrenaline and phenylephrine on milk extraction during the mechanical milking of cows].

During mechanical milking in the morning between days 60 and 130 of lactation, 6 or 10 French Friesian Pie-Noire (FFPN) cows were given an intrajugular injection of 0.3 mg of adrenaline or 5 mg of phenylephrine (table 1). The treatments, each given 7 times to each cow, were alternated every other day with a control injection of 0.9% NaCl. The adrenaline caused: - a non-significant decrease in total milk yield (-4.9%: 11.57 l vs 12.17 l with NaCl) and in the volume of machine-stripped milk (0.360 l vs 0.430 l with NaCl); - an increase (+8.7%) in milk flow (1.165 l/min vs 1.072 l/min with NaCl; table 4). Phenylephrine caused a significant 10% reduction in total milk yield (13.35 l vs 14.84 l with NaCl) but had no effect on the volume of machine-stripped milk (0.235 l vs 0.295 l with NaCl) or on milk flow (0.961 l/min vs 0.962 l/min with NaCl; table 3). In agreement with our previous results (Bernabé and Peeters, 1980; Bernabé and Ricordel, 1985), beta-receptor (adrenaline) stimulation appeared to increase milk flow by relaxing the teat muscles. However, when contact was avoided between the teats and the milking machine, the stimulation of teat alpha-receptors (phenylephrine) did not inhibit milk flow. It is supposed that during milking the machine caused the teat tissue to contract enough to mask the effect of the alpha-mimetic treatment on milk flow.

Animals↗

PubMed1984

The electrophysiological actions of phenylephrine on the rabbit S-A node.

This study characterizes the electrophysiologic effects of the alpha agonist phenylephrine on the rabbit sinus node. Phenylephrine increased sinus node firing rate and increased slope of Phase 4 depolarization. It shortened action potential duration. It had no effect on maximum diastolic potential or action potential amplitude. These actions were blocked by propranolol. These data imply phenylephrine may exert an effect on the sinus node through a beta-adrenoreceptor.

Action Potentials↗

PubMed1978

[Ocular blood flow of cats after local administration of pilocarpine, phenylephrine, and of a mixture of both drugs (author's transl)].

Radioactively labelled microspheres (size 15 micron) were used to determine the regional blood flow in cats before and 15, 30 and 45 minutes after unilateral drug administration. In four experimental groups, each consisting of five animals, two drops of the drug were administered into the conjunctival sac. The blood flow increased in both eyes after administration of 2% pilocarpine and of Glauko Biciron, a mixture of 2% pilocarpine and 0.06% phenylephrine. No significant differences in the regional blood flows between the treated and untreated eye were found. After administration of 2% phenylephrine a decrease in blood flow was observed in both eyes, however earlier and more pronounced in the left eye. Thus, phenylephrine evoked the expected vasoconstrictive effect on the treated side. In the control group, which received physiological salt solution, the blood flow on the treated side decreased in most tissues, while an increase was observed on the untreated side.

Administration, Topical↗

PubMed1983

Effect of hormones on urethral sensitivity to phenylephrine in normal and incontinent dogs.

The effects of stilboestrol and progesterone on pressure responses of the urethra to the alpha-adrenergic agonist, phenylephrine, were investigated in normal and incontinent ovariectomised dogs. It was found that progesterone had no significant effect on normal dogs but after pretreatment with stilboestrol the dose response curve was shifted to the left so that one third to one eighth of the original dose of phenylephrine produced the same response. In incontinent animals the sensitivity to phenylephrine was reduced compared with normal animals and stilboestrol either had no effect or only partially restored normal sensitivity. These results suggest that incontinence may result in part from decreased effectiveness of adrenergic innervation to the urethra.

Animals↗

PubMed1980

Nitroglycerin therapy for phenylephrine-induced hypertension in pregnant ewes.

