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PubMed1989

The pressor hyperresponsiveness to phenylephrine unmasks sympathetic hypofunction in migraine.

The pressor responsiveness to phenylephrine, an almost pure agonist of peripheral alpha-1-adrenoceptors, was studied in 32 migraine patients in headache-free intervals. Eighteen healthy volunteers served as a control group. Fourteen patients and 14 controls also underwent the tilt test. The following observations were made: (1) the pressor response to phenylephrine was significantly greater and longer lasting in patients than in controls; (2) the reflex decrease of heart rate did not differ in the two groups; (3) a normal orthostatic increase of blood pressure and heart rate occurred in migraineurs with hyperresponsiveness to phenylephrine. These findings suggest a supersensitivity of vascular adrenoceptors which is compatible with a chronic adrenergic deficiency in migraineurs. Since patients did not show an orthostatic hypotension in attack-free periods, the compensatory character of receptoral supersensitivity and the possible mechanisms of cardiovascular dysautonomia, which may occur during migraineous attack, were discussed.

Adult↗

PubMed1975

Reversal by phenylephrine of the beneficial effects of intravenous nitroglycerin in patients with acute myocardial infarction.

Nitroglycerin has been shown to reduce ST-segment elevation during acute myocardial infarction, an effect potentiated in the dog by agents that reverse nitroglycerin-induced hypotension. Our study was designed to determine the effects of combined nitroglycerin and phenylephrine therapy. Ten patients with acute transmural myocardial infarctions received intravenous nitroglycerin, sufficient to reduce mean arterial pressure from 107 +/- 6 to 85 +/- 6 mm Hg (P less than 0.001), for 60 minutes. Left ventricular filling pressure decreased from 19 +/- 2 to 11 +/- 2 mm Hg (P less than 0.001). SigmaST, the sum of ST-segment elevations in 16 precordial leads, decreased (P less than 0.02) with intravenous nitroglycerin. Subsequent addition of phenylephrine infusion, sufficient to re-elevate mean arterial pressure to 106 +/- 4 mm Hg (P less than 0.001) for 30 minutes, increased left ventricular filling pressure to 17 +/- 2 mm Hg (P less than 0.05) and also significantly increased sigmaST (P less than 0.05). Our results suggest that addition of phenylephrine to nitroglycerin is not beneficial in the treatment of patients with acute myocardial infarction.

Acute Disease↗

PubMedDate not supplied

The presence of the endothelial layer reduces nitric oxide-induced hyporesponsiveness to phenylephrine in rat aorta.

A single exposure to nitric oxide (NO) donors produces a long-lasting hyporesponsiveness to phenylephrine (HRP) in rat aorta rings. Here the authors investigate the role of the endothelial layer in the development of NO-induced HRP and the putative role of endothelium-derived vasoconstrictors in counteracting it. The NO donor S-nitrosoacetyl-D,L-penicillamine (SNAP) induced a dose-dependent reduction in the maximal effect (Emax) of phenylephrine. In rings without endothelium, Emax dropped to 60%, 25%, and 10% of control values 1 h after a 30-min incubation with SNAP (2, 20, and 200 microM, respectively). In contrast, the presence of endothelium prevented the HRP induced by 2 microM SNAP and significantly reduced the HRP elicited by 20 and 200 microM SNAP (Emax reductions of 50% and 65%, respectively), thereby characterizing the endothelium protective effect. Superoxide dismutase (SOD; 100 IU/mL), MnTBAP (a nonenzymatic SOD mimetic; 100 microM), captopril (10 microM), MK886 (a lipoxygenase inhibitor; 10 microM) and BQ 123 (endothelin receptor A antagonist; 1 microM) did not change the endothelium protective effect. Therefore, increased release of vasoconstrictors that would counteract NO-induced loss in phenylephrine responses cannot account for the protective effect of endothelium. In contrast, oxidation of sulphydryls with DTNB prevented the onset of SNAP-induced HRP. A better understanding of mechanisms by which the endothelial layer (or protein sulphydryl groups present in it) exerts its protective effect towards the NO-induced loss in physiological vasoconstriction is likely to be of value in cardiovascular conditions such as ischemia/reperfusion and septic shock.

Animals↗

PubMed1991

Insulin attenuation of vasoconstrictor responses to phenylephrine in Zucker lean and obese rats.

