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PubMed1995

The circulatory regulation of TPA and UPA secretion, clearance, and inhibition during exercise and during the infusion of isoproterenol and phenylephrine.

BACKGROUND: Exercise to exhaustion and infusions of isoproterenol and phenylephrine were used to study interactions between plasminogen activator regulation and the control of regional blood flow in 10 healthy males. METHODS AND RESULTS: Experimental measurements of cardiac output, heart rate, tissue plasminogen activator (TPA), urokinase plasminogen activator (UPA), plasminogen activator inhibitor (PAI-1), C1-inhibitor, and TPA/C1-inhibitor complex during the infusions and exercise were used to develop a comprehensive fluid-phase model of the circulatory regulation of fibrinolysis. alpha- and beta-adrenergic agonists increased TPA and UPA in plasma by different mechanisms: Phenylephrine decreased hepatic blood flow and thus clearance while isoproterenol stimulated increased secretion of TPA and UPA. Exercise to exhaustion increased TPA and UPA through a combination of increased secretion and decreased clearance. The time course of UPA and TPA release were similar, but the magnitude of their secretion responses differed. In vivo, C1-inhibitor bound to TPA at a rate of 553 mol-1.s-1. C1-inhibitor contributed equally with PAI-1 to TPA inhibition when active PAI-1 levels were low (20 to 50 pmol/L) but was less important when active PAI-1 levels were high. CONCLUSIONS: We conclude that secretion, inhibition, clearance, and regional blood flow effects must all be taken into account when evaluating changes in plasminogen activator levels.

Adrenergic alpha-Agonists↗

PubMed1996

Noninvasive assessment of baroreflex control in borderline hypertension. Comparison with the phenylephrine method.

In this study, we examined the sensitivity of two recently developed noninvasive baroreflex measurement techniques to assess baroreflex control in hypertension. We assessed baroreflex sensitivity noninvasively from covariations of systolic pressure and RR interval using spectral analysis and sequence detection. The noninvasive estimates of baroreflex control were compared with estimates derived from phenylephrine-induced increases in systolic pressure and RR interval in normotensive subjects (n = 27) and borderline hypertensive subjects (n = 15). Baroreflex sensitivity was significantly reduced in the borderline hypertensive group relative to the normotensive group when assessed with the use of either the noninvasive or invasive methods to index baroreflex control. In addition, estimates obtained from the noninvasive methods were significantly correlated with baroreflex sensitivity assessed with the phenylephrine method (spectral: r = .48, P < .001; sequence: r = .50, P < .001). These findings suggest that spectral analysis and the sequence method provide viable alternatives to the pharmacological approach for estimation of baroreflex sensitivity in hypertension.

Adult↗

PubMed1996

Depletion of mitogen-activated protein kinase using an antisense oligodeoxynucleotide approach downregulates the phenylephrine-induced hypertrophic response in rat cardiac myocytes.

An antisense oligodeoxynucleotide (ODN) approach was used to investigate whether mitogen-activated protein kinase (MAPK) is necessary for the hypertrophic response in cardiac myocytes. A phosphorothioate-protected 17-mer directed against the initiation of translation sites of the p42 and p44 MAPK isoform mRNAs was introduced into cultured cardiac myocytes by liposomal transfection. At an antisense ODN concentration of 0.2 mumol/L, p42 MAPK protein was reduced by 82% (immunoblot) after 48 hours, and p42 and p44 MAPK activities were reduced by 44% and 60%, respectively. The same concentration of anti-MAPK ODN inhibited development of the morphological features of hypertrophy (sarcomerogenesis, increased cell size) in myocytes exposed to phenylephrine. Phenylephrine-induced activation of the atrial natriuretic factor (ANF) promoter (measured by the activity of a transfected ANF promoter/luciferase reporter gene) and induction of ANF mRNA (measured by RNase protection assay) were also attenuated. We conclude that MAPK is important for the development of the hypertrophic phenotype in this model of hypertrophy.

Amino Acid Sequence↗

PubMed1987

Phenylephrine-induced reversible cataract in the mouse.

Topical 10% phenylephrine will produce lens opacities in several strains of mouse. These lens opacities resolve spontaneously within 24 hours, leaving an apparently normal eye. Phenylephrine-induced lens opacification in the mouse can be prevented by covering the eye with ointment, suggesting that the underlying mechanism is transcorneal dehydration.

Animals↗

PubMed1990

Third place--Resident Clinical Science Award 1990. The in vivo and in vitro effect of phenylephrine (Neo Synephrine) on nasal ciliary beat frequency and mucociliary transport.

