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PubMed2004

Obligatory role for endogenous endothelin in mediating the hypertrophic effects of phenylephrine and angiotensin II in neonatal rat ventricular myocytes: evidence for two distinct mechanisms for endothelin regulation.

Various Gq protein-coupled receptor agonists such as the alpha1 adrenoceptor agonist phenylephrine, angiotensin II, and endothelin-1 are potent hypertrophic factors. There is evidence of potential cross talk between these agents, particularly in terms of endothelin-1 as playing a central role in mediating the actions of other hypertrophic factors. Using cultured rat neonatal ventricular myocytes, we assessed the potential cross talk between these factors and sought to examine the potential underlying mechanisms. Twenty-four-hour exposure to either agent produced significant hypertrophy as determined by cell size and molecular markers. Although the hypertrophic effects of phenylephrine and angiotensin II were expectedly prevented by alpha1 and AT1 receptor antagonists, respectively, these effects were also blocked by the ETA receptor antagonist BQ123 [cyclo(D-Asp-Pro-D-Val-Leu-D-Trp)] but not by the ETB antagonist BQ788 (N-cis-2,6-dimethylpiperidinocarbonyl-L-gamma-methylleucyl-D-1-methoxycarbonyltryptophanyl-D-norleucine). Both phenylephrine and angiotensin II significantly increased protein expression of both endothelin receptor subtypes. Both phenylephrine and angiotensin II produced significant activation of p38 as well as extracellular signal-regulated protein kinase and c-Jun NH2-terminal kinase, although this was unaffected by endothelin receptor blockade. Further studies revealed that the effects of phenylephrine and angiotensin II were mediated by stimulated endothelin-1 production occurring via two separate mechanisms: angiotensin II by increasing the levels of the endothelin-1 precursor prepro endothelin-1 and phenylephrine by upregulating endothelin-converting enzyme 1. Our results indicate that the endothelin-1 system plays an obligatory role in the hypertrophic response to both phenylephrine and angiotensin II in cultured myocytes through a mechanism independent of mitogenactivated protein kinase activation.

Angiotensin II↗

PubMed2004

Inhibition of phenylephrine-induced cardiomyocyte hypertrophy by activation of multiple adenosine receptor subtypes.

Plasma adenosine levels are elevated in cardiovascular disease including hypertension and heart failure, and the nucleoside has been proposed to serve as an endogenous antimyocardial remodeling factor. We studied the modulation of phenylephrine-induced hypertrophy by adenosine receptor activation in isolated neonatal cultured ventricular myocytes. Phenylephrine (10 muM) increased cell size by 35% and significantly increased expression of atrial natriuretic peptide. These effects were reduced by the stable adenosine analog 2-chloroadenosine and were completely blocked by the adenosine A(1) receptor agonist N(6)-cyclopentyladenosine (1 microM), the A(2A) receptor agonist 2-p-(2-carboxyethyl)-phenethylamino-5'-N-ethylcarboxamidoadenosine (100 nM), and the A(3) receptor agonist N(6)-(3-iodobenzyl)adenosine-5'-methyluronamide (100 nM). The antihypertrophic effects of all three agonists were completely reversed by their respective antagonists. Phenylephrine significantly up-regulated expression of the immediate early gene c-fos especially within the first 30 min of phenylephrine treatment. These effects were almost completely inhibited by all adenosine receptor agonists. Although phenylephrine also induced early stimulation of both p38 mitogen-activated protein kinase and extracellular signal-regulated kinase, these responses were unaffected by adenosine agonists. The expression of the G-protein regulatory factors RGS2 and RGS4 were increased by nearly 3-fold by phenylephrine treatment although this was completely prevented by adenosine receptor agonists. These agents also blocked the ability of phenylephrine to up-regulate Na/H exchange isoform 1 (NHE1) expression in hypertrophied myocytes. Thus, our results demonstrate an antihypertrophic effect of adenosine acting via multiple receptor subtypes through a mechanism involving down-regulation of NHE1 expression. The ability to prevent regulators of G-protein signaling (RGS) up-regulation further suggests that adenosine receptor activation minimizes signaling which leads to hypertrophic responses.

Adenosine↗

PubMed2005

Haeme oxygenase mediates hyporeactivity to phenylephrine in the mesenteric vessels of cirrhotic rats with ascites.

