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PubMed1990

Stimulation of mitochondrial pyruvate transport in rat renal cortex by phenylephrine.

Phenylephrine effect on liver and kidney cortex mitochondrial pyruvate concentration was investigated. While in liver the alpha 1-adrenergic agent produced a decrease in pyruvate content, a significant increase was observed in kidney, even in the presence of 0.5 mM alpha-cyano-4-hydroxy-cinnamate. These changes were not observed when pyruvate was formed by intramitochondrial transamination of alanine, suggesting a role for the pyruvate transport across mitochondrial membranes in the regulation of mitochondrial pyruvate metabolism in kidney cortex. This was corroborated measuring the phenylephrine effect on pyruvate carboxylation.

Alanine↗

PubMed1990

Epidermal growth factor concentrations in submandibular salivary gland, plasma, liver, bile, kidneys and urine of male mice: dynamics after phenylephrine injection.

To elucidate the dynamics of epidermal growth factor (EGF) in mice, I studied the effects of excision of the submandibular salivary gland (SMG) and intravenous injection of phenylephrine in adult male mice on the concentration of EGF in plasma, bile, urine, the SMG, the liver and the kidneys. After excision of SMG (sx), the mean concentration of EGF in the liver decreased. Phenylephrine increased the concentrations of EGF in the plasma and liver in both intact and sx mice. In the intact mice, the EGF concentrations also increased in the bile and kidneys but not in the urine. The expected dramatic decrease occurred in the SMG EGF. I conclude that alpha-adrenergic stimulation causes 1) in intact mice release of EGF from SMG into blood, from which it is excreted into bile but not into urine, and 2) release of EGF even from tissues other than SMG.

Analysis of Variance↗

PubMed1995

Effects of phenylephrine induced increase in arterial pressure and closure of the ductus arteriosus on the secretion of atrial natriuretic peptide (ANP) and renin in the ovine fetus.

Although atrial natriuretic peptide (ANP) has been detected in the plasma of late gestation fetal sheep, stimuli that control its secretion and its function in regulating fluid volume are unclear. To determine stimuli that increase ANP secretion and to ascertain whether the response is a function of gestation we studied 20 chronically cannulated fetal sheep. The fetuses were divided into 3 groups; Group I (age range 118-129 days), Group II (age range 129-141 days) and Group III (age range 127-137 days) gestation. Arterial pressure was increased to within a physiologic range by infusing phenylephrine at 6 micrograms/min at 0.1 ml/min into the inferior vena cava of the fetus (Groups I and II). Corrected for body weight fetuses in Group I received 2 micrograms/kg/min whereas fetuses in Group II received 1.66 micrograms/kg/min. In the fetuses in Group III preload to the right side of the heart was increased by inflating an occluder cuff was placed around the ductus arteriosus. Systemic mean arterial pressure (MAP) increased significantly in fetuses in Groups I and II. Plasma ANP concentrations increased significantly in all fetuses. Plasma Renin Activity (PRA) decreased significantly in the fetuses in Group II. These results suggest that phenylephrine infusion and closure of the ductus arteriosus in utero increase circulating ANP in fetal sheep.

Animals↗

PubMed1991

Suppression of feeding induced by phenylephrine microinjections within the paraventricular hypothalamus in rats.

