SEARCH · PubMed Health

Results for “phenylephrine”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources

PubMed1993

Alpha 1-adrenoceptor subtype involved in the positive inotropic response to phenylephrine in rat atria.

Phenylephrine produced positive inotropic responses in isolated rat right and left atria. The responses were competitively inhibited by alpha 1-adrenoceptor antagonists (prazosin, WB4101 and HV723) with relatively low affinities (pA2 values close to 8.0). Chloroethylclonidine had no significant effect on the responses to phenylephrine. These results suggest that the positive inotropic response to phenylephrine in rat atria is mediated through alpha 1-adrenoceptors which cannot be defined by the alpha 1A, alpha 1B subclassification.

Acetonitriles↗

PubMed1994

Effect of carbachol in the absence and presence of phenylephrine on Rb+ efflux and tension in rabbit left atria.

The muscarinic agonist carbachol produced a concentration-dependent increase in 86Rb+ efflux and decrease in tension in isolated, electrically stimulated rabbit left atria. However, the lowest concentration of carbachol tested produced only a very small increase in 86Rb+ efflux, while it caused a relatively greater decrease in tension. 4-Aminopyridine and pertussis toxin attenuated the carbachol-stimulated 86Rb+ efflux and negative inotropic effect. However, 4-aminopyridine had a greater inhibitory effect on carbachol-stimulated 86Rb+ efflux than on carbachol-induced decreases in tension. Pre-treatment of rabbits with pertussis toxin completely abolished the increase in 86Rb+ efflux and decrease in tension produced by carbachol in the presence of the alpha-adrenoceptor agonist phenylephrine. 4-Aminopyridine attenuated the negative inotropic response to carbachol in the presence of phenylephrine, but had less effect on the carbachol-induced increase in 86Rb+ efflux under these conditions. These results suggest that carbachol-induced increases in K+ efflux may contribute at least in part to the negative inotropic responses to carbachol in the presence and absence of phenylephrine. However, this may not be sufficient to explain the direct negative inotropic response of left atria to carbachol.

4-Aminopyridine↗

PubMed1987

Increased outputs of lymphocytes in lymph efferent from the lymph nodes of sheep during systemic arterial hypertension induced by phenylephrine or dopamine.

Induced systemic arterial hypotension by intravenous nitroprusside administration and by acute arterial occlusion in sheep have been found to reduce lymphocyte traffic as mirrored in the output of lymphocytes into the efferent lymph of peripheral lymph nodes. In the present series of experiments in sheep with chronically cannulated efferent lymphatics of peripheral lymph nodes, induced and monitored systemic arterial hypertension with intravenous pump infusions of phenylephrine or dopamine both produced sharp increases in the output of lymphocytes into efferent lymph in all of 27 studies. The increases in lymphocyte output with dopamine were more sustained and less associated with evidence of lymphoid tissue damage than with phenylephrine. Phenylephrine infusions were attended by a high incidence of gross bleeding into the efferent lymph, of increased coagulability of efferent lymph in the absence of gross bleeding and of prolonged depression of lymphocyte outputs after the cessation of intravenous infusion.

Animals↗

PubMed1986

The comparative effects of epinephrine versus phenylephrine on regional cerebral blood flow during cardiopulmonary resuscitation.

Epinephrine in larger doses than currently recommended during cardiopulmonary resuscitation (CPR) has been shown to improve cerebral blood flow (CBF) following a 10-min arrest in a swine model. The purpose of this pilot study was to measure CBF during CPR, comparing high-dose epinephrine to a pure alpha-1 agonist, phenylephrine. Ten swine each weighing greater than 15 kg, were instrumented for regional CBF measurements using tracer microspheres. CBF was measured during normal sinus rhythm (NSR). Following 10 min of ventricular fibrillation, CPR was begun and regional CBF was again measured. Following 3 min of CPR, the swine were randomized to receive either epinephrine (0.2 mg/kg), or phenylephrine (0.1 mg/kg), through a peripheral intravenous line. Regional CBF was again measured 1 min after drug administration. Regional CBF following drug administration was compared using an analysis of covariance. Adjusted CBFs are expressed in ml/min per 100 g for epinephrine and phenylephrine, respectively: left cerebral cortex (12.5 vs. 2.3, P = 0.002); right cerebral cortex (13.0 vs. 2.8, P = 0.003); cerebellum (32.9 vs. 4.1, P = 0.004); midbrain (35.7 vs. 2.6, P = 0.0004), pons (30.3 vs. 2.9, P = O.006); medulla (49.5 vs. 13.6, P = 0.02) and cervical spinal cord (49.6 vs. 14.1, P = 0.003).

