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PubMed1991

Phenylephrine prodrug. Report of clinical trials.

The authors evaluated the mydriatic effect of phenylephrine oxazolidine prodrug, a lipophilic sympathomimetic that undergoes hydrolysis to phenylephrine as it passes through the cornea and aqueous humor. Double-masked clinical trials were performed randomizing 66 healthy subjects to receive either the silicone vehicle as a placebo, 10% viscous phenylephrine hydrochloride (HCl), or prodrug in 0.25%, 0.50%, or 1.0% concentrations. A mean horizontal pupillary diameter of 8.8 mm was achieved in 30 minutes in those receiving 1% prodrug versus 6.5 mm obtained at 30 minutes with 10% viscous phenylephrine HCl. Statistically, this difference was highly significant at P less than or equal to 0.0001. There were minimal systemic or ocular adverse effects from any preparation.

Administration, Topical↗

PubMed1975

Effects of isoprenaline and phenylephrine on plasma potassium: role of the liver.

A dog liver preparation in situ was used. Intravenous infusion of isoprenaline caused a decrease of plasma potassium levels, which was preceded, in some of the animals infused with higher doses, by a rise in plasma potassium. Propranolol abolished both these effects of isoprenaline, whereas phentolamine was devoided of effects. Liver potassium was not affected by isoprenaline infusions. Phenylephrine caused release of potassium from the liver; this effect was blocked by phentolamine, but not by propranolol. Combination of phenylephrine and isoprenaline induced a super-additive hyperkalemia. Analysis of these results led to the conclusion that the rise in plasma potassium due to phenylephrine might reflect a direct kalemotropic effect and an indirect hypoxemic effect. Isoprenaline seems to increase the hypoxemia caused by phenylephrine by opening the intrahepatic vascular shunts.

Adrenergic alpha-Antagonists↗

PubMed1978

Rat jugular vein relaxes to norepinephrine, phenylephrine and histamine.

Circular muscle of the rat external jugular vein contracted to serotonin, angiotensin and potassium chloride but not to norepinephrine, phenylephrine, histamine or carbamylcholine. In contrast, rabbit and guinea-pig jugular veins contracted to norepinephrine, phenylephrine and histamine, although contractions to norepinephrine were small in guinea-pig jugular veins. Norepinephrine, phenylephrine and histamine produced a concentration-dependent sustained relaxation of serotonin-induced contractions in the rat jugular vein, as did isoproterenol, nitroglycerin and papaverine. Propranolol blocked relaxation to norepinephrine, phenylephrine and isoproterenol whereas metiamide, a H2 receptor antagonist blocked relaxation to histamine. alpha adrenergic receptor blockade with phentolamine or prazosin resulted in greater relaxation to norepinephrine whereas cocaine did not enhance norepinephrine-induced vasodilation. This study supports the premise that norepinephrine may exert prominent beta adrenergic receptor stimulation in some blood vessels and that this effect may be more apparent in veins than arteries.

Adrenergic alpha-Antagonists↗

PubMed1989

[The effects of ephedrine and phenylephrine on arterial partial pressure of oxygen].

The changes in arterial partial pressure of oxygen were studied following intravenous injections of either ephedrine, 0.2mg.kg-1, or phenylephrine 2.5 micrograms.kg-1, to restore arterial hypotension. Eighty one adult patients underwent general anesthesia, being mechanically ventilated, were divided into two groups; both lung ventilation group (68 patients) and one lung ventilation group (13). In both lung ventilation group, PaO2/FIO2 changed from 390 +/- 132 to 400 +/- 137 mmHg, and 428 +/- 124 to 438 +/- 136 following administrations of ephedrine and phenylephrine, respectively. The results were not statistically significant. In the one lung ventilation group, PaO2/FIO2 did not change significantly from 190 +/- 45 to 186 +/- 29 with ephedrine and 267 +/- 138 to 317 +/- 230 with phenylephrine. We observed neither arrhythmia, severe hypoxemia, nor decrease in PaO2/FIO2 by more than 100mmHg. These results indicate that with respect to changes in arterial partial pressure of oxygen, the clinical doses of ephedrine and phenylephrine can be safely administered to patients under general anesthesia to restore arterial hypotension.