BACKGROUND AND AIMS: Haeme oxygenase could play a role in the pathogenesis of arterial vasodilation in cirrhosis. The aim of this study was to verify the role of haeme oxygenase in the hyporesponsiveness to phenylephrine of small mesenteric arteries in rats with CCl(4) induced cirrhosis, with and without ascites. METHODS: Pressurised small resistance mesenteric arteries were challenged with increasing doses of phenylephrine. Dose-response curves were evaluated under basal conditions, after inhibition of haeme oxygenase with chromium-mesoporphyrin, after inhibition of nitric oxide synthase (NOS) with N(G)-nitro-L-arginine-methyl-ester (L-NAME), and then after inhibition of both NOS and haeme oxygenase. Haeme oxygenase protein expression was also analysed. RESULTS: Twenty six control rats and 35 rats with cirrhosis (17 with and 18 without ascites) were studied. Response to phenylephrine was lower in non-ascitic and ascitic cirrhosis than in controls. Chromium-mesoporphyrin increased the response to phenylephrine only in ascitic cirrhosis (p<0.001). L-NAME increased the response to phenylephrine in controls (p<0.001) and in ascitic and non-ascitic cirrhosis (p = 0.002, p<0.001, respectively) but the final response in non-ascitic cirrhosis was similar to that of control rats while it remained impaired in ascitic cirrhosis. Addition of chromium-mesoporphyrin to L-NAME improved the response to phenylephrine in ascitic cirrhosis (p<0.01), with final values not different from those of the other two groups. Protein expression of the inducible isoform of haeme oxygenase was increased in the mesenteric vessels of cirrhotic rats. CONCLUSION: Haeme oxygenase mediates hyporeactivity to phenylephrine in the mesenteric vessels of experimental cirrhosis with ascites. NOS plays a major role only in the first stage of the disease.

Animals↗

PubMed2001

beta-Receptor agonist activity of phenylephrine in the human forearm.

Phenylephrine is generally regarded as a "pure" alpha(1)-agonist. However, after treatment of the forearm with the alpha-adrenergic-blocking drug phentolamine, brachial artery infusion of phenylephrine can cause transient forearm vasodilation. To determine whether this response was beta-receptor mediated, phenylephrine, phentolamine, and propranolol were infused into the brachial arteries of six healthy volunteers. Forearm vascular conductance (FVC) was also calculated and expressed as arbitrary units (units). Infusion of phenylephrine by itself (0.5 microg. dl forearm volume(-1). min(-1)) caused a sustained decrease (P < 0.05) in FVC from 3.5 +/- 0.7 to 0.9 +/- 0.2 units (P < 0.05). Infusion of the alpha-blocker phentolamine increased (P < 0.05) baseline FVC to 5.7 +/- 1.3 units. Subsequent infusion of phenylephrine after alpha-blockade caused FVC to increase (P < 0.05) for ~1 min from 5.7 +/- 1.3 to a peak of 13.1 +/- 1.8 units. Propranolol had no effect on baseline flow, and subsequent phenylephrine infusion after alpha- and beta-blockade caused a small, but significant, sustained decrease in FVC from 5.1 +/- 1.0 to 3.6 +/- 0.8 units. There were no systemic effects from the infusions, and saline infusion at the same rate (1-2 ml/min) had no forearm vasoconstrictor or dilator effects. These data indicate that in humans phenylephrine can exert transient beta(2)-vasodilator activity when its predominant alpha-constrictor effects are blocked.

Adrenergic alpha-Agonists↗

PubMed1996

Age-related changes in alpha-adrenoceptor-mediated blood pressure in the rat: relationship between the potency for phenylephrine and the maximum number of binding sites.