Animals↗

PubMed1983

Mechanism of action of phenylephrine on isolated guinea-pig atria rate.

1. Phenylephrine has a positive chronotropic effect on the right isolated guinea-pig atria and this effect is not modified by alpha-adrenergic blocker (phentolamine) but it is drastically inhibited by beta-adrenergic antagonists (practolol or propranolol). 2. The effect is substantially reduced by treatment with cocaine or pretreatment with reserpine. 3. Cocaine plus reserpine shift the dose-response curve for phenylephrine to the left. 4. It is concluded that positive chronotropic effect of phenylephrine has two components: direct action on beta-adrenergic receptors and an indirect action due to norepinephrine release.

Adrenergic alpha-Antagonists↗

PubMed1996

High-performance liquid chromatographic determination of phenylephrine and its conjugates in human plasma using solid-phase extraction and electrochemical detection.

An HPLC method for the determination of phenylephrine and its conjugates in human plasma was developed and validated. The method for quantitation involved extraction of diluted plasma (subject to hydrolysis with beta-glucuronidase for 30 min with 500 units of enzyme per 0.1 ml of plasma at 37 degrees C for the conjugates) on solid-phase weak cation-exchange cartridges followed by elution of the analyte and the internal standard (ethylnorphenylephrine) with 5% triethylamine in methanol. Analysis was carried out on a 15 cm ODS stationary phase using ion-pair reversed-phase chromatography. An electrochemical detector operated at + 1.15 V vs. Ag/AgCl was employed for detection. The standard curves were linear in the range 1.0-50.0 ng ml-1 for phenylephrine and 25.0-500.0 ng ml-1 for phenylephrine obtained from its conjugates. The limit of quantitation was 2.0 ng ml-1 (RSD = 17%) and 25.0 ng ml-1 (RSD = 18%), respectively. Acceptable accuracy and precision were obtained during intra- and inter-batch analyses for both the assays.

Adrenergic alpha-Agonists↗

PubMed1990

Preservation of ventricular function by treatment of ventricular fibrillation with phenylephrine.

Epinephrine promotes resuscitation from ventricular fibrillation because of its peripheral vasoconstrictive effects. However, the beta-adrenergic effects of epinephrine may be detrimental because of the stimulation of myocardial oxygen demand. To test whether functional recovery from fibrillation in hearts treated with a selective alpha-adrenergic agent is greater than in hearts treated with epinephrine, ventricular fibrillation was induced in eight isolated dog hearts while coronary perfusion pressure was maintained at 30 mm Hg. In random order, epinephrine (5 micrograms/min), phenylephrine (50 micrograms/min) or no drug was infused for 5 min. The heart was then defibrillated, the drug infusion stopped and coronary perfusion pressure increased to 100 mm Hg. Coronary blood flow (ml/min per 100 g), arteriovenous oxygen difference (ml O2/dl) and myocardial oxygen consumption (ml O2/min per 100 g) measured after 4 min of ventricular fibrillation were greater with epinephrine (mean +/- SD 30.9 +/- 11.7, 17.5 +/- 1.6 and 5.4 +/- 1.9, respectively) than with phenylephrine (24.4 +/- 6.0, 15.7 +/- 2.6 and 3.8 +/- 1.1, respectively) or no drug (19.8 +/- 5.2, 12.8 +/- 1.8 and 2.6 +/- 0.7, respectively) (p less than 0.05, p less than 0.05 and p less than 0.05, respectively). The slope of the end-systolic pressure-volume relation 10 min after defibrillation and restoration of normal coronary perfusion pressure was depressed (percent of prefibrillation value) most by epinephrine infusion (72 +/- 17%, n = 6), less by no drug infusion (82 +/- 12%, n = 4) and was increased after phenylephrine infusion (143 +/- 17%, n = 6) (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Effects of phenylephrine and dopamine on cerebral blood flow, blood volume, and oxygenation in young rabbits.

The effects of phenylephrine and dopamine on cerebral blood flow, blood volume, and oxygenation were studied in young rabbits using a hydrogen gas clearance method and near-infrared spectrometry. Phenylephrine infusion led to an increase in blood pressure and cerebral blood flow without changes in cerebral blood volume and oxygenation. This result suggests that phenylephrine increases arterial blood flow and vascular resistance in vascular beds which may lead to the rupture of weak vessels in premature infants. Cytochrome a, a3, however, was not affected by the drug. Conversely, a low-dose dopamine infusion had no effect on cerebral hemodynamics, but high-dose decreased blood pressure and cerebral oxyhemoglobin, and increased deoxyhemoglobin without appreciable changes in cerebral blood flow, which suggests venous congestion and arterial blood reduction in the brain.