Adult↗

PubMed1988

[Effects of phenylephrine on atrial natriuretic factor and the renin-aldosterone axis in normal patients and essential hypertensive patients].

Phenylephrine infusions enhance diuresis and natriuresis both in normal subjects and patients with essential hypertension, whereas they have an opposite effect on urinary aldosterone excretion, decreasing it in normal subjects and enhancing it in hypertensive patients. With the new knowledge concerning the atrial natriuretic factor (ANF), it seemed a strong possibility that in normal subjects phenylephrine infusions should exert its effect through the increased release of ANF, as suggested by in vitro studies. Phenylephrine infusions at high pressor dose (to increase diastolic pressure by 25 mmHg) in six healthy volunteers increased plasma ANF and cGMP and decreased plasma renin activity and aldosterone concentrations. Urinary volume, sodium, and cGMP excretion were also increased. Phenylephrine infusions at low pressor dose (to increase diastolic pressure by 12-15 mmHg), in healthy subjects and in five patients with mild essential hypertension, significantly increased plasma ANF concentrations and decreased plasma renin activity to the same degree in both groups. But, whereas in normal subjects plasma aldosterone decreased significantly, it increased in patients with mild essential hypertension despite the simultaneous rise in plasma ANF concentration.

Adult↗

PubMed1988

Reducing cocaine solution use by promoting the use of a lidocaine-phenylephrine solution.

A program to reduce the use of cocaine solution in a university teaching hospital by promoting the use of a lidocaine-phenylephrine solution is described. To reduce the use of cocaine solution, pharmacists promoted the use of a mixture of lidocaine 3% and phenylephrine 0.25% in place of cocaine solution for nasotracheal intubation procedures. Because initial clinical use of the lidocaine-phenylephrine solution by the anesthesia service was successful, the pharmacy department began in December 1986 to actively promote use of the solution to the bronchoscopy service, the emergency service, and select inpatient nursing units. Educational measures included an article in the pharmacy and therapeutics newsletter detailing the safety and efficacy of the solution, pharmacist description of the program to physicians and nurses, and designation of the solution as a free floor stock item on nursing units. By 1988, total cocaine solution use had decreased by 66% from the 1984 average of 145.7 doses per month to an average of 50.0 doses per month; overall use of topical anesthetics remained constant. The nursing staff supported the use of the lidocaine-phenylephrine solution because it eliminated the extensive record keeping necessary for the cocaine solution. The program to decrease the amount of cocaine solution used was successful and will be expanded to other areas of the hospital.

Anesthesia↗

PubMed1986

Prolongation of lidocaine spinal anesthesia with phenylephrine.

The effect of added phenylephrine on the duration of sensory analgesia during lidocaine spinal anesthesia was determined in 65 ASA class I-III patients randomly divided into three groups. Group 1 (n = 25) received 62.5 mg lidocaine in 7.5% glucose; group 2 (n = 21) received lidocaine with 2 mg phenylephrine; and group 3 (n = 19) received lidocaine with 5 mg phenylephrine. The level of analgesia to pin prick was assessed by an anesthesiologist unaware of the drug combination used. The mean +/- SD cephalad level of analgesia did not differ among the groups. In group 1, the times for two- and for four-segment regression of the level of analgesia, and the time for regression of analgesia to the T-12 dermatome, were 77 +/- 19 (1 SD), 99 +/- 24, and 109 +/- 26 min, respectively. The corresponding values were 98 +/- 25, 118 +/- 27, and 130 +/- 36 min in group 2 and 124 +/- 32, 142 +/- 31, and 162 +/- 35 min in group 3. All the regression times in group 2 were significantly longer than those in group 1 (P less than 0.05). All the regression times in group 3 were significantly longer than those in group 2 (P less than 0.02). It is concluded that clinically useful prolongation of sensory analgesia may be obtained by addition of phenylephrine to lidocaine during spinal anesthesia.

Aged↗

PubMed1979

Effect of phenylephrine on normal and regenerated endothelial cells in cat cornea.