To study the effects of aging on the blood pressure potency of phenylephrine, 6-, 10- and 40-week-old rats were used. In anesthetized rats, the potency (pD2 value) of phenylephrine on the blood pressure tended to increase with age from 6 to 10 weeks, but significantly decreased thereafter with age from 10 to 40 weeks. Similarly, in pithed rats, the potency of phenylephrine significantly increased, but decreased thereafter. In isolated rat thoracic aorta, the pD2 value of phenylephrine from the contractile responses significantly increased with age from 6 to 10 weeks, but decreased thereafter from 10 to 40 weeks. The change in the potency of phenylephrine on the blood pressure was proportional to the pD2 value of phenylephrine estimated in aortic preparations. The specific binding of [3H]prazosin to single smooth muscle cells of thoracic aorta from different aged rats was saturable. The maximum number of binding sites (Bmax) significantly increased with age from 6 to 10 weeks, but decreased thereafter from 10 to 40 weeks. However, the dissociation constant of [3H]prazosin (Kd) did not alter with age. The changes in the potencies (pD2 values) of phenylephrine on the pressure responses and on the contractile responses were proportional to the logarithm of the maximum number of binding sites. The present study suggests that age-related changes in blood pressure are due to changes in the maximum number of binding sites (receptor density) of alpha 1-adrenoceptors.

Adrenergic alpha-Agonists↗

PubMed2004

Effects of topically instilled bunazosin, an alpha1-adrenoceptor antagonist, on constrictions induced by phenylephrine and ET-1 in rabbit retinal arteries.

PURPOSE: To examine the inhibitory effects of topically instilled bunazosin hydrochloride (bunazosin), a selective alpha1-adrenoceptor antagonist, on the retinal artery constrictions induced by intravitreous phenylephrine hydrochloride (phenylephrine) and endothelin (ET)-1 in rabbits. METHODS: Phenylephrine or ET-1 (20 microL) was injected into the central part of the vitreous in both eyes in pigmented rabbits. Color fundus photographs were taken at 5 minutes before and 60 minutes after the injection. The average diameter of the major retinal arteries at the rim of the optic nerve head (ONH) was normalized with respect to ONH diameter. Bunazosin was instilled into one eye (chosen randomly) and vehicle into the fellow eye at 60 minutes before the intravitreous injection. To examine any interaction between the alpha1-adrenoceptor and ET receptor, phenylephrine and ET-1 were co-injected at individually ineffective doses. In addition, ET-1-induced vasoconstriction was examined after unilateral superior cervical ganglionectomy. The binding affinities of bunazosin for ETA and ETB receptors were also evaluated. The series of experiments was performed as masked tests. RESULTS: Retinal arteries were dose-dependently constricted by both intravitreous phenylephrine and intravitreous ET-1. Topically instilled bunazosin at 0.01% partly inhibited both of these vasoconstrictions on the ipsilateral side, but not on the contralateral side. Bunazosin did not bind to ET receptors. Co-injection of phenylephrine and ET-1 at individually ineffective doses constricted retinal arteries significantly. An adrenergic supersensitivity in retinal arteries was observed after superior cervical ganglionectomy only on the ganglionectomized eye. The ET-1-induced vasoconstriction was significantly weaker in cervical ganglionectomized eyes than in sham-surgery eyes. CONCLUSIONS: The present findings suggest that topically instilled bunazosin reaches the posterior retina by local penetration at concentrations sufficient to attenuate the phenylephrine- or ET-1-induced constriction of retinal arteries in normal rabbit eyes, and that the inhibitory effect of bunazosin on the ET-1-induced vasoconstriction in this tissue may be partly attributable to an interaction between the alpha1-adrenoceptor and ET receptor.

Administration, Topical↗

PubMed1991

Myocardial oxygen supply/demand relations during phenylephrine infusions in dogs.

Experiments were performed on 14 fentanyl-pentobarbital-anesthetized dogs to assess changes in myocardial oxygen supply/demand relations during intravenous infusions of phenylephrine (2.8 micrograms.kg-1.min-1). Myocardial blood flow was measured with radioactive microspheres. Myocardial oxygen and lactate extraction were determined. Myocardial oxygen consumption was calculated with the Fick equation. In series 1, measurements were obtained during phenylephrine-induced pressor responses. In series 2, measurements were obtained with aortic pressure maintained constant with an extracorporeal reservoir during phenylephrine infusion, so that coronary vasomotor responses could be assessed in the absence of increases in ventricular afterload and perfusion pressure. In series 1, the phenylephrine-induced increase in mean aortic pressure (+42%) was accompanied by proportional (60%) increases in myocardial blood flow and myocardial oxygen consumption and with no change in the endocardium-to-epicardium flow ratio, oxygen extraction, coronary sinus oxygen tension and oxygen saturation, or myocardial lactate extraction. In series 2, phenylephrine infusion caused a transmurally uniform 15% decrease in myocardial blood flow combined with a 10% decrease in myocardial oxygen consumption. The coronary arteriovenous oxygen difference increased modestly (+5%), resulting in small decreases in coronary sinus oxygen tension and oxygen saturation, whereas lactate extraction was unaffected. The present findings suggest that phenylephrine has a direct vasoconstrictor effect in the coronary circulation that is weak and completely overridden by metabolic autoregulatory mechanisms in response to pressure-induced augmentations in cardiac workload. The authors conclude that the myocardium is not at risk when phenylephrine is used to treat hypotension in patients with adequate cardiac function and coronary vasodilator reserve.