Animals↗

PubMed1995

The effect of chronic treatment with imipramine on the responsiveness of hippocampal CA1 neurons to phenylephrine and serotonin in a chronic mild stress model of depression.

The effect of chronic mild stress (CMS) and chronic treatment with the tricyclic antidepressant drug imipramine (10 mg/kg/day for 5 weeks) on neuronal responsiveness to the alpha 1-noradrenergic agonist phenylephrine and serotonin (5-HT) was examined ex vivo, in the CA1 cell layer of the rat hippocampal slice preparation. We corroborated some previous findings that CMS, which had been used as an animal model of depression, decreased the consumption of a 1% sucrose solution and that that effect was reversed by chronic administration of imipramine. Imipramine did not change the sucrose consumption in control animals. In both control and stressed animals, phenylephrine (5 microM) and 5-HT (10 microM) attenuated the amplitude of the population spikes evoked in the CA1 pyramidal cell layer by stimulation of Schaffer collateral/commissural fibers. Those inhibitory effects of phenylephrine and 5-HT were significantly potentiated by chronic treatment with imipramine. The imipramine-induced potentiation was similar in slices from control and stressed animals. These results suggest that the imipramine-induced functional changes in alpha 1-noradrenergic and serotonergic receptors in the hippocampus are not involved in the anti-anhedonic effect of chronic imipramine administration in the CMS model of depression.

Animals↗

PubMed2006

Intraoperative assessment of mitral regurgitation: role of phenylephrine challenge.

OBJECTIVES: We defined the effects of the operative (OP) state and phenylephrine challenge on the assessment of mitral regurgitation (MR) severity. METHODS: In all, 57 patients underwent transesophageal echocardiographic assessment of MR severity pre-OP (PREOP) and intra-OP. MR severity was assessed PREOP under conscious sedation and intra-OP with general anesthesia, before and after hemodynamic manipulation with vasoactive agents, to match intra-OP and PREOP transesophageal echocardiographic mean arterial blood pressures. RESULTS: Intra-OP MR and mean arterial pressure were less than PREOP in 27 patients (both P < .001). When PREOP and OP blood pressures were matched using phenylephrine, there was no significant difference in MR severity between the two states (P = 1.0). Nonetheless, MR severity was still underestimated in 6 patients and overestimated in 7 patients intra-OP. CONCLUSIONS: Intra-OP transesophageal echocardiography underestimates MR severity. Phenylephrine reduces, yet does not eliminate, intra-OP underestimation of MR severity.

Adult↗

PubMed2006

Phenylephrine and pilocarpine eye drop test for dementia with Lewy bodies and Alzheimer's disease.

Pupillary response test using dilute phenylephrine, a sympathetic agonist, and dilute pilocarpine, a cholinergic agonist, were performed in 24 patients with dementia with Lewy bodies (DLB), 40 patients with Alzheimer's disease (AD), and 23 normal elderly subjects. The mydriatic response to 0.5% phenylephrine was significantly greater in the DLB group than in the AD and control groups. The mydriatic change correlated inversely with the reduction in cardiac 123I-metaiodobenzylguanidine uptake. In contrast, miotic response to 0.0625% pilocarpine was significantly greater in the DLB and AD groups than in the control group. The pupil assay using combined phenylephrine and pilocarpine eye drop test may be useful in the detection of patients with DLB and AD and in distinguishing between them.

3-Iodobenzylguanidine↗

PubMed2005

Angiopoietin-1 increases arteriolar vasoconstriction to phenylephrine during sepsis.

Sepsis leads to a reduction in vascular tone and a loss of vasoconstriction in response to catecholamines. We propose that angiopoietin-1 (Ang-1), which is known to modulate vascular inflammation and nitric oxide (NO), could improve responsiveness to vasopressor agents during sepsis. Mesenteric arterioles (300-400 microm) from rats (n=19) were mounted in a pressurized myograph and incubated with lipopolysaccharide (LPS, 50 microg/mL) for up to 4 h to model sepsis. Vasoconstriction (mean+/-SD) to phenylephrine (10(-8)-10(-3) M) was reduced in the presence of LPS (4 h, pD2: 5.8+/-0.2 (controls, n=6), 1.4+/-2.2 (LPS, n=6); maximal constriction: 48.2+/-4.8% (controls), 2.6+/-5.8% (LPS), P<0.05). However, in the presence of Ang-1 (250 ng/mL) phenylephrine caused greater vasoconstriction compared to LPS alone (4 h, pD2: 4.5+/-2.1; maximal constriction: 12.6+/-4.0% (n=7), P<0.05). In conclusion, Ang-1 increases vasoconstriction to phenylephrine in the presence of LPS. During sepsis therefore, Ang-1 increases vascular reactivity and has the potential to increase blood pressure and decrease vasopressor requirements in vivo.