Twenty volunteers with normal noses were studied to determine the effect of phenylephrine on nasal ciliary function. In vivo study of this drug was performed in 15 patients and revealed a significant increase in their ciliary beat frequency from a control of 11 Hz to 12.03 Hz (p = 0.001). Mucociliary transit times in these volunteers were also studied, revealing a mean of 9.9 minutes prestimulation and 10.2 minutes poststimulation, which was not statistically significant (p = 0.77). Five additional subjects donated ciliated mucosal samples for in vitro analysis of varying concentrations of this agent that showed a significant ciliostimulatory effect at lower concentrations (0.01%), with a progressive cilioinhibitory effect at higher concentrations (0.25%, 0.5%). The 0.05% concentration showed no significant change in ciliary activity compared to control measurements. These data demonstrate that phenylephrine has a ciliostimulatory effect in vivo, as well as in appropriate concentrations in vitro, and should be safe and relatively nontoxic to the mucociliary apparatus for short-term use.

Awards and Prizes↗

PubMed1993

The effect of phenylephrine bolus administration on left ventricular function during isoflurane-induced hypotension.

By using transesophageal echocardiography, we examined the effect of phenylephrine (PHE) bolus administration on left ventricular function in 16 patients with no known cardiovascular disease during isoflurane-induced hypotension. PHE was compared with norepinephrine (NE). The patients received an intravenous bolus of PHE (2 micrograms/kg) or NE (0.1 microgram/kg) in random order. The second substance was administered after levels of arterial blood pressure and heart rate returned to baseline levels. We determined fractional area change, end-systolic wall stress, and rate-corrected mean velocity of circumferential fiber shortening. Both substances effectively restored arterial blood pressure. However, after PHE, fractional area change decreased from 0.45 to 0.31 (mean) and rate corrected mean velocity of circumferential fiber shortening from 0.88 to 0.57 circumference/s, whereas both variables remained unchanged in response to NE. End-systolic wall stress increased after PHE and NE from 47.4 to 91.2 and from 54.0 to 65.2 10(3) dyne/cm2, respectively. We conclude that phenylephrine, given as intravenous bolus to patients under isoflurane hypotension, causes a transient impairment of left ventricular systolic performance.

Adult↗

PubMed1979

Cerebral arterial spasm: part 9. In vitro effects of nifedipine on serotonin-, phenylephrine-, and potassium-induced contractions of canine basilar and femoral arteries.

We performed in vitro experiments with a small volume chamber to determine the inhibitory effect of nifedipine on serotonin-, phenylephrine-, and potassium-induced contractions of canine basilar and femoral arteries. Nifedipine, an inhibitor of the influx of extracellular calcium into smooth muscle cells, was found to be a sensitive inhibitor of contractions of the basilar artery induced by all three agents. In contrast, nifedipine did not significantly inhibit the serotonin- and phenylephrine-induced contractions of the femoral artery but did inhibit potassium-induced contractions of the femoral artery. Calcium-induced contractions of the basilar artery were also inhibited by nifedipine. These experiments demonstrate a relatively selective effect of nifedipine on the basilar artery, and a mechanism to explain this selective effect is postulated.

Animals↗

PubMed1979

Treatment of subarachnoid hemorrhage with sodium nitroprusside and phenylephrine: an experimental study.

The effectiveness of simultaneous intravenous sodium nitroprusside and phenylephrine in improving the cerebrovascular disturbances and survival rate after induced subarachnoid hemorrhage (SAH) was studied in the cynomolgus monkey. We measured regional cerebral blood flow (rCBF) using the intra-arterial xenon-133 clearance technique. In our experimental animal model, SAH was associated with a persistent reduction in rCBF, elevation of cerebrovascular resistance (CVR), cerebral vasospasm for the duration of the study (150 minutes), and poor survival. For animals receiving the treatment regime (administered approximately 25 minutes after the induced SAH), rCBF remained low, CVR was high, and cerebral vasospasm was persistent. Survival in this group was the same as that observed for the untreated animals. Simultaneous administration of sodium nitroprusside and phenylephrine was ineffective in improving rCBF, CVR, cerebral vasospasm, or survival after SAH. In the control group (receiving only the treatment and not an intracranial insult), rCBF was below resting levels both during and after therapy, indicating impaired cerebral autoregulation. (Neurosurgery, 5: 688--595, 1979).