Recent data from this laboratory indicate that insulin resistant obese Zucker rats exhibit hypertension associated with exaggerated in vitro vascular reactivity to phenylephrine, serotonin, and KCl, and we have found insulin to attenuate vascular reactivity responses to these agonists. Accordingly, in the present study we evaluated the possibility that exaggerated vascular reactivity responses in obese Zucker rats may result from insulin resistance and a consequent failure of insulin to attenuate vasoactive responses. Thoracic aortae were isolated from male 16 week old lean and obese Zucker rats, and replicate helical strips from each animal were suspended in a muscle bath under a resting tension of 1.4 g in the presence or absence of insulin (0.1 mU/mL) for 1 h. The insulin was then washed out, and vascular reactivity responses to phenylephrine were determined. The obese rats exhibited greater reactivity to phenylephrine (ED50:1.10 +/- 90 X 10(-8) v 7.57 +/- 0.88 X 10(-10) mol/L in lean and obese rats, respectively, P less than .025). Insulin caused a significant attenuation of the contractile response in both the lean and obese aortae. However, lean rats exhibited a markedly greater attenuation than the obese rats (46.0 +/- 17.0 v 17.8 +/- 7.5% attenuation in the lean and obese rats, respectively, P less than .01). These data suggest that increased vascular reactivity responses in obese Zucker rats may result from their insulin resistant state and, consequently, a diminished ability of insulin to attenuate vasoconstrictor responses.

Animals↗

PubMed1994

Spinal anaesthesia for caesarean section: comparison of infusions of phenylephrine and ephedrine.

Maternal cardiovascular changes and neonatal acid-base status were assessed in 29 healthy women undergoing elective lower segment Caesarean section under spinal anaesthesia. The patients were allocated randomly to one of three groups to receive an i.v. infusion of one of the following: ephedrine 1 mg min-1 (group E1: n = 10), ephedrine 2 mg min-1 (group E2: n = 9), or phenylephrine 10 micrograms min-1 (group P: n = 10). Invasive arterial pressure was monitored continuously and if hypotension occurred (defined as a 20% decrease from baseline, taken after i.v. preload administration), bolus doses of either ephedrine (6 mg in groups E1 and E2) or phenylephrine (20 micrograms in group P) were given. Only four patients became hypotensive in group E2, compared with eight patients in group E1 and nine patients in group P. The total time that the patients remained hypotensive was greatest in group P (P < 0.005), less in group E1 and least in group E2. Neonatal Apgar scores and acid-base profiles were similar in all three groups. In this study, an infusion of phenylephrine 10 micrograms min-1 with bolus doses of 20 micrograms was shown to be significantly less effective in maintaining systolic arterial pressure within 20% limits of baseline compared with an infusion of ephedrine 1 or 2 mg min-1 with bolus doses of 6 mg.

Adult↗

PubMed1999

Effect of mild hypothermia on the vascular actions of phenylephrine in rat aortic rings.

Intraoperative mild hypothermia is common. We have investigated the effects of mild hypothermia (34 vs 38 degrees C) on phenylephrine--(10(-8) to 10(-5) mol litre-1) induced contractions of rat aortic rings mounted for isometric tension recordings. A marked decrease in Emax (maximal tension) (P < 0.05) and significant increase in EC50 (phenylephrine concentration producing 50% of maximal tension) were observed at the lower temperature in endothelium intact rings, but there was no effect of temperature when the endothelium had been removed. The decreased contraction with hypothermia in the endothelium intact vessels was restored to 84% by administration of the nitric oxide synthase inhibitor L-NNA and a small additional amount of tone was restored in the presence of the cyclooxygenase inhibitor, indomethacin. We conclude that mild hypothermia markedly decreased phenylephrine-induced rat aortic contraction in vitro by endothelium dependent mechanisms, largely related to increased nitric oxide production or action.

Animals↗

PubMed2002

Intraoperative pulmonary oedema in a child following systemic absorption of phenylephrine eyedrops.

Ophthalmic surgeons often apply phenylephrine topically to effect pupillary dilatation. We describe a paediatric patient in whom cardiac arrhythmias, severe hypertension and pulmonary oedema occurred following intraoperative ocular phenylephrine administration. We believe that systemic absorption of the drug was responsible and discuss ways in which this might be reduced when ocular phenylephrine is used in this context.