Topical commercial phenylephrine HCl (Neo-Synephrine 10%) has been shown to cause an increase in corneal thickness and reversible vacuolization of corneal endothelial cells in rabbits. Using an in vivo model of regenerated corneal endothelial cells in the cat, we compared the cytotoxicity of phenylephrine-HCl 10% to regenerated and to normal, nonregenerated cells. Following removal of the epithelium, topical application of the drug causes the appearance of anterior and posterior bands of stromal edema and reversible vacuolization in both normal and regenerated endothelial cells. Phenylephrine was not more damaging to the regenerated cells. Polymorphonuclear leukocytes infiltrated between the regenerating cells 24 hr after treatment but did not appear to destroy them. Phenylephrine may therefore be implicated as a causative factor of corneal edema and postoperative inflammation.

Animals↗

PubMed1983

Effects of insulin on phenylephrine-induced activation of phosphorylase and phosphatidylinositol turnover in isolated hepatocytes.

Treatment of isolated hepatocytes with the alpha-agonist phenylephrine led to a rapid increase in the activity of phosphorylase a and an increase in the rate of 32P incorporation into phosphatidylinositol. After pretreatment of the cells with insulin, this activation of phosphorylase was reduced by about 50% but there was no alteration in either the basal or phenylephrine-stimulated rate of phosphatidylinositol turnover. This difference in the sensitivity of these two processes to insulin was observed at all times and concentrations of phenylephrine examined. Direct measurement of phosphatidylinositol breakdown and phosphatidic acid formation confirmed that the activation of the phosphatidylinositol cycle by phenylephrine was not blocked by insulin. These data suggest that insulin antagonism of alpha-adrenergic effects on glycogenolysis in liver is mediated at a step distal to hormone binding to the alpha 1-receptor and activation of inositol lipid breakdown but prior to intracellular Ca2+ mobilization.

Animals↗

PubMed1984

Vasoconstrictors in spinal anesthesia with tetracaine--a comparison of epinephrine and phenylephrine.

A randomized double-blind study was conducted in 50 orthopedic patients to determine the effect of epinephrine and phenylephrine on the anesthetic properties of intrathecally administered tetracaine. Two doses of each vasoconstrictor agent were studied: 0.2 mg of epinephrine, 0.3 mg of epinephrine, 1 mg of phenylephrine, and 2 mg of phenylephrine. The results show that both vasoconstrictor agents in the doses used significantly prolong duration of sensory anesthesia and motor blockade produced by the subarachnoid administration of tetracaine. At equipotent doses no differences existed between the ability of epinephrine and phenylephrine to prolong the duration of spinal anesthesia produced by tetracaine.

Adult↗

PubMed1982

Intranasally administered phenylephrine and blood pressure.

The possibility that intranasally administered phenylephrine might cause systemic vasoconstriction and an important increase in blood pressure if administered to susceptible individuals in higher doses was investigated in two groups potentially at high risk: 12 patients with chronic nasal congestion whose blood pressure was normal and 14 patients with hypertension receiving the beta-blocker metoprolol. On two separate days increasing doses (0.5 to 4 mg) of phenylephrine or a placebo of identical appearance were instilled into the nostrils at hourly intervals. The blood pressure and the heart rate were recorded every 10 minutes. The total amount of phenylephrine administered (7.5 to 15 mg) was 4 to 30 times the manufacturer's recommended dose. No significant changes in blood pressure or heart rate occurred in either group after the instillation of phenylephrine.

Administration, Intranasal↗

PubMed1980

Blockade of the rate and force responses to phenylephrine on rat atria with labetalol.

Evidence suggests that the combined alpha and beta adrenergic agonist phenylephrine influences cardiac tissue through stimulation of both alpha and beta adrenoceptors. Phenylephrine effected a positive inotropic and chronotropic response in paced (1 Hz) left and spontaneously beating right atria, respectively. In the presence of the combined alpha and beta adrenoceptor antagonist labetalol (5 x 10(-6)M) the rate and force responses to phenylephrine were completely abolished. The data suggest that phenylephrine exerts its inotropic and chronotropic effects through both alpha and beta adrenoceptors in such a way that both adrenoceptors must be blocked in order to completely abolish the responses induced by the dual agonist.