Rats were treated with the alpha-2 agonist clonidine (4, 20 and 50 nMol) and with the alpha-1 agonist 1-phenylephrine (50, 100, 200 and 400 nMol). Phenylpropanolamine (PPA) is a phenythylamine anorectic drug that exerts direct agonist effects predominantly on alpha-1 adrenergic receptors, with some alpha-2 adrenergic activity. We recently reported that injection of PPA significantly suppressed feeding in rats. Prior studies have noted that into the paraventricular hypothalamus (PVN) microinjections of the alpha-2 adrenergic receptor agonist clonidine into the PVN induced feeding behavior in satiated rats. However, the effect on feeding of administration of alpha-1 adrenergic agonists within the PVN remains unknown. In the present study, unilateral guide cannulae aimed at the PVN were surgically implanted in adult male rats. In an initial 60 min feeding test conducted under free-feeding ("non-deprived") conditions, each rat was found to eat significantly more food after injection of 25 nMol norepinephrine (NE) into the PVN. In subsequent tests, the feeding increased significantly to 4 nMol clonidine; however, feeding was suppressed by 50 nMol clonidine. Food intake after 20 nMol clonidine was not significantly different from that recorded after vehicle. In contrast, phenylephrine (100-400 nMol) reliably suppressed feeding behavior. In the final phase of the study, the rats ate significantly less food after injection of 160 nMol PPA into the PVN but consumed significantly more food after a final injection of 25 nMol NE into the PVN. These results suggest that the anorexic action of PPA may be linked to activation of alpha-1 adrenergic receptors within the PVN.

Analysis of Variance↗

PubMed1988

Activators of protein kinase C and phenylephrine depolarize the astrocyte membrane by reducing the K+ permeability.

The membrane potential of astrocytes has been measured by monitoring the absorbance of a cyanine dye DiS-C2-(5). Ba2+, the phorbol ester 12-tetradecanoylphorbol myristateacetate (TPA) and the diglyceride, dioctanoylglycerol (DiC8) depolarize the membrane. Valinomycin which makes the membrane potential dependent on the K+ electrochemical potential evokes a hyperpolarization when added subsequently. The alpha-adrenergic receptor agonist phenylephrine was blocked by Ba2+, TPA, DiC8 and valinomycin. The results suggest that a protein kinase C-mediated reduction in the K+ permeability is responsible for the depolarizing effect of TPA, DiC8 and phenylephrine.

Animals↗

PubMed1991

In vivo activation of pineal N-acetyltransferase but not type II thyroxine 5'-deiodinase by phenylephrine in young rats.

The regulation by alpha- and beta-adrenergic agonists of pineal N-acetyltransferase (NAT) and type II thyroxine 5'-deiodinase (5'-D) in rats at either 2 or 6 weeks of age was studied. The pattern of stimulation was different because NAT activity could be clearly activated by an alpha-adrenergic agonist, phenylephrine, only in 2-week-old rats. However, isoproterenol, a beta-adrenergic agonist, was able to stimulate NAT activity in rats at both 2 and 6 weeks of life. On the other hand, phenylephrine was always ineffective in stimulating 5'-D activity, while isoproterenol clearly activated it at both ages. These results strongly suggest a role for alpha-adrenergic receptors, in addition to beta-adrenergic receptors, in regulating rat pineal NAT activity during development.

Adrenergic alpha-Agonists↗

PubMed1996

Synthesis and preliminary evaluation of [11C]-(-)-phenylephrine as a functional heart neuronal PET agent.

The in vivo behavior of (-)-[11C]phenylephrine (PHEN) is compared with the structurally similar but monoamine oxidase (MAO)-resistant analog (-)-[11C]-m-hydroxyephedrine (HED), which is an established heart neuronal marker. The chiral synthesis of PHEN has been achieved by direct methylation of (-)-m-octopamine with either 11CH3I or CF3SO311CH3. These synthetic methods produced PHEN with a specific activity ranging from 500-1000 Ci/mmol, in a radiochemical yield of > 50% (EOS) and with an enantiomeric purity of 94-96%. Biodistribution studies indicate the initial uptake of PHEN in rat heart is approximately half that of HED. Following PHEN injection, radioactivity egresses from the rat heart rapidly, with 50% washout occurring from 5 to 60 min. HED washout over this interval was less than 20%. The heart neuronal selectivity determined by desipramine blockade of the amine neuronal transporter was 75-77% compared to 92-95% for HED. Ring-labeled (-)-[3H]phenylephrine gave tissue-to-blood concentration ratios and heart clearance times very similar to PHEN. Rats pretreated with the MAO A inhibitor clorgyline showed higher levels of activity in the heart at 15 and 60 min. Tandem PET studies with PHEN and HED in the closed-chest dog provided excellent heart images with both tracers.