Child↗

PubMed2003

Transient hyperaemic response to assess vascular reactivity of skin: effect of locally iontophoresed acetylcholine, bradykinin, epinephrine and phenylephrine.

BACKGROUND: Recently, the transient hyperaemic response (THR) to brief compression (20 s) of the brachial artery has been described as a way to assess vascular reactivity of the forearm skin. We studied the effects of locally iontophoresed vasoactive agents on this response in 20 male volunteers. METHODS: An iontophoresis chamber attached to the anterior forearm permitted simultaneous administration of drugs by iontophoresis and measurement of skin blood flow-flux by laser Doppler probe. Three THR tests were performed before and after iontophoresis by compressing the brachial artery with digital pressure for 20 s and then releasing. The following were iontophoresed: saline 0.9% (iontophoresis vehicle control), acetylcholine, bradykinin, epinephrine and phenylephrine. The THR ratio (THRR) was calculated as F2/F1 where F1 was baseline blood flow-flux immediately before compression and F2 was peak blood flow-flux after release. RESULTS: When compared with saline 0.9%, acetylcholine and bradykinin increased median F1 from 9.2 (range 5.2-23.8) to 22.1 (8.7-61.5) and from 4.8 (3.0-23.2) to 15.0 (2.5-31.8), respectively, and reduced THRR from 1.26 (1.07-2.2) to 0.99 (0.93-1.04) and from 1.63 (1.06-2.58) to 1.09 (0.93-1.19), respectively. Epinephrine, but not phenylephrine, caused a significant reduction in F1 from 9.2 (5.2-23.8) to 4.0 (1.5-22.3). Neither epinephrine nor phenylephrine had significant effect on THRR. CONCLUSIONS: Iontophoresed acetylcholine and bradykinin significantly increase the flow-flux and impair THR in forearm skin, further validating the concept that THR represents true vasodilatation during arterial occlusion. In addition, iontophoresis of vasoconstrictors does not appear to have any consistent effect.

Acetylcholine↗

PubMed2002

Vascular responsiveness to brachial artery infusions of phenylephrine during isoflurane and desflurane anesthesia.

UNLABELLED: Compared with equi-minimum alveolar anesthetic concentration (MAC) isoflurane, desflurane is associated with greater levels of sympathetic nerve activity in humans but similar reductions in blood pressure. To explore these divergent effects, we evaluated vascular alpha(1)-adrenoceptor responses in the human forearm during isoflurane and desflurane anesthesia to determine if alpha(1)-adrenoceptor responses were more substantially attenuated during desflurane administration. Bilateral forearm venous occlusion plethysmography was used to examine arterial blood flow and to determine changes in forearm vascular resistance during brachial artery infusions of saline and phenylephrine (0.2, 0.4, 0.8, and 1.6 microg/min) in 22 conscious subjects and during anesthesia with 0.65 and 1.3 MAC isoflurane or desflurane. Infusion of phenylephrine into the brachial artery increased the forearm vascular resistance in a dose-dependent manner. The arterial response to phenylephrine was significantly attenuated by 0.65 and 1.3 MAC desflurane and similarly attenuated during 1.3 MAC isoflurane (P < 0.05). Impaired arterial alpha(1)-adrenoceptor responsiveness occurred during desflurane. However, this effect was statistically similar (P > 0.05) to the impaired responses during isoflurane. Blood pressure decreases during volatile anesthesia may be, in part, caused by decreased alpha(1)-adrenoceptor responsiveness. IMPLICATIONS: alpha-receptors on blood vessels regulate constriction and dilation and therefore modulate blood pressure. This research indicates that vasoconstriction via the alpha(1)-receptor vascular response is impaired during isoflurane and desflurane anesthesia.

Adrenergic alpha-Agonists↗

PubMed1988

Does anesthetic technique make a difference? Augmentation of systolic blood pressure during carotid endarterectomy: effects of phenylephrine versus light anesthesia and of isoflurane versus halothane on the incidence of myocardial ischemia.