Obstetrical situations in which endogenous or exogenous vasoactive amines precipitously increase maternal blood pressure and decrease uterine blood flow may be associated with increased maternal morbidity and mortality and with development of fetal acidosis and distress. We examined the effectiveness of nitroglycerin in lowering maternal blood pressure and increasing uterine blood flow during the infusion of the alpha-adrenergic agent phenylephrine. During the phenylephrine infusion maternal blood pressure increased 20%, cardiac output decreased 25%, total peripheral vascular resistance increased 60%, pulmonary arterial pressure increased 40%, uterine blood flow decreased 50%, and fetal arterial pH decreased from 7.37 to 7.30 (p less than 0.05). While maintaining the phenylephrine infusion at a constant rate, the infusion of nitroglycerin rapidly returned maternal systemic pressure and pulmonary arterial pressure to control values, decreased total peripheral resistance to 18% above control, increased cardiac output to 12% below control, increased uterine artery blood flow to 30% below control, and increased the fetal arterial pH from 7.30 to 7.35 (p less than 0.05). It is concluded that maternal hypertension resulting from intense alpha-adrenergic stimulation may be treated rapidly and effectively by the intravenous infusion of nitroglycerin with a partial restoration (20%) of uterine artery blood flow toward control.

Animals↗

PubMedDate not supplied

[Decrease of the hypertensive responses to phenylephrine in the rat submitted to a sublethal dose of E. coli endotoxin. Restoration by indomethacin (author's transl)].

E. Coli endotoxin was injected by i.v. route to rats at a dose immediately lower than the minimal lethal dose. Assays were performed on anesthetized rats (urethane 1 g/kg i.p.). The carotid arterial pressure was recorded 1, 2, 4, 16 and 24 hours after endotoxin administration, and hypertensive responses to three successive doses of phenylephrine (2; 5 or 10 micrograms/kg i.v.) was measured until return to initial values. Compared to control rats the hypertensive responses in the endotoxin-treated rats were depressed. This depression was evident at the first hour following endotoxin administration and was maintained at least for four hours. This lower response was improved by a treatment of the rats with indomethacin (10 mg/kg i.v.) when this drug was administered half an hour before, or concomitantly with endotoxin. When indomethacin (10 mg/kg) was given two hours after endotoxin the improvement was less marked. So did indomethacin at 5 mg/kg dose level. Indomethacin alone did not potentiate the pressive responses to phenylephrine. These results show that the endotoxin-induced decrease in the hypertensive responses to phenylephrine does not appear to depend on its hypotensive or lethal effects. It can be brought together with the low cardiovascular responses to different drugs found in animals under endotoxin shock. These results show moreover that an early increase in prostaglandin synthesis under the influence of endotoxin may be involved in this depressant effect.

Animals↗

PubMed1980

Effect of sodium nitroprusside on directly measured myocardial oxygen consumption during phenylephrine-induced hypertension in dogs anesthetized with halothane.

Regional myocardial O2 consumption (MVO2) was measured directly as the product of left anterior descending coronary artery blood flow and coronary arteriovenous O2 content difference in eight dogs anesthetized with 1% halothane in O2 following thiopental induction. Changes in MVO2, brought about by infusions of phenylephrine and sodium nitroprusside, were compared with simultaneously observed changes in some readily obtainable indirect induces of MVO2 such as the tension-time index and the heart rate-blood pressure product. During halothane alone average values of mean arterial pressure and regional MVO2 were, respectively, 81 mm Hg and 3.6 ml of O2/min. When mean arterial pressure was increased to 126 mm Hg (average) and held there for 27 minutes by continuously infusing a dilute solution of phenylephrine, regional MVO2 averaged 5.4 ml/min. When mean arterial pressure was lowered to 77 mm Hg for a 36-minute period by infusing sodium nitroprusside (phenylephrine infusion maintained), regional MVO2 fell to 2.5 ml/min. There was a high and significant correlation between changes in directly measured regional MVO2 and simultaneously observed changes in mean arterial pressure, tension-time index, and heart rate-blood pressure. These results indicate that during halothane anesthesia in healthy dogs, changes in readily obtainable indirect indices of MVO2 such as the tension-time index and heart rate-blood pressure product, accurately characterize changes in MVO2 directly measured.