Animals↗

PubMed1995

The effect of intravenous phenylephrine on airway calibre in asthma.

Tracheobronchial vasoconstriction and subsequent reduction of airway wall thickness due to the alpha 1-agonist methoxamine, might be responsible for prevention of exercise-induced asthma, and reduction of bronchial hyperresponsiveness to methacholine increase in exercise performance in patients with impaired left ventricular function. Since bronchial wall oedema plays an important role in asthma, we have now investigated the bronchial response to the intravenously administered alpha 1-agonist, phenylephrine, in asthma of various severity. Increasing noncumulative intravenous phenylephrine doses (100 to 600 micrograms) were injected in 18 asthmatic subjects (three groups: mild asthma, mild asthma with recent acute attack, severe obstructive asthma) and in 11 control subjects. Changes in specific airways resistance (sRaw) on phenylephrine were linearly related to the dose administered in 16 out of 18 asthmatic subjects, and in only 3 out of 11 control subjects. In the asthmatic subjects, sRaw increased in 10 patients whose asthma was mild, or bronchial obstruction mild to moderate, and decreased in the remaining 8 asthmatic subjects with more severe disease or with a higher degree of bronchial obstruction. Changes in forced expiratory volume in one second (FEV1) were consistent with those of sRaw. In the five asthmatic subjects who underwent the protocol twice, results were reproducible. There was no difference in the responses of heart rate between the three groups of asthmatic subjects. It is likely that phenylephrine acts both via airway smooth muscle contraction, an effect which might predominate in mild asthma, and via mucosal vasoconstriction, which might overcome the effect on smooth muscle in more severe asthma with bronchial wall oedema.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Differential activation of protein kinase C isoforms by endothelin-1 and phenylephrine and subsequent stimulation of p42 and p44 mitogen-activated protein kinases in ventricular myocytes cultured from neonatal rat hearts.

The translocation of protein kinase C (PKC) isoforms PKC-alpha, PKC-delta, PKC-epsilon, and PKC-zeta from soluble to particulate fractions was studied in ventricular cardiomyocytes cultured from neonatal rats. Endothelin-1 (ET-1) caused a rapid ETA receptor-mediated translocation of PKC-delta and PKC-epsilon (complete in 0.5-1 min). By 3-5 min, both isoforms were returning to the soluble fraction, but a greater proportion of PKC-epsilon remained associated with the particulate fraction. The EC50 of translocation for PKC-delta was 11-15 nM ET-1 whereas that for PKC-epsilon was 1.4-1.7 nM. Phenylephrine caused a rapid translocation of PKC-epsilon (EC50 = 0.9 microM) but the proportion lost from the soluble fraction was less than with ET-1. Translocation of PKC-delta was barely detectable with phenylephrine. Neither agonist caused any consistent translocation of PKC-alpha or PKC-zeta. Activation of p42 and p44 mitogen-activated protein kinase (MAPK) by ET-1 or phenylephrine followed more slowly (complete in 3-5 min). Phosphorylation of p42-MAPK occurred simultaneously with its activation. The proportion of the total p42-MAPK pool phosphorylated in response to ET-1 (50%) was greater than with phenylephrine (20%). In addition to activation of MAPK, an unidentified p85 protein kinase was activated by ET-1 in the soluble fraction whereas an unidentified p58 protein kinase was activated in the particulate fraction.

Amino Acid Sequence↗

PubMed1999

A retrospective analysis of left dorsal displacement of the large colon treated with phenylephrine hydrochloride and exercise in 12 horses (1996-98).

AIM: To review the outcome of cases of left dorsal displacement of the large colon (LDDLC) treated with phenylephrine HCl and mild exercise. METHODS: Physical parameters, laboratory data, ultrasonographic findings and outcome were analysed in a retrospective study of 12 horses with a confirmed diagnosis of LDDLC which were treated with phenylephrine HCl and mild exercise. RESULTS: Administration of phenylephrine HCl and mild exercise resulted in the resolution of LDDLC in 11 of 12 treated horses. One horse failed to resolve the entrapment and required surgical correction. CONCLUSION: Administration of phenylephrine HCl appears to be an effective treatment for horses with confirmed diagnosis of LDDLC presented with mild to moderate colonic distention.