Animals↗

PubMed2005

Comparison of the inhibitory effects of docosahexaenoic acid (DHA) on U46619- and phenylephrine-induced contractions in guinea-pig aorta.

Inhibitory effects of docosahexaenoic acid (DHA) on the muscle contractions induced by U46619, a thromboxane A2 (TXA2) mimetic, and phenylephrine were compared in guinea-pig aorta. In de-endothelialized guinea-pig aortic ring preparations, DHA at 10 microM strongly inhibited a sustained contraction produced by U46619 (3-100 nM) whereas it did not exhibit an appreciable effect on phenylephrine (3-10 microM)-induced contraction. The present findings indicate that DHA inhibits more selectively TXA2 receptor (TP receptor)-mediated vascular contraction than alpha-adrenoceptor-mediated response. Selective inhibition by DHA of TP receptor-mediated contraction of blood vessels seems underlie in part the mechanisms by which this polyunsaturated fatty acid exerts its circulatory-protective effects.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1986

Effects of vasopressin, angiotensin II and phenylephrine on hepatic ketogenesis and fatty acid synthesis.

Studies were conducted to clarify the effects of vasopressin, angiotensin II and phenylephrine on hepatic ketogenesis and fatty acid synthesis. Hepatocytes from fed rats were incubated with oleate or octanoate. Vasopressin stimulated fatty acid synthesis as well as lactate and pyruvate accumulation in the presence of oleate. In accordance with this action, vasopressin caused a marked decrease in ketogenesis from oleate. When octanoate was added as a substrate, vasopressin failed to inhibit ketogenesis. Neither angiotensin II nor phenylephrine affected ketogenesis or fatty acid synthesis. The results in the present study show that there are vasopressin-mediated reciprocal changes in ketogenesis from oleate and fatty acid synthesis in isolated hepatocytes.

Angiotensin II↗

PubMed2005

Responsiveness of vascular alpha1-adrenoceptors of diabetic rat knee joint to phenylephrine in acute inflammation.

In diabetic angiopathy, responsiveness of alphal-adrenoceptors in blood vessels increases. The aim of this study was to investigate the vasoconstrictor response of knee joint blood vessels to phenylephrine (a 1-adrenoceptor agonist) in diabetes and acute inflammation. Acute knee joint inflammation was induced by the intraarticular injection of a 3% kaolin/3% carrageenan suspension. Diabetes was induced by the intravenous injection of alloxan (70 mg/kg). Male albino rats weighing 70 to 90 g each were divided into the following 4 groups: untreated controls, diabetic, inflammatory, and diabetic inflammatory. The blood flow of the knee joint was measured using the laser Doppler flowmetry (LDF) technique. Vasoconstriction of the articular microvascular was measured in response to the topical application of different concentrations (10(-7) to 10(-3) mol) phenylephrine. The results of this study show that (a) increased knee joint diameter and circumference due to inflammation and the knee joint basal blood flow were significantly lower in diabetic than in control rats; (b) the responsiveness of alphal-adrenoceptors decreased in kaolin/carrageenan-induced acute inflammation; (c) carrageenan-induced acute inflammation did not decrease the responsiveness of alphal-adrenoceptors in diabetic rats. We conclude that diabetes inhibits the reductive effect of acute inflammation on the responsiveness of alpha1-adrenoceptors in rats.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

[The pupil in the chronic phase of Chagas disease and the reaction to pilocarpine and phenylephrine].

To develop a method to analyse pupillary disturbances in patients with chronic Chagas disease in an endemic area, ten chagasic and ten normal subjects were matched according to sex, age and race. Pupillary diameter and area were determined using projection and topography techniques and compared between groups. Both pupils were visualised simultaneously. In each case three photographs were taken under standardised illumination. The first photo was obtained without medication, the second, 30 minutes after instillation of 0,1% pilocarpine and the last 30 minutes after instillation of 3% phenylephrine (60 minutes after pilocarpine). Pupils of chagasic patients had a statistically significant greater initial diameter and area, irregularity of the pupil border, greater percentual reduction in diameter and area after pilocarpine 0.1% and greater percentual increase in diameter and area after 3% phenylephrine eyedrops. The method developed for this study was considered satisfactory. The results suggest ocular autonomic nervous system disturbances in chagasic patients.

Chagas Disease↗

PubMed1977

Effect of topical application of phenylephrine hydrochloride on hyperplastic gingivitis.