Anesthesia↗

PubMed1980

Effect of phenoxybenzamine, propranolol, phenylephrine and isoproterenol on the circulation of rats bearing Guérin carcinoma.

Effects of phenoxybenzamine (1 mg per 100 g i.v.), propranolol (0.2 mg per 100 g i.v.), phenylephrine (0.1--0.3--1.0--3.0 micrograms per 100 g per min) and isoproterenol (0.01--0.03--0.1--0.3 micrograms per 100 g per min) were studied on cardiac output (Evans-blue dilution), organ and tumour blood flows (Sapirstein's isotope indicator dilution technique) in rats bearing Guérin carcinoma. In agreement with our earlier results data for haematocrit, blood pressure, TPR and organ vascular resistance were lower whereas cardiac index and organ blood flow were higher in control untreated tumour-bearing animals than in untreated normal rats. Phenoxybenzamine, depending on tumour size, decreased blood pressure, TPR and vascular resistance of organs, while it was found ineffective in rats with tumours of very large size (60--80 g). Propranolol treatment produced slight and similar effects in both normal and tumour-bearing rats. Phenylephrine enhanced peripheral resistance as a function of log dose in both normal and tumour bearing animals, nevertheless in the latter group it elicited more marked responses in the vascular bed of the kidneys, intestines and skin. The vasodilatory log dose dependent effect of isoproterenol was not present in tumour-bearing rats. In addition to the anaemia, the continuous decrease of alpha adrenergic activity in the systemic circulation parallel with tumour growth appears to be the most reasonable explanation for the "hyperkinesis" observed in tumour-bearing rats. Resistance of tumour vascular bed was increased by both phenoxybenzamine and propranolol. During the course of phenylephrine infusion (1.0 or 3.0 micrograms per min) the resistance of tumour vessels was more increased than that of other organs. Isoproterenol infusion resulted in a vasoconstriction of the tumour vessel. It appears that with maximally dilated vessels, vasoconstriction remains the only possible vascular response in Guérin carcinoma. In the vascular bed of the tumour a preponderance of beta adrenergic receptors also seems to be feasible.

Animals↗

PubMed1994

Arterial hypertension associated with topical ocular use of phenylephrine in dogs.

In 3 dogs scheduled for surgical removal of cataracts, systemic and topical treatment with antibiotics and topical ocular treatment with prednisolone, atropine, flurbiprofen, and phenylephrine were used to achieve maximal mydriasis, with minimal risk of pupillary constriction in response to surgery. Each dog developed arterial hypertension, with systolic, diastolic, and mean arterial pressures ranging from 170 to 205, 90 to 112, and 123 to 148 mm of Hg, respectively. Hypertension was treated with acepromazine maleate (0.001 to 0.005 mg/kg of body weight) i.v., decreasing arterial pressures to reference values. Phenylephrine dosages for topical use ranged from 50 to 367 times greater than the i.v. dose required to increase arterial pressure by 50% in anesthetized dogs. Although adverse sequelae to these episodes of hypertension were not noticed, this report documents the uptake of phenylephrine from topical ocular application and suggests the need for dose-response measurements for this adjunct to mydriatic treatment in dogs.

Acepromazine↗

PubMed1994

Enhanced contractile response to phenylephrine and increased density of [3H]PN200-110 binding sites in thoracic aorta isolated from dietary magnesium-deficient rats.

The present study was undertaken to examine whether the enhanced contractile response to phenylephrine observed in thoracic aorta isolated from dietary magnesium-deficient rats depends on an increased density of alpha 1-adrenoceptor or calcium channels. Adult male Wistar rats were fed with a magnesium-deficient diet (0.001 per cent magnesium) for 30 days with control groups (0.07 per cent magnesium). The contractile response to phenylephrine was significantly inhibited by nifedipine in both aortas without endothelium, and the degree of the inhibition was significantly greater in magnesium-deficient rats than in controls. Membranes were isolated from both thoracic aortas without endothelium, and the binding of [3H]PN200-110 or [3H]prazosin to the membranes was studied. A single binding site for [3H]PN200-110 or [3H]prazosin was evident for both membranes with high affinity. Dietary magnesium-deficiency increased significantly the maximal number (Bmax) of [3H]PN200-110 binding sites, but not Bmax of [3H]prazosin, and did not alter the binding affinity of both ligands. These results suggest that increased density of calcium channels participates in the enhanced contractile response to phenylephrine in thoracic aortas isolated from dietary magnesium-deficient rats.