Anesthesia, Intravenous↗

PubMed1992

Phenylephrine does not limit myocardial blood flow or oxygen delivery during isoflurane-induced hypotension in dogs.

Experiments were performed on seven fentanyl-pentobarbital-anesthetized, open-chest dogs to determine whether stimulation of coronary alpha 1-adrenergic receptors by phenylephrine causes coronary vasoconstriction and impaired myocardial oxygen delivery when phenylephrine is infused to correct isoflurane-induced hypotension. Myocardial blood flow was measured with radioactive microspheres, and myocardial oxygen and lactate extraction were determined. The Fick equation was used to calculate myocardial oxygen consumption. Measurements were obtained (a) under control conditions, (b) after a 30-min inhalation of isoflurane sufficient to decrease mean aortic pressure by 30%, and (c) while maintaining administration of isoflurane, 5-10 min after restoration of mean aortic pressure by intravenous infusion of phenylephrine. Isoflurane-induced hypotension was accompanied by a baroreceptor-mediated increase in heart rate and by a decrease in myocardial oxygen consumption; however, myocardial blood flow was maintained, resulting in decreased oxygen extraction and increased coronary sinus PO2, thus implying a direct coronary vasodilating effect for isoflurane. Lactate extraction was unaffected. Phenylephrine infusion during inhalation of isoflurane returned mean aortic pressure and heart rate to their respective control values, and it did not change myocardial oxygen consumption, myocardial blood flow, myocardial oxygen extraction, coronary sinus PO2, or lactate extraction from values obtained during isoflurane alone. These latter findings are consistent with undiminished coronary vasodilation by isoflurane in the presence of phenylephrine. In conclusion, infused phenylephrine to restore aortic pressure during isoflurane administration had no vasoconstrictor effect in the coronary circulation and did not impair myocardial oxygen delivery. Apparently, the direct coronary vasodilating action of isoflurane completely nullified phenylephrine-induced vasoconstriction via local alpha 1-adrenergic receptors.

Animals↗

PubMed1979

Inhibitory alpha-adrenergic action of phenylephrine in guinea pig taenia caecum.

Phenylephrine, a selective alpha-adrenergic stimulant, caused a maximal relaxation of the taenia from guinea pig caecum in the concentration of 10(-6) g/ml. Phenylephrine in this concentration did not influence intracellular cyclic AMP and cyclic GMP levels. Although phenylephrine abolished the spontaneous spike discharge, no change was detected in 45Ca-uptake and 45Ca-efflux on the tissue level after phenylephrine. Ca-uptake and Ca-release on the subcellular level were also not influenced by phenylephrine. In Ca free-solution phenylephrine inhibited the response to CaCl2. Phenylephrine increased 42K-efflux in the normally polarized taenia and also in the K-depolarized taenia.

Action Potentials↗

PubMed1996

Alpha 1B-adrenoceptor subtype mediating the phenylephrine-induced contractile response in rabbit corpus cavernosum penis.