Whether anesthetic technique affected the incidence of myocardial ischemia in 60 patients undergoing carotid endarterectomy was investigated. The patients were randomly assigned to receive halothane or isoflurane (with nitrous oxide) either at a low concentration alone or at a higher concentration with phenylephrine added to support blood pressure. Blood pressure was maintained within 20% of each patient's average ward systolic pressure. Seven leads of electrocardiograms (ECG) and echocardiograms were analyzed for segmental wall motion. The echocardiograms were analyzed using standard formulae for end-systolic meridional wall stress (SWS) and rate-corrected velocity of fiber shortening (Vcfc). Because of the nature of these calculations, only echocardiograms with normal regional wall motion could be accurately analyzed. The patients had postoperative ECG and creatinine phosphokinase (CPK) isoenzyme determinations and regularly scheduled clinical examinations to detect perioperative myocardial infarction and neurologic deficits. Although blood pressures were similar, the patients who received a higher concentration of anesthetic plus phenylephrine had a higher wall stress, regardless of the choice of anesthetic agent. All four techniques allowed provision of the same stump pressures (the marker surgeons used for adequacy of collateral carotid flow). No difference could be found in wall stress or incidence of myocardial ischemia between isoflurane and halothane. The patients who received phenylephrine had a threefold greater incidence of myocardial ischemia than did the patients who had light anesthesia to maintain similar systolic blood pressures and stump pressures. The groups were demographically and hemodynamically similar; in particular, the heart rates were not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed2003

Role of endothelium-derived hyperpolarizing factor in phenylephrine-induced oscillatory vasomotion in rat small mesenteric artery.

BACKGROUND: In small mesenteric arteries, endothelium-derived hyperpolarizing factor (EDHF) in addition to endothelium-derived relaxing factors (EDRFs) including NO plays an important role in acetylcholine-induced vasodilation. It has been reported that EDRFs play an important role in alpha(1)-adrenoceptor agonist-induced oscillatory vasomotion and in limiting vasoconstrictor response to the agonists; however, contribution of EDHF to the alpha(1)-agonist-induced oscillation is unknown. METHODS: Rat small mesenteric arteries were isolated and cannulated at each end with a glass micropipette. The vessels were immersed in a bath (37 degrees C) containing physiologic saline solution. Changes in vessel diameter were measured using an optical density video detection system. RESULTS: Denudation of the endothelium and inhibition of NO synthesis caused a leftward shift in the concentration-response relation for phenylephrine in the mesenteric arteries, whereas inhibition of cyclooxygenase by indomethacin had no effect. Blockade of Ca2+-activated K+ (K(Ca)) channels by charybdotoxin and apamin caused a further leftward shift in the concentration-response relation in the vessels pretreated with Nomega-nitro-l-arginine methylester and indomethacin. Phenylephrine at concentrations higher than 10(-6) m caused endothelium-dependent oscillatory vasomotion, which was reduced but not abolished after combined inhibition of the cyclooxygenase and NO synthase pathways. However, the K(Ca) channel blockers completely abolished the remaining component of oscillation. CONCLUSIONS: Endothelially-derived NO is an important modulator of sustained agonist-induced vasoconstriction. NO, as well as endothelially-derived cyclooxygenase products and EDHF, also contribute significantly to phenylephrine-induced oscillatory vasomotion.

Animals↗

PubMed1982

Circulatory responses to afterloading with phenylephrine in hyperdynamic sepsis.

We assessed cardiac function by acute pressure loading with phenylephrine in 7 patients who had hyperdynamic sepsis and in 8 patients who had heart disease. All patients with sepsis had a positive Limulus lysate teat, a septic focus, and a cardiac output (CO) greater than 6.0 L/min. Phenylephrine was given iv to elevate systolic arterial pressure by 30 mm Hg. Cardiac index (CI) and stroke index (SI) increased significantly in patients with hyperdynamic sepsis, whereas systemic vascular resistance index (SVRI) showed no change. In patients with heart disease, CI and SI decreased significantly, whereas SVRI increased significantly. The marked differences in response to phenylephrine by the two groups suggest lack of cardiac dysfunction in patients with hyperdynamic sepsis.

Aged↗

PubMed1990

Decreased responsiveness of superficial hand veins to phenylephrine in black normotensive males.