Animals↗

PubMed1994

Effects of WB4101 and chloroethylclonidine on the positive and negative inotropic actions of phenylephrine in rat cardiac muscle.

This study was designed to determine if the positive and negative inotropic actions of alpha-1-adrenergic agonists in rat atrial and ventricular myocardium are mediated via different alpha-1-adrenergic receptor (AR) subtypes. Inotropic effects of phenylephrine were examined in isolated left atrial and papillary muscle before and after treatment with prazosin, WB4101 (N-[2-(2,6-dimethoxyphenoxy)ethyl]-2,3-dihydro-1,4-benzodioxin+ ++-2-methanamine), chloroethylclonidine (CEC) and WB4101 plus CEC. Phenylephrine (10 microM) elicited a monophasic positive inotropic response in left atrial muscle and a triphasic inotropic action in papillary muscle (transient positive, then negative inotropic components preceding a sustained positive inotropic response). CEC, WB4101 and prazosin each antagonized the monophasic response in isolated left atria and the sustained positive inotropic response in papillary muscle. CEC and prazosin each antagonized the transient negative inotropic component in papillary muscle. The transient positive inotropic response was not affected by CEC, WB4101 or CEC plus WB4101, but was antagonized by higher concentrations of prazosin. These data suggest that the sustained positive inotropic effect of alpha-1-adrenergic agonists in rat atrial and ventricular myocardium results from stimulation of alpha-1A and alpha-1B ARs, whereas the transient negative inotropic component of the triphasic response in ventricular preparations is mediated via alpha-1B ARs. However, present data do not exclude the possibility that the CEC-sensitive inotropic responses elicited by phenylephrine may be mediated in part by other recently described alpha-1 subtypes. The receptors involved in the transient positive inotropic action cannot be identified by current results.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1996

Clinical evaluation of carbon-11-phenylephrine: MAO-sensitive marker of cardiac sympathetic neurons.

UNLABELLED: The sympathomimetic drug phenylephrine recently has been labeled with 11C for use in PET studies of cardiac sympathetic innervation. Previous reports using isolated perfused rat heart models indicate that phenylephrine is metabolized by intraneuronal monoamine oxidase (MAO). This report compares the imaging characteristics, neuronal selectivity and kinetics of (-)-[11C]phenylephrine (PHEN) to the structurally similar but MAO-resistant analog (-)-[11C]-meta-hydroxyephedrine (HED), an established heart neuronal marker. METHODS: Fourteen healthy volunteers were studied with PET and PHEN. Ten had paired studies with HED; four of the 10 were scanned a second time with each tracer after oral administration of desipramine, a selective neuronal transport blocker. Hemodynamic and electrocardiographic responses were monitored. Blood levels of intact radiotracer and radiolabeled metabolites were determined from venous blood samples taken during the PET study. Myocardial retention indices for both tracers were calculated. RESULTS: No hemodynamic or electrocardiographic effects were observed with either tracer. PHEN showed reduced myocardial retention at 50 min compared to HED; however, image quality and uniformity of distribution were comparable. PHEN cleared from myocardium with a mean half-time of 59 +/- 5 min, while myocardial levels of HED remained constant. PHEN metabolites appeared in the blood approximately three times faster than HED metabolites. Desipramine pretreatment markedly reduced (> 60%) myocardial retention of both PHEN and HED. CONCLUSION: PHEN provides PET images of human heart comparable in quality and uniformity to HED. Like HED, PHEN localizes in the sympathetic nerves of the heart. However, the more rapid efflux of PHEN, that is likely mediated by MAO, may provide information on the functional status of cardiac sympathetic neurons unobtainable with HED.

Adult↗