The alpha 1-adrenoceptor subtype mediating contraction to phenylephrine in rabbit corpus cavernosum penis (CCP) was investigated using selective alpha 1-adrenoceptor subtype antagonists. WB4101 ((2-(2,6-dimethoxy-phenoxyethyl)-aminomethyl-1, 4-benzodioxane) hydrochloride), 5-methylurapidil and tamsulosin concentration-dependently produced a parallel rightward shift of the concentration-response curve to phenylephrine, yielding pKB values of 8.05, 7.59 and 9.21, respectively. The slopes of the Schild plots were not different from unity. These antagonists did not affect the maximum response to phenylephrine. Oxymetazoline (1 microM), which initially caused a small contraction, produced a parallel rightward shift of the concentration-response curve to phenylephrine with an apparent pKB value of 6.99. However, oxymetazoline seemed to act as a non-surmountable antagonist to the phenylephrine-induced contraction, reducing the maximum response by 71.1%. Chloroethylclonidine (25 and 100 microM) produced a parallel rightward shift of the concentration-response curve to phenylephrine without altering the maximum response. These results show that the alpha 1-adrenoceptor in rabbit CCP has a relatively low affinity for WB4101, 5-methylurapidil, tamsulosin and oxymetazoline and is sensitive to inactivation by chloroethylclonidine. It is suggested that the alpha 1-adrenoceptor subtype mediating contraction to phenylephrine in rabbit CCP has the characteristics of the alpha 1B-adrenoceptor subtype.

Adrenergic alpha-Agonists↗

PubMed2006

Different effects of propranolol, phenylephrine, and saline volume loading on catecholamine-induced left ventricular outflow tract obstruction in acute coronary syndrome.

Hemodynamic deterioration due to left ventricular outflow tract (LVOT) obstruction can occur during catecholamine infusion in patients with acute coronary syndrome (ACS). The purpose of the present study was to compare the utility of propranolol, phenylephrine infusion, and rapid saline loading for reversal of dobutamine-induced LVOT obstruction in a canine model of ACS. ACS was induced via left anterior descending artery ligation in 21 open-chest anesthetized dogs, and LVOT obstruction, defined as an LVOT gradient > 30 mmHg, was induced by dobutamine infusion (20 to 40 microg/kg/min). Subsequently, the effects of propranolol infusion (0.7 to 1.0 microg/kg/min, n = 8), phenylephrine infusion (10 to 200 microg/kg/min, n = 7), and saline loading (200 to 400 mL/hr, n = 6) were assessed by serial hemodynamic measurements. All interventions produced significant and comparable improvements in the LVOT pressure gradient (propranolol: 60 +/- 16 to 15 +/- 12; phenylephrine: 68 +/- 15 to 12 +/- 10; saline loading: 58 +/- 18 to 22 +/- 10 mmHg; P < 0.001 for baseline versus postintervention; P = NS for comparison between interventions). Phenylephrine produced the greatest elevation in aortic pressure (propranolol: +15 +/- 13; phenylephrine: +51 +/- 36; saline loading: +15 +/- 15 mmHg; P < 0.05), while saline loading produced the greatest increase in cardiac output (propranolol: +0.05 +/- 0.12; phenylephrine: +0.28 +/- 0.37; saline loading: +0.73 +/- 0.48 L/min; P < 0.05). Propranolol was the only intervention that produced a significant decrease in diastolic pulmonary artery pressure (16 +/- 5 to 11 +/- 3 mmHg, P < 0.05). Propranolol, phenylephrine infusion, and saline volume loading were similarly effective in reversing dobutamine-induced LVOT obstruction in this canine model of ACS. However, each intervention produced different hemodynamic effects with potentially different clinical indications.

Adrenergic beta-Antagonists↗

PubMed1982

Increased numbers of sperm in the oviducts and improved fertilization rates in rabbits after administration of phenylephrine or ergonovine near the time of insemination.

Phenylephrine, an alpha-adrenoceptor agonist, was administered im to does near the time of mating or insemination. The treatment increased sperm numbers in the oviducts by about 50-fold and in the uterus by about 10-fold at 2 or 2.5 h after insemination. Methoxamine, another alpha-adrenoceptor agonist that was given im, did not increase sperm numbers, although both phenylephrine' and methoxamine significantly increased the number and amplitude of uterine contractions when contractions were measured by strain gauge force transducers attached to the uterus of conscious does. Ergonovine, an ergot derivative given im, increased sperm numbers more than 10-fold in the oviducts and five to 10-fold in the uterus at 2 or 2.5 h after insemination. Ergonovine increased the frequency and amplitude of uterine contractions when given iv but not when given im. In tests with a range of doses of phenylephrine and ergonovine, 5 mg of phenylephrine and .6 mg of ergonovine appeared to be near optimal for maximizing the number of sperm in the uterus and oviducts at 2.5 h after insemination. Phenoxybenzamine, an alpha-adrenoceptor blocking agent, prevented the phenylephrine-induced increases in both uterine contractions and sperm numbers in the oviducts and uterus. Phenoxybenzamine also prevented the effect of ergonovine on sperm numbers. In does inseminated with low numbers of sperm (92,000; an inseminate selected to result in a low fertilization rate in control does), the administration of phenylephrine or ergonovine significantly increased ovum fertilization rates (16% for control does, 52 and 63%, respectively, for phenylephrine- and ergonovine-treated does).