A double blind study was conducted to evaluate the effectiveness of Phenodent Type A (brand of phenylephrine hydrochloride) on decongesting hyperplastic gingivitis. Three solutions were used: a 0.5% a placebo, and a 0.25% concentration of phenylephrine hydrochloride. The periodontal disease index was used to score variables which might have an effect on gingival response to local irritants. Impressions were taken and casts were made on 45 subjects at 0, 1, 3, and 6-week intervals. An instrument with accuracy of 0.001 inch was constructed to measure the changes in the interdental papillae of the stone casts. No significant reduction of gingival volume was established for any of the three solutions.

Administration, Topical↗

PubMed2006

Accuracy of an oscillometric blood pressure monitor during phenylephrine-induced hypertension in dogs.

OBJECTIVE: To examine the agreement between direct arterial blood pressure measurements obtained from 2 arteries and indirect blood pressure measurements obtained with an oscillometric blood pressure monitor (OBPM) during normotension and phenylephrine-induced hypertension in dogs. ANIMALS: 16 male Beagles. PROCEDURES: In anesthetized dogs, arterial catheters were placed in the lingual and dorsal pedal arteries for measurement of arterial blood pressure. A blood pressure cuff was placed on either the dog's fore- or hind limb and connected to an OBPM. Systolic, diastolic, and mean arterial blood pressures (SAP, DAP, and MAP, respectively) were recorded from both arteries and the OBPM every 5 minutes for 30 minutes (baseline), during a 30-minute period in which dogs received a phenylephrine infusion IV to induce hypertension, and for 30 minutes after discontinuation of the infusion. Mean differences in blood pressure values and confidence intervals were calculated to compare the indirect and direct measurement techniques. RESULTS: In dogs, oscillometry underestimated SAP during normotension, and the difference between oscillometric and direct measurements increased during hypertension. Oscillometry underestimated DAP, but the difference between oscillometric and direct measurements decreased during hypertension. There was close agreement among techniques for MAP determinations. Biases between direct measurements and OPBM blood pressure values measured from dogs' forelimbs or hind limbs were not significantly different. CONCLUSIONS AND CLINICAL RELEVANCE: In normotensive dogs, oscillometric measurements of MAP and SAP agreed more closely with direct arterial pressure measurements than oscillometric estimates of DAP. Oscillometric measurement of MAP was accurate during both normotension and hypertension in dogs.

Animals↗

PubMed1988

Toxicity and carcinogenicity studies of phenylephrine hydrochloride in F344/N rats and B6C3F1 mice.

Phenylephrine HCl was incorporated into feed given to male and female F344/N rats and B6C3F1 mice in studies of 14 days, 12 weeks, and 2 years duration. In 12-week studies, body weight gains decreased with dose, and deaths of male rats and mice occurred at concentrations of 5,000 ppm and above; however, no organ-specific toxicity was evident. During 2-year studies, body weights of rats receiving diets at 620 and 1,250 ppm and mice at 1,250 and 2,500 ppm ranged up to 16% less than control. Survival of high dose male rats was substantially greater than controls. Survivals of other dose groups of rats and mice were similar to controls. Chronic focal inflammation of the liver, and inflammation of the prostate were increased in dosed rats. No increases in neoplasms were observed in rats or mice consuming diets containing phenylephrine HCl for 2 years. The incidences of mononuclear cell leukemia and pheochromocytomas of the adrenal gland were decreased in dosed male rats. Approximate time weighted average doses ranged up to 54 mg/kg/day for rats and 280 mg/kg/day for mice during the 2-year studies.

Adrenal Glands↗

PubMedDate not supplied

Effect of phenylephrine on aqueous humor flow.

The effect of topical 2.5% phenylephrine hydrochloride, an alpha adrenergic agonist, on the rate of aqueous humor flow was studied in the eyes of 22 normal human subjects. The drug and a placebo were administered by random assignment from coded containers with the fellow eye serving as the control. Intraocular pressure, anterior chamber volume, corneal thickness and the rate of clearance of topically applied fluorescein from the anterior chamber were measured. Four of the 22 subjects underwent a study of the effect of phenylephrine on the permeability to fluorescein of the blood-aqueous barrier. No statistically significant effect of the drug was found on the rate of aqueous humor flow, intraocular pressure, anterior chamber volume, corneal thickness or permeability of the blood-aqueous barrier.

Anterior Chamber↗

PubMed1999

Sensitivity of [11C]phenylephrine kinetics to monoamine oxidase activity in normal human heart.