Angiopoietin-1↗

PubMed2004

Phenylephrine and endothelin-1 upregulate connective tissue growth factor in neonatal rat cardiac myocytes.

Cardiac hypertrophy is associated with hypertrophic growth of cardiac myocytes and increased fibrosis. Much is known of the stimuli which promote myocyte hypertrophy and the changes associated with the response, but the links between the two are largely unknown. Using subtractive hybridization, we identified three genes which are acutely (<1 h) upregulated in neonatal rat ventricular myocytes exposed to the alpha-adrenergic agonist, phenylephrine. One represented connective tissue growth factor (CTGF) which is implicated in fibrosis and promotes hypertrophy in other cells. We further examined the expression of CTGF mRNA and protein in cardiac myocytes using quantitative PCR and immunoblotting, confirming that phenylephrine increased CTGF mRNA (maximal within 1 h) and protein (increased over 4 - 24 h). Endothelin-1 promoted a greater, though transient, increase in CTGF mRNA, but the increase in CTGF protein was sustained over 8 h. Neither agonist increased CTGF mRNA in cardiac non-myocytes. By increasing the expression of CTGF in cardiac myocytes, hypertrophic agonists such as phenylephrine and endothelin-1 may promote fibrosis. CTGF may also propagate the hypertrophic response initiated by these agonists.

Animals↗

PubMed1978

Hypertensive reactions to phenylephrine eyedrops in patients with sympathetic denervation.

We studied the effects of topical phenylephrine eyedrops on systemic blood pressure in 298 patients about to undergo ocular surgical procedures by comparing their blood pressure on admission to the hospital with that measured immediately before surgery. The patients were divided into three groups. Group 1 consisted of 230 patients who had neither history of insulin-dependent diabetes nor prior teatment with reserpine or guanethidine. Group 2 included 41 insulin-dependent diabetic patients. Group 3 contained 27 hypertensive patients who had been taking reserpine or guanethidine. Patients in each group were divided into two subgroups (A and B). The 202 patients in the three A subgroups received preoperative phenylephrine eyedrops, whereas the 96 patients in the three B subgroups did not. All three B subgroups and Group 1A (176 patients) did not show significant increases in blood pressure. There was a statistically significant increase in both systolic and diastolic pressures in Group 2A (14 patients) and in Group 3A (12 patients). From this study, we concluded that administration of preoperative phenylephrine eyedrops can be hazardous in patients with long-standing insulin-dependent diabetes or in hypertensive patients receiving reserpine or guanethidine.

Aged↗

PubMed2000

Effects of neutral sphingomyelinase on phenylephrine-induced vasoconstriction and Ca(2+) mobilization in rat aortic smooth muscle.

The sphingomyelin pathway is now recognized as an important signal transduction system regulating various cellular functions, in which activation of a neutral sphingomyelinase induced by various extracellular stimulants results in selective degradation of sphingomyelin, yielding bioactive lipid intermediates, ceramides and phosphorylcholine. In the present study, our emphasis has been to examine the effects of exogenous Mg(2+)-dependent neutral sphingomyelinase, in physiological and pathophysiological magnesium concentrations, on phenylephrine-induced vasomotor tone and on intracellular free Ca(2+)([Ca(2+)](i)) mobilization in vitro. Neutral sphingomyelinase (0.001-0.1 U/ml), alone, did not elicit any significant changes in either basal tension or resting levels of [Ca(2+)](i) in rat aortic smooth muscle; similar results were obtained with phosphorylcholine. However, neutral sphingomyelinase (0.001-0.1 U/ml) and C(2)-ceramide or ceramide-1-phosphate, but not phosphorylcholine, attenuated phenylephrine-induced contractions, in isolated rat aortic rings, in a concentration-related manner. The addition of extracellular magnesium in different concentrations (0, 0.3, 1.2, 2.4 mM) modulated the neutral sphingomyelinase-vasorelaxant action in a concentration-dependent manner. Neutral sphingomyelinase-evoked relaxation was only partially endothelium-dependent. Nitric oxide synthase inhibitors, N(G)-nitro-L-arginine (L-NNA) and L-N(G)-monomethyl-arginine (L-NMMA), an inhibitor of prostanoid synthesis (indomethacin), and pharmacologic amine antagonists, such as atropine, diphenhydramine, cimetidine, propranolol, and methysergide as well as an opiate antagonist, naloxone, all failed to attenuate or interfere with the vasorelaxant responses of neutral sphingomyelinase. Three different inhibitors of protein kinase C (i.e., staurosporine, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) or bisindolylmaleimide I), when used over a wide concentration range, also failed to interfere with the neutral sphingomyelinase-induced relaxations. Neutral sphingomyelinase inhibited the elevations in [Ca(2+)](i) in cultured rat aortic smooth muscle cells caused by phenylephrine. Our results suggest that a Mg(2+)-dependent sphingomyelin signaling pathway may play an important regulatory role in arterial wall tone.