Essential hypertension is more prevalent among blacks than whites although the explanation is unknown. It is possible that an altered vascular adrenoceptor responsiveness in blacks may play a role in the etiology of this racial difference. To test this hypothesis, we have compared the diameter changes in superficial veins in response to phenylephrine, an alpha-adrenergic agonist, and to isoproterenol, a beta-adrenergic agonist, in black and white young normotensive males using the dorsal hand vein compliance technique. The maximal venoconstriction after phenylephrine (Emax) was 92 +/- 9% (mean +/- SD) in the whites but only 74 +/- 12% in the blacks (p = 0.00046). The ED50 of phenylephrine was 342 ng/min (geometric mean) in whites and 245 ng/min in blacks (p = 0.50). The Emax and ED50 for isoproterenol-mediated venodilation was not significantly different between the racial groups. These results indicate a decreased maximal responsiveness to alpha-adrenergic stimulation in normotensive blacks. How these changes relate to cardiovascular alterations in hypertensive blacks requires further study.

Adolescent↗

PubMed1994

Ischaemia/reperfusion enhances phenylephrine-induced contraction of rabbit aorta due to impairment of neuronal uptake.

We studied the effect of ischaemia and reperfusion on vasoconstrictor and vasodilator mechanisms. Anaesthetized rabbits were subjected to 4-h abdominal aortic occlusion and 1-h reperfusion in vivo. Segments of the abdominal (ischaemic-reperfused) and thoracic (control) aorta were then removed for in vitro studies. Ischaemia/reperfusion had no significant effect on relaxant responses to either acetylcholine (ACh:endothelium-dependent) or sodium nitroprusside (SNP:endothelium-independent). The sensitivity of the aorta to contraction by phenylephrine was significantly increased in aortic rings with or without endothelium (by 2.2- and 3.7-fold, respectively), but was not different after 4-h ischaemia without reperfusion. In contrast, responses to methoxamine, serotonin, and U46619 were not affected by ischaemia/reperfusion. Moreover, the relative increase in aortic sensitivity to phenylephrine was prevented by treatment of control and ischaemic-reperfused aortic rings with the neuronal uptake inhibitor cocaine (10(-5) M). These results suggest that after 4-h ischaemia, reperfusion damages sympathetic neuronal uptake mechanisms in rabbit aorta. As a result, phenylephrine, an agonist normally susceptible to neuronal uptake, may exert more potent contractile effects. Endothelium-dependent and endothelium-independent relaxant mechanisms in the aorta appear to be resistant to acute ischaemia and reperfusion.

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

PubMed1999

Vasoconstrictor effects of various melatonin analogs on the rat tail artery in the presence of phenylephrine.

We performed a pharmacologic analysis of the increase in perfusion pressure induced by melatonin and related analogues in the perfused rat tail artery precontracted by 1 microM phenylephrine. Melatonin, 2-iodomelatonin, 6-chloromelatonin, and S20098 (N-[2-(7-methoxy-1-naphthyl)ethyl]acetamide) produced a concentration-dependent enhancement of the vasoconstrictor response evoked by 1 microM phenylephrine with a rank order of potency compatible with the pharmacologic profile defined for high-affinity melatonin receptors. Melatonin had no effect on electrically induced [3H]noradrenaline release, but the neurogenic vasoconstriction was increased at melatonin concentrations of 100 and 300 nM. Increasing concentrations of the naphthalenic-based antagonist S20928 (N-[2-(1-naphthyl)ethyl]cyclobutanecarboxamide) caused a parallel rightward shift in the melatonin concentration-response curve without depressing the maximal response. The pA2 value of S20928 was 7.01 +/- 0.08. Luzindole, 1 microM, an antagonist of Mel1b melatonin receptors, was without effect on melatonin-induced responses. By using reverse transcription-polymerase chain reaction (RT-PCR), we found that messenger RNA (mRNA) encoding for Mel1a is transcribed in the rat tail artery. In conclusion, the results show that melatonin produced an enhancement of the contractile response elicited by phenylephrine in the perfused rat tail artery. This vasoconstrictor response appears to be mediated through activation of Mel1a receptors located on smooth-muscle cells. No evidence for an action of melatonin on either the endothelium or sympathetic nerve endings was found.

Acetamides↗

PubMed1999

Enhancement of constrictor response of spastic coronary arteries to acetylcholine but not to phenylephrine in patients with coronary spastic angina.