UNLABELLED: Phenylephrine labeled with 11C was developed as a radiotracer for imaging studies of cardiac sympathetic nerves with PET. A structural analog of norepinephrine, (-)-[11C]phenylephrine (PHEN) is transported into cardiac sympathetic nerve varicosities by the neuronal norepinephrine transporter and stored in vesicles. PHEN is also a substrate for monoamine oxidase (MAO). The goal of this study was to assess the importance of neuronal MAO activity on the kinetics of PHEN in the normal human heart. MAO metabolism of PHEN was inhibited at the tracer level by substituting deuterium atoms for the two hydrogen atoms at the alpha-carbon side chain position to yield the MAO-resistant analog D2-PHEN. METHODS: Paired PET studies of PHEN and D2-PHEN were performed in six normal volunteers. Hemodynamic and electrocardiographic responses were monitored. Blood levels of intact radiotracer and radiolabeled metabolites were measured in venous samples taken during the 60 min dynamic PET study. Myocardial retention of the tracers was regionally quantified as a retention index. Tracer efflux between 6 and 50 min after tracer injection was fit to a single exponential process to obtain a washout half-time for all left ventricular regions. RESULTS: Although initial heart uptake of the two tracers was similar, D2-PHEN cleared from the heart 2.6 times more slowly than PHEN (mean half-time 155+/-52 versus 55+/-10 min, respectively; P < 0.01). Correspondingly, heart retention of D2-PHEN at 40-60 min after tracer injection was higher than PHEN (mean retention indices 0.086+/-0.018 versus 0.066+/-0.011 mL blood/ min/mL tissue, respectively; P < 0.003). CONCLUSION: Efflux of radioactivity from normal human heart after uptake of PHEN is primarily due to metabolism of the tracer by neuronal MAO. Related mechanistic studies in the isolated rat heart indicate that vesicular storage of PHEN protects the tracer from rapid metabolism by neuronal MAO, suggesting that MAO metabolism of PHEN leaking from storage vesicles leads to the gradual loss of PHEN from the neurons. Thus, although MAO metabolism influences the rate of clearance of PHEN from the neurons, MAO metabolism is not the rate-determining step in the observed efflux rate under normal conditions. Rather, the rate at which PHEN leaks from storage vesicles is likely to be the rate-limiting step in the observed efflux rate.

Adult↗

PubMed1999

Influence of vesicular storage and monoamine oxidase activity on [11C]phenylephrine kinetics: studies in isolated rat heart.

UNLABELLED: [11C]Phenylephrine (PHEN) is a radiolabeled analogue of norepinephrine that is transported into cardiac sympathetic nerve varicosities by the neuronal norepinephrine transporter and taken up into storage vesicles localized within the nerve varicosities by the vesicular monoamine transporter. PHEN is structurally related to two previously developed sympathetic nerve markers: [11C]-meta-hydroxyephedrine and [11C]epinephrine. To better characterize the neuronal handling of PHEN, particularly its sensitivity to neuronal monoamine oxidase (MAO) activity, kinetic studies in an isolated working rat heart system were performed. METHODS: Radiotracer was administered to the isolated working heart as a 10-min constant infusion followed by a 110-min washout period. Two distinctly different approaches were used to assess the sensitivity of the kinetics of PHEN to MAO activity. In the first approach, oxidation of PHEN by MAO was inhibited at the enzymatic level with the MAO inhibitor pargyline. In the second approach, the two hydrogen atoms on the a-carbon of the side chain of PHEN were replaced with deuterium atoms ([11C](-)-alpha-alpha-dideutero-phenylephrine [D2-PHEN]) to inhibit MAO activity at the tracer level. The importance of vesicular uptake on the kinetics of PHEN and D2-PHEN was assessed by inhibiting vesicular monoamine transporter-mediated storage into vesicles with reserpine. RESULTS: Under control conditions, PHEN initially accumulated into the heart at a rate of 0.72+/-0.15 mL/min/g wet. Inhibition of MAO activity with either pargyline or di-deuterium substitution did not significantly alter this rate. However, MAO inhibition did significantly slow the clearance of radioactivity from the heart during the washout phase of the study. Blocking vesicular uptake with reserpine reduced the initial uptake rates of PHEN and D2-PHEN, as well as greatly accelerated the clearance of radioactivity from the heart during washout. CONCLUSION: These studies indicate that PHEN kinetics are sensitive to neuronal MAO activity. Under normal conditions, efficient vesicular storage of PHEN serves to protect the tracer from rapid metabolism by neuronal MAO. However, it is likely that leakage of PHEN from the storage vesicles and subsequent metabolism by MAO lead to an appreciable clearance of radioactivity from the heart.

Animals↗