PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “phenylephrine”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

Topical phenylephrine may result in worsening of visual loss when used to dilate pupils in patients with vaso-occlusive disease of the optic nerve.

Four patients (age range 54-82, 1F 3M) diagnosed with non-arteritic ischemic optic neuropathy experienced acute worsening of visual function after instillation of phenylephrine for dilated funduscopic examination. They experienced decreased visual function immediately or shortly after administration of topical mydriatic drops given in preparation for funduscopy. In all cases one drop each of 2.5% phenylephrine and 0.5-1% tropicamide was used. Three patients had classical risk factors such as hypertension, diabetes, and had a contralateral "disc-at-risk". The female and youngest patient had ischemic optic neuropathy presumed secondary to lupus erythematosus. The time from acute visual loss to presentation to neuro-ophthalmic care ranged from 1-6 days. The time of onset of the decline in visual function varied from 45 minutes (patient with lupus) to 12 hours after instillation of mydriatic drops. Visual acuity at diagnosis ranged from 20/40-20/400. Phenylephrine is a mydriatic with vasoconstrictive properties, which may be absorbed through the cornea, thus yielding non-negligible intraocular concentrations. Vasoconstriction of the watershed posterior ciliary capillary beds may result in further precipitating infarction of already compromised circulatory territories in edematous optic nerves. Because phenylephrine is a known vasoconstrictor in vivo and in vitro, it is more likely to cause deleterious vasoconstriction and an acute decline in visual function in patients with acute ischemic optic neuropathy than tropicamide. The routine practice of using phenylephrine to prepare patients for funduscopic assessment should be re-examined, particularly in patients with ischemic optic neuropathy.

Administration, Topical↗

Vascular smooth muscle responsiveness to noradrenaline and phenylephrine following experimental heart failure in dogs.

Adrenergic vascular responsiveness was assessed in the dorsal pedal artery and the saphenous vein in dogs before and after the development of congestive heart failure (CHF). Following development of severe CHF, both noradrenaline and phenylephrine could produce a greater maximum tension and a shift of the resultant concentration-effect curve to the left compared to the curves seen before the development of CHF. The saphenous vein was more sensitive than the dorsal pedal artery to both agonists before CHF. After CHF, the sensitivity difference to noradrenaline increased significantly but it remained unaltered to phenylephrine. Relative to noradrenaline, phenylephrine became more potent on the artery at peak CHF, whereas the potency ratio was unchanged in the saphenous vein at peak CHF. Prazosin was a competitive antagonist only against phenylephrine prior to CHF; competitive antagonism was not seen against noradrenaline or following CHF. Prazosin was less effective in antagonising noradrenaline induced contractions, as shown by an increase in IC50 values. These results are consistent with increased tissue sensitivity to adrenergic agents during CHF. The greater potency of phenylephrine in the artery at peak CHF suggests the presence of a greater proportion of alpha 1 adrenoceptors, which is consistent with the decrease in effectiveness of prazosin after the development of CHF.

Animals↗

Amplification by phenylephrine and serotonin of coronary vasoconstriction induced by a high arterial blood oxygen tension.

OBJECTIVE: The aim was to investigate the effect on the coronary network of the interaction between high arterial blood oxygen tension (PaO2) and stimulation by the alpha adrenergic agonist phenylephrine or by serotonin in an isolated, blood perfused rabbit heart preparation. METHODS: Fresh pig erythrocytes in Krebs-Henseleit buffer were oxygenated to reach normal PaO2 [19.4(SEM 0.7) kPa] or high PaO2 [53.2(5.5) kPa]. Blood oxygen content was kept constant despite the higher PaO2, by slightly reducing the haemoglobin concentration from 9.3(0.2) to 8.8(0.2) g.100 ml-1 (p < 0.01). Coronary blood flow was kept constant throughout the study, so that the oxygen supply would not vary with the rise in PaO2. Increases in coronary resistance were therefore reflected by increased perfusion pressure. RESULTS: Switching from normal to high PaO2 induced coronary vasoconstriction, reflected by enhanced perfusion pressure of +21(5)%. After pretreatment with the alpha adrenergic agonist phenylephrine, perfusion of a high PaO2 solution increased coronary resistance by +35(7)% (p < 0.05), a value significantly higher than that found without phenylephrine. Oxygen consumption and myocardial performance did not vary throughout the study. To determine whether this amplification of the response was specifically due to alpha agonist stimulation or could be observed with other vasoactive agents, we applied the same protocol using serotonin instead of phenylephrine. Here again, coronary vasoconstriction rose in response to high PaO2 after serotonin infusion [+25(5)% versus +59(10)%]. CONCLUSIONS: The response of the coronary network to high PaO2 is amplified by pretreatment with the alpha adrenergic agonist phenylephrine or with serotonin, regardless of any changes in metabolic status.

Animals↗

Effects of age and gender on cardiovascular responses to phenylephrine.

BACKGROUND: The age-associated impairment in left ventricular (LV) systolic function appears to be mostly detectable during exercise or sympathetic stimulation. We hypothesized that the decline in cardiac function could be unmasked by an acute increase in afterload induced by phenylephrine. We further sought to examine whether the deterioration in cardiac function is influenced by gender. METHODS: We studied 17 young (20-31 years old) and 21 older healthy subjects (60-75 years old) who were given infusions of incremental doses of phenylephrine following cardiac muscarinic receptor blockade with atropine. Left ventricular systolic function was assessed with 2-D echocardiography. RESULTS: The young subjects exhibited a paradoxical increase in heart rate in response to alpha-adrenergic stimulation, but the older subjects did not (p < .01). The increase in systolic blood pressure in response to phenylephrine was influenced by age and gender (i.e., greater in the younger men and older women), whereas the increase in diastolic blood pressure was greater in the younger than the older subjects of both sexes. The changes in LV end-diastolic diameter with phenylephrine were unaffected by age or gender. The slope of the systolic shortening-end systolic wall stress relationship was significantly steeper in the older subjects, suggesting a decline in the contractile response to an acute increase in afterload with aging. CONCLUSIONS: This study's findings suggest that age can significantly influence the cardiovascular responses to alpha-adrenergic stimulation and that phenylephrine, by acutely increasing afterload, is effective in unmasking the age-associated deterioration in left ventricular systolic function. Further, it appears that the increase in systolic blood pressure in response to an alpha-adrenergic challenge is significantly influenced not only by age but also by gender.

Adrenergic alpha-Agonists↗

Intraoperative phenylephrine infusion decreases the magnitude of redistribution hypothermia.

UNLABELLED: Core hypothermia during the first hour after induction of general anesthesia results largely from an internal core-to-peripheral redistribution of body heat. This redistribution results from both central inhibition of tonic thermoregulatory vasoconstriction in the arteriovenous shunt and anesthetic-induced vasodilation. We therefore tested the hypothesis that acute administration of phenylephrine, a pure alpha-adrenergic agonist, reduces the magnitude of anesthetic-induced core-to-peripheral redistribution of body heat. Patients undergoing minor oral surgery were randomly assigned to an infusion of 0.5 microgram.kg-1.min-1 phenylephrine i.v. or no treatment (control). The phenylephrine infusion was started immediately before anesthesia was induced with 2.5 mg/kg propofol i.v. Subsequently, anesthesia was maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe, skin-temperature gradients < 0 degree C