This study examined the direct response of smooth muscle of coronary spasm sites to alpha1-adrenergic stimulation in patients with coronary spastic angina. Phenylephrine (1 microM in the coronary circulation, for 5 min), a stimulator of alpha1-adrenoreceptors, was directly infused into coronary arteries with spasm in 10 patients with coronary spastic angina and into normal coronary arteries in 10 control patients. The luminal diameter of epicardial coronary arteries was determined by computer-assisted quantitative angiography. The constrictor response to intracoronary injection of acetylcholine (ACh; 50 microg) was greater in spastic arteries than in control arteries (decrease from baseline, 48+/-2% vs. 12+/-2%, respectively; p<0.001). ACh (50 or 100 microg) induced coronary spasm associated with myocardial ischemia in all of patients with coronary spastic angina but not in any control patients. On the other hand, phenylephrine infusion did not induce coronary spasm in any of patients with coronary spastic angina or in control subjects. The constrictor response to phenylephrine infusion was comparable between spasm and control coronary arteries (decrease from baseline, 11+/-2% vs. 9+/-2%, respectively; p = NS). The results indicate that smooth muscle of spastic coronary arteries does not exhibit enhancement of constrictor response to direct stimulation of alpha1-adrenoreceptor on coronary smooth muscle. There may be receptor-specific enhancement of constrictor response to agonists in smooth muscle of spastic coronary arteries in patients with coronary spastic angina.

Acetylcholine↗

PubMed2005

Hypertension increases the participation of vasoconstrictor prostanoids from cyclooxygenase-2 in phenylephrine responses.

OBJECTIVE: The present study was designed to analyse whether hypertension alters the involvement of cyclooxygenase-2-derived mediators in phenylephrine-induced vasoconstrictor responses. METHODS: Vascular reactivity experiments were performed in aortic segments from normotensive, Wistar-Kyoto, and spontaneously hypertensive rats (SHR); protein expression was measured by western blot and/or immunohistochemistry, and prostaglandin F2alpha (PGF2alpha), 8-isoprostane and prostacyclin release were determined by enzyme immunoassay commercial kits. RESULTS: The protein synthesis inhibitor dexamethasone (1 micromol/l), the non-selective cyclooxygenase inhibitor indomethacin (10 micromol/l), the selective cyclooxygenase-2 inhibitor NS 398 (1 micromol/l), and the thromboxane A2/prostaglandin H2 (TP) receptor antagonist SQ 29,548 (1 micromol/l), reduced the concentration-response curves to phenylephrine more in segments from hypertensive than from normotensive rats; however, the thromboxane A2 (TxA2) synthase inhibitors furegrelate (10 micromol/l) and OKY 046 (1 and 10 micromol/l) had no effect in either strain. Removing endothelium or adding dexamethasone almost abolished the NS 398 effect. Cyclooxygenase-2 protein expression, which was reduced by dexamethasone, was higher in aorta from hypertensive animals. In both strains cyclooxygenase-2 was localized mainly in endothelial cells and adventitial fibroblasts. 13,14-Dihydro-15-keto-PGF2alpha, 6-keto-PGF1alpha and 8-isoprostane levels were greater in the medium from hypertensive than from normotensive rats; NS 398 decreased levels of the three metabolites studied only in the medium from SHR. CONCLUSIONS: PGF2alpha and 8-isoprostane seem to be involved in the response to phenylephrine in rat aorta; this involvement is greater in hypertensive rats, probably due to a higher endothelial induction of cyclooxygenase-2.

Animals↗

PubMed2005

Open sky Müller muscle-conjunctival resection in phenylephrine test-negative blepharoptosis patients.

PURPOSE: To assess the efficacy of Müller muscle-conjunctival resection in patients in whom the phenylephrine test was negative. METHODS: A non-randomized, prospective clinical trial was conducted on 20 eyelids of 15 consecutive patients with blepharoptosis who showed no change in the upper eyelid margin-reflex distance (MRD1) following instillation of topical phenylephrine. The technique used was open sky Müller muscle-conjunctival resection. RESULTS: The mean MRD1 increased by 3.3 mm. No patient required augmentation of the procedure, and all patients had excellent appearance of their skin crease and eyelid contour. No complications arose from the procedure, including no incidence of dry eye symptoms or signs. CONCLUSIONS: Müller muscle-conjunctival resection may offer a safe and effective means of treating blepharoptosis despite a negative phenylephrine test.

Adult↗