Animals↗

PubMedDate not supplied

The effects of clonidine, guanfacine and phenylephrine on the excitatory and inhibitory responses of the rat anococcygeus muscle.

The effects of clonidine, guanfacine and phenylephrine on twitch responses and the basal tone of the rat anococcygeus muscle were investigated. Clonidine (10(-9)-3 x 10(-8) M) and guanfacine (10(-9)-10(-7) M) inhibited the twitch responses with the same potency, whereas phenylephrine (10(-9)-10(-7) M) was found ineffective. The inhibitory effect of clonidine and guanfacine was antagonized by yohimbine. Higher concentrations of clonidine and guanfacine increased the muscle tone and elicited inhibitory responses during field stimulation. Phenylephrine at concentrations greater than 10(-7) M also increased the muscle tone but induced biphasic responses. Clonidine (10(-7)-3 x 10(-5) M), guanfacine (3 x 10(-7)-3 x 10(-5) M) and phenylephrine (3 x 10(-7)-10(-5) M) caused concentration-dependent increases in the basal tone. The order of potency of these agonists in increasing the basal tone was clonidine > guanfacine > phenylephrine. Both yohimbine (10(-8)-10(-5) M) and prazosin (10(-9)-10(-7) M) antagonized these tonic contractions. Prazosin was found to be 39-, 122- and 83-fold more potent than yohimbine in antagonizing clonidine, guanfacine and phenylephrine-induced tonic contractions, respectively. Clonidine and guanfacine inhibited twitch responses through stimulation of presynaptic alpha-2 adrenoceptors. Postsynaptic alpha-1 adrenoceptors seem responsible for the contractile effects of clonidine, guanfacine and phenylephrine in the rat anococcygeus muscle.

Animals↗

PubMed2000

Transesophageal atrial pacing reduces phenylephrine needed for blood pressure support during carotid endarterectomy.

OBJECTIVE: To determine whether transesophageal atrial pacing reduces phenylephrine requirement for blood pressure support during general anesthesia for carotid endarterectomy. DESIGN: Prospective randomized clinical study. SETTING: University hospital. PARTICIPANTS: Thirty-six patients undergoing elective carotid endarterectomy under general anesthesia. INTERVENTIONS: Adults of either sex (n = 36) received general anesthesia using a standardized anesthetic regimen for elective carotid endarterectomy. Phenylephrine requirements were measured in patients having carotid endarterectomy and randomized to phenylephrine infusion (group 1, 19 patients) or phenylephrine infusion plus transesophageal atrial pacing (group 2, 17 patients) to maintain systolic blood pressure within +/-20% of baseline systolic blood pressure. MEASUREMENTS AND MAIN RESULTS: Measurements included (1) the amount of phenylephrine required in each group, (2) the variance of systolic blood pressure outside the desired range, and (3) the occurrence of postoperative electrocardiogram or myocardial enzyme changes suggesting myocardial ischemia. The average requirement for phenylephrine was less for group 2 (0.28+/-0.16 microg/kg/min) than for group 1 patients (0.46+/-0.23 microg/kg/min) (p = 0.02 by t-test). CONCLUSIONS: Under controlled conditions of general anesthesia for carotid endarterectomy, transesophageal atrial pacing reduced by 40% the amount of phenylephrine needed for blood pressure support and helped in the treatment of disadvantageous sinus bradycardia.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Failure of phenylephrine to prolong isobaric bupivacaine spinal anesthesia in elderly patients.