Animals↗

PubMed2005

Prominent positive U waves appearing with high-dose intravenous phenylephrine.

A 71-year-old woman who had critical cerebral ischemia secondary to a carotid artery occlusion was receiving high-dose intravenous phenylephrine for a trial of hypertensive therapy. While on a maximal dose of phenylephrine she developed prominent positive U waves, which disappeared with the cessation of the drug. The possible underlying electrophysiological mechanisms of this phenomenon are discussed in this paper.

Aged↗

PubMed2004

CE versus HPLC for the dissolution test in a pharmaceutical formulation containing acetaminophen, phenylephrine and chlorpheniramine.

A new polar reverse phase stationary phase has permitted our group to develop and validate an isocratic HPLC method for the simultaneous determination of acetaminophen, phenylephrine and chlorpheniramine in capsules as pharmaceutical formulation after their dissolution test. Final optimised chromatographic conditions employed a Supelco Discovery HS PEG column (polyethylene glycol), 5 microm, 15 cm x 0.46 cm. The mobile phase was 20 mM phosphate buffer at pH 7.0/acetonitrile 80:20 (v/v) at a flow rate of 1 ml/min. UV detection was performed at 210 nm for phenylephrine and chlorpheniramine and at 305 nm for acetaminophen. On the other hand, to evaluate the capability of CE to work in a routine analytical method fulfilling the pharmaceutical requirements and to study the behaviour of the technique with these compounds, we developed a CE method with the same objective. Normal and reverted polarity, the pH and concentration of the buffer, and the presence and concentration of surfactants were assayed. Forty millimolar phosphate buffer at pH 6.20 with 0.5 mM SDS at 30k V in an uncoated silica capillary provided a runtime of 4.5 min to separate the three analytes and the excipients. Moreover, parameters affecting precision in CE, such as the injection of buffer after the sample to refill the capillary were also tested. After development, the validation was performed in parallel for HPLC and CE with the same standards and samples to avoid differences due to the manipulation. The validation parameters of both techniques were adequate for the intended purpose.

Acetaminophen↗

PubMed2004

Charge-transfer complexes of phenylephrine with nitrobenzene derivatives.

The molecular charge-transfer complexes of phenylephrine with picric acid and m-dinitrobenzene have been studied and investigated by IR, 1H NMR electronic spectra in organic solvents and buffer solutions, respectively. Simple and selective methods are proposed for the determination of phenylephrine hydrochloride in bulk form and in tablets. The two methods are based on the formation of charge-transfer complexes between drug base as a n-donor (D) and picric acid, m-dinitrobenzene as pi-acceptor (A). The products exhibit absorption maxima at 497 and 560 nm in acetonitrile for picric acid and m-dinitrobenzene, respectively. The coloured product exhibits an absorption maximum at 650 nm in dioxane. The sensitive kinetic methods for the determination phynylephrine hydrochloride are described. The method is based upon a kinetic investigation of the oxidation reaction of the drug with alkaline potassium permanganate at room temperature for a fixed time at 20 min.

Electrons↗

PubMed2003

Patient safety first alert--epinephrine and phenylephrine in surgical settings.

Epinephrine and phenylephrine always should be used with extreme caution, especially in their most concentrated solutions. This is especially true in the OR where these medications are used for purposes involving extreme variations in doses and strengths. Although these medications may be handled and administered daily, clinicians must be vigilant in their efforts to ensure safe handling practices. Clinicians should monitor patients carefully for any adverse side effects. Practitioners should review up-to-date references for all products, including epinephrine and phenylephrine, and follow the recommended strategies and measures to reduce risks when preparing, handling, or administering these medications in the OR.