Journal Article↗

PubMed2026

Effects of phenylephrine and norepinephrine with restrictive infusion on oxygenation during one-lung ventilation for lung surgery: a randomized controlled trial.

OBJECTIVE: This study compared the effects of norepinephrine or phenylephrine combined with restrictive infusion on the oxygenation during thoracoscopic one-lung ventilation (OLV). METHODS: Ninety patients were randomly divided into three groups: the norepinephrine group (Group N), the phenylephrine group (Group P), and the control group (Group C). Arterial partial pressure of oxygen (PaO2) and intrapulmonary shunt fraction (Qs/Qt) were measured with patients in lateral positions during two-lung ventilation (TLV) at 10 min (T1), and during OLV at 15 min (T2) and 45 min (T3). Lung tissue samples were analyzed for endothelin and COX-2 levels after surgery. RESULTS: At T3, Group P had significantly higher PaO2 and lower Qs/Qt than Groups N and C (all p < 0.05), with no significant differences between Groups N and C (all p > 0.05). Compared to T1, Groups N and C showed significantly lower PaO2 and higher Qs/Qt at T2 and T3 (all p < 0.05), with no significant differences in PaO2 and Qs/Qt at T3 compared with T2 (all p > 0.05). Group P patients had lower PaO2 and higher Qs/Qt at T2 and T3 compared to T1 (all p < 0.05), but at T3, PaO2 increased and Qs/Qt decreased compared to T2 (all p < 0.05). Lung tissue levels of endothelin and COX-2 were significantly elevated in group P compared to groups N and C (all p < 0.05). CONCLUSION: Combining phenylephrine with restrictive infusion during OLV improved oxygenation by increasing PaO2, decreasing Qs/Qt, and raising endothelin and COX-2 levels in lung tissue, thereby enhancing the HPV effect.

Humans↗

PubMed1979

The effect of phenylephrine on the cornea.

Rabbit corneas were treated with three drops of phenylephrine hydrochloride with the epithelium intact or denuded. Corneal thickness was measured before and after drug treatment, and at various times after treatment the corneas were fixed for scanning and transmission electron microscopic observation. The results of this study show that phenylephrine caused a dramatic increase in corneal thickness (drug-induced edema) and cellular vacuolation within the keratocytes and endothelial cells in the corneas without the epithelium. Corneal thickness did not change and the ultrastructural changes were minimal following drug application in those corneas with the epithelium intact. Results of this study also suggest that phenylephrine has a cytotoxic effect on the corneal endothelium and keratocytes when used in corneas where the epithelium has been removed. In coreas with intact epithelium, the damage was less severe and limited to the epithelium.

Animals↗

PubMed1986

Aqueous vs viscous phenylephrine. II. Mydriatic effects.

We performed four studies to determine whether there is a difference in the mydriatic effect of 2.5% aqueous vs 2.5% viscous phenylephrine hydrochloride solutions. The first study was performed under "room light" conditions, and the mean (+/- SD) dilation at one hour was 0.87 +/- 1.18 mm for the aqueous and 0.86 +/- 1.14 mm for the viscous solutions. The second study was performed in a darkened room, and the mean dilation at one hour was slightly greater than in room light but was still minimal (aqueous, 1.14 +/- 1.00 mm; viscous, 1.07 +/- 1.11 mm). In the third study, patients were pretreated with a topical anesthetic (0.5% proparacaine hydrochloride), and the mean one-hour dilation was approximately twice (aqueous, 2.30 +/- 0.81 mm; viscous, 2.41 +/- 0.88 mm) that found in patients who were not pretreated with proparacaine. In the fourth study, the two phenylephrine solutions were used in combination with 1% tropicamide, and the mean one-hour dilation was 3.8 +/- 0.82 mm for the aqueous and 3.8 +/- 0.98 mm for the viscous solutions. Our studies show that there is no difference in the mydriatic effect of 2.5% aqueous vs 2.5% viscous phenylephrine solutions when used alone or in combination with 0.5% proparacaine or 1% tropicamide.

Adult↗