BACKGROUND AND OBJECTIVES: The effects of phenylephrine on the duration of spinal anesthesia produced by plain bupivacaine were investigated in a double-blind study of 100 elderly patients. METHODS: Each patient received a basic solution of 3 ml 0.5% plain bupivacaine to which was added either 1 ml physiologic saline, 0.2 ml (1 mg) 0.5% phenylephrine plus 0.8 ml normal saline, 0.4 ml phenylephrine plus 0.6 ml normal saline, 0.6 ml phenylephrine plus 0.4 ml normal saline, or 0.8 ml phenylephrine plus 0.2 ml normal saline. RESULTS: The duration of sensory block (measured by two- and four-segment regression times and times to regression to T12 and L2 dermatomes) was not statistically prolonged by addition of phenylephrine. CONCLUSION: It is concluded that, in an attempt to prolong plain bupivacaine spinal anesthesia, the addition of phenylephrine does not appear to be advantageous for routine clinical practice.

Aged↗

PubMed1994

Phenylephrine eye drops in ophthalmic surgery--a clinical study on cardiovascular effects.

Phenylephrine in concentrations of either 2.5% or 10% is widely used as a mydriatic agent in ophthalmic surgery. Its potential cardiovascular effects are seldom recorded as ophthalmic surgery is not usually monitored by an anaesthetist. A prospective randomised double blind study was carried out in 89 consecutive cases of uncomplicated cataract surgery in the presence of an anaesthesiologist ensuring the continuous monitoring of blood pressure, heart rate, electrocardiography and pulse oximetry. All these patients were given a drop of either normal saline, 2.5% or 10% phenylephrine in addition to mydriacyl prior to surgery. Blood pressure readings were found to be significantly higher in non-hypertensive patients receiving phenylephrine at the start of the operation and at five, 10, 15 and 20 minutes intra-operatively and the first three hours post-operatively. Blood pressure readings in hypertensive patients, on the other hand, were also found to increase after phenylephrine administration, though not statistically significant. 10.3% of the 10% phenylephrine group and 3% of the 2.5% phenylephrine group required intraoperative intravenous hypotensive agent to control the blood pressure. There were no arrhythmias or ischaemic changes observed intraoperatively. None of the patients complained of palpitation, headache or chest discomfort. There was no oxygen desaturation observed. We concluded that significant hypertensive effects can arise after phenylephrine eye drop administration. Hence, it should be used cautiously with intraoperative monitoring of the cardiovascular status during cataract surgery.

Aged↗

PubMed1980

Is phenylephrine pivalate a prodrug?

Phenylephrine pivalate has been assumed to be a prodrug devoid of important intrinsic activity because of its structural similarity to dipivefrin (dipivaly epinephrine). However, unlike dipivefrin, the pharmacologic activity of phenylephrine pivalate was not prevented by prior administration of echothiophate iodide. Rabbits pretreated bilaterally with 0.25% echothiophate for two and seven days had similar mydriasis, both in quantity and duration, after receiving 10% phenylephrine hydrochloride to one eye and 1% phenylephrine pivalate to the other eye. This as consistent with the hypothesis that the phenylephrine pivalate molecule has important alpha-adrenergic activity regardless of whether it is converted to phenylephrine.

Animals↗

PubMed2001

Novel site-specific chemical delivery system as a potential mydriatic agent: formation of phenylephrine in the iris-ciliary body from phenylephrone chemical delivery systems.

The objective of this study was to test the three novel ester derivatives of phenylephrone (isovaleryl, phenylacetyl, and pivalyl esters) as potential site-specific chemical delivery systems. The mydriatic effect and ocular distribution/metabolism of these compounds were studied by topical application to the eyes of normal rabbits. It was assumed that a reduction-hydrolysis sequence could produce the active phenylephrine in the iris-ciliary body tissues. All the derivatives showed a more pronounced mydriatic effect than that of phenylephrine, whereas phenylephrone was completely devoid of any mydriatic activity. Phenylacetyl ester was the most potent drug, with short duration of action, and showed maximum activity in the presence of 0.01% benzalkonium chloride without causing any visible irritation to the rabbit eye. Administration of the novel compounds to the eyes of the rabbits showed no traces of phenylephrine in the systemic circulation, contrary to topical administration of phenylephrine. Phenylephrone was detected in different compartments of the eye, whereas phenylephrine was present only in the iris-ciliary body tissues following administration of phenylacetyl ester. The conversion of phenylephrone esters to the active drug, phenylephrine, and thus their subsequent activity was dependent on the physicochemical characteristics of the drugs. The results suggest the potential use of phenylacetyl ester as a potent short-term mydriatic agent without systemic side effects.

Animals↗