Adrenergic alpha-Agonists↗

PubMed2000

Effect of phenylephrine with and without atropine on QT dispersion in healthy normotensive men.

The present study examined if changes in cardiac after-load would affect QT interval dispersion. QT dispersion (QTd) on the 12-lead electrocardiogram is believed to be a noninvasive measure of electrical inhomogeneity in the heart and has recently been identified as a sensitive predictor of sudden cardiac death. In experimental models, an increase in cardiac afterload has been shown to alter action potential durations through mechanoelectrical feedback. This may result in an altered dispersion of action potential repolarization in the ventricle. Until now, there has been little evidence for this occurring in man in vivo. In the present study, the effects of afterload on QTd were examined in 10 healthy male volunteers (mean age [SD] 25 years [4.5]) who received an intravenous infusion of phenylephrine (0.2 to 3.6 microg/kg/min) given in incremental doses, and placebo in a blinded, crossover fashion. Because phenylephrine is known to alter heart rate (HR) significantly (via a reflex vagal response), the study was performed with and without atropine. We found a significant positive correlation between acute changes in blood pressure (BP) and changes in all QTd indexes (deltaQTd/delta systolic BP and deltaQTcd/deltasystolic BP r values 0.67 and 0.60, respectively; p <0.001). This relation was independent of HR changes or reflex vagal activity. Atropine had no significant effect on QTd. These observations have important clinical implications and may partly account for why sudden deaths and arrhythmic complications occur so frequently in conditions associated with increased after-load, such as hypertension and heart failure.

Adrenergic alpha-Agonists↗

PubMed1978

Effects of tricyclic antidepressants on cardiovascular responses to norepinephrine and phenylephrine during pregnancy.

The effects of imipramine and amitriptyline on the responses of the uteroplacental vasculature to norepinephrine and phenylephrine were investigated in the pregnant ewe. Experiments were performed on conscious animals in which electromagnetic flow transducers were chronically implanted on the uterine arteries. Administered alone, the tricyclic antidepressants had no effect on mean arterial pressure (MAP) or estimated uteroplacental vascular conductance (UPVCe). Following intravenous infusion of either imipramine (1 mg. per kilogram) or amitriptyline (2.5 mg. per kilogram), the pressor response to norepinephrine (1 microgram per kilogram) and the duration of that response were significantly increased (p less than 0.05). In addition, both the duration of the norepinephrine-produced decrease in uteroplacental blood flow (UPBF) and the amplitude of the decrease in UPVCe were enhanced. In contrast, responses to phenylephrine (2.5 microgram per kilogram) were unaffected by prior administration of either imipramine or amitriptyline. Of additional interest were findings suggesting differential sensitivities to alpha-agonists of the uteroplacental compared with other vascular beds. These observations bring attention to the possibility of interactions between endogenous or exogenous norepinephrine and the tricyclic antidepressants and suggest that the possibly unique sensitivities of the uteroplacental bed should be considered when prescribing drugs during pregnancy.

Amitriptyline↗

PubMed1990

The effect of phenylephrine on inositol 1,4,5-trisphosphate levels in vascular smooth muscle measured using a protein binding assay system.

This study utilizes a protein binding assay system to evaluate agonist-induced changes in inositol 1,4,5-trisphosphate (IP3) in rat aorta. Phenylephrine induced a rapid transient increase in IP3 content of rat aorta which was concentration dependent and blocked by prazosin. The concentration response curve to IP3 formation was shifted to the right of the concentration-response curve for contraction in normal calcium-containing buffer but was close to that obtained in calcium-free medium. This suggests that although IP3 may play an important role in mediating release of intracellular Ca2+, other factors (e.g. Ca2(+)-influx) may be involved in determining the magnitude of vascular smooth muscle contraction in Ca2(+)-containing solutions. Both 8-bromo cyclic GMP and sodium nitroprusside significantly attenuated the phenylephrine-induced IP3 formation. Removal of the endothelium did not alter the generation of IP3.