Animals↗

PubMed1997

Alpha 1D-adrenoceptors play little role in the positive inotropic action of phenylephrine.

This study was designed to determine if the positive inotropic action of alpha 1-adrenergic stimulation in rat heart is mediated via alpha 1D-adrenoceptors. Isolated left atrial and papillary muscle were suspended in oxygenated Krebs-Henseleit buffer (37 degrees C) containing 1 microM nadolol and paced at 3.0 Hz. Isometric tension was continuously monitored. Cumulative concentration-response curves for phenylephrine were obtained in the presence and absence of BMY 7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspirol[4.5] decane-7,9-dione), a selective competitive alpha 1D-adrenoceptor antagonist. BMY 7378 at concentrations up to 30 nM did not significantly affect the positive inotropic response to phenylephrine. In contrast, as reported by other investigators, alpha 1D-adrenoceptor-selective concentrations of this antagonist (3 and 10 nM) did elicit a concentration-dependent right-ward shift in the vasoconstrictor response to phenylephrine in rat abdominal aorta. These data suggest that alpha 1D-adrenoceptors do not play a major role in the positive inotropic action of alpha-adrenoceptor stimulation in rat cardiac muscle.

Adrenergic alpha-Agonists↗

PubMed1987

Alcoholic cardiomyopathy in rats: inotropic responses to phenylephrine, glucagon, ouabain, and dobutamine.

The inotropic responses of chronic alcoholic and control rat hearts to phenylephrine, glucagon, ouabain, and dobutamine were studied to determine if the reported beta-adrenergic subsensitivity of alcoholic rat hearts was a specific defect. Male Long-Evans rats were maintained on nutritionally-complete liquid diets for 10 to 12 months; alcoholic rats received 38% of their calories from ethanol. Dry heart weight/body weight ratios indicated an average 15% hypertrophy of the alcoholic rat hearts. The function of isolated working hearts from these animals was studied at a constant heart rate and afterload. Ventricular function curves indicated significantly lower basal function of alcoholic rat hearts, as evident from their lower peak left ventricular relaxation rate, lower isovolumic relaxation rate, and lower peak power compared to controls. The alcoholic rat hearts had significantly lower inotropic (stroke work and peak power) responses to phenylephrine, glucagon, and dobutamine compared to controls, whereas the response of the alcoholics to ouabain was not significantly different from that of controls. Oxygen supply-to-utilization ratios decreased similarly in alcoholics and controls during treatment with the inotropic agents, as a result of increases in myocardial oxygen consumption and effects on coronary flow that were similar in both groups of animals. Thus the differences in inotropic responses observed with the alcoholic rat hearts were not primarily the result of compromised oxygen supply. Rather, the decreased stroke work response of the alcoholic hearts which occurred despite an increase in oxygen consumption suggested that the alcoholic rat hearts did not utilize oxygen as efficiently as did control hearts to perform external work. This was reflected in the significant differences between alcoholics and controls in the response of calculated external work efficiency to phenylephrine, glucagon, and dobutamine. Thus, alcohol-induced cardiac hypertrophy was associated with depressed basal left ventricular contractile function and decreased responsiveness to alpha 1-adrenergic, beta 1-adrenergic, and glucagon stimulation, but the responsiveness to ouabain was not significantly affected. These characteristics are similar to those of hearts hypertrophied by other causes.

Animals↗

PubMed1980

3. Phenylephrine hydrochloride.

Phenylephrine hydrochloride is a potent, effective, relatively safe drug with few ocular side effects. Side effects from topical instillation are uncommon but include severe systemic cardiovascular effects with elevated blood pressure and stroke. Ten percent phenylephrine should be used with caution in patients with known cardiac disease, hypertension, aneurysms, long-standing insulin-dependent diabetes, or advanced arteriosclerosis. A 2.5% concentration is generally indicated for ophthalmic examination as well as for use in infants and in the elderly. Phenylephrine should not be used in patients with narrow-angle glaucoma, and it is also contraindicated in patients taking monoamine oxidase inhibitors or tricyclic antidepressants.

Administration, Topical↗