Animals↗

PubMed1987

Ethanol inhibits dual receptor stimulation of pineal cAMP and cGMP by vasoactive intestinal peptide and phenylephrine.

Concurrent activation of vasoactive intestinal peptide and alpha 1-adrenergic receptor resulted in greater than 20-fold increases in pineal cAMP and cGMP accumulation. We now find that an intoxicating level of ethanol (0.2%, 34 mM) inhibits greater than 50% the large increases in pineal cAMP and cGMP produced by concurrent treatment with vasoactive intestinal peptide and phenylephrine. The potency of the various alcohols tested was directly related to their chain length. This inhibition appears to be specific since a five-fold higher concentration of ethanol does not inhibit the stimulation of cAMP and cGMP accumulation produced by concurrent treatment with isoproterenol and phenylephrine. Accordingly, it seems that one mechanism of action of ethanol on neural function may be its ability to selectively inhibit ethanol-sensitive integrative mechanisms which regulate cyclic nucleotides.

Alcohols↗

PubMed1988

Adenosine inhibits phenylephrine activation of phospholipase A in hamster brown adipocytes.

Exposure of brown adipocytes to phenylephrine activates a phospholipase A2 producing arachidonic acid and lysophospholipids. When adipocytes were incubated with adenosine deaminase, a greater release of arachidonic acid and accumulation of lysophosphatidyl-choline in response to phenylephrine was noted. The potentiating effect of adenosine deaminase was also observed in the presence of A23187 and for both stimuli, the effect of adenosine deaminase was reversed by phenylisopropyladenosine. These results suggest the presence of an heretofore unrecognized action of adenosine, namely inhibition of phospholipase A2 activity in brown fat cells.

Adenosine↗

PubMed2000

Effects of ouabain on the pressor response to phenylephrine and on the sodium pump activity in diabetic rats.

The diabetes mellitus insulin-dependent is usually associated with cardiovascular disorders and with changes in the activity of the Na(+),K(+)-ATPase. The effects of ouabain, a Na(+),K(+)-ATPase inhibitor, on the pressor response of 7-day streptozotocin-induced diabetes were investigated in anesthetized rats and on the vascular reactivity of the perfused rat tail vascular bed. Diabetes was characterized by hyperglycemia (86+/-7.8 vs. 471+/-18.5 mg/dl) without changes in arterial blood pressure. Blood pressure increased after the treatment with 18 microg/kg ouabain in controls but not in diabetic rats; acute hyperglycemia, in non-treated rats, did not change these effects. Control tail vascular beds showed increased maximal response to phenylephrine after treatment with 10 nM ouabain for 1 h; this response was abolished in streptozotocin-treated rats. These rats showed an increased sensitivity to phenylephrine without changing the maximal vasoconstrictor response when compared to control rats. The relaxation induced by acetylcholine was reduced in diabetic rats. The functional activity of the Na(+),K(+)-ATPase was inhibited in vascular beds from diabetic rats, when compared to control rats, and the inhibition of the Na(+),K(+)-ATPase with 10 nM ouabain was not effective in these rats. Results suggested that in 7-day diabetic rats, the increase of arterial blood pressure or the sensitization of the vascular bed produced by ouabain is lost as a consequence of the reduction of the functional activity of the Na(+), K(+)-ATPase probably as a result of insulin lack and a deficient endothelial nitric oxide activity.

Anesthesia↗

PubMed1991

Treatment of pharmacological priapism with phenylephrine.

Pharmacological prolonged erections or priapism due to anesthesia were treated in 36 patients with intracorporeal injections of phenylephrine. Detumescence was obtained rapidly in every case and no marked side effect was reported. Considering the possible toxicity of other adrenergic agents, phenylephrine is strongly recommended in the treatment of priapism.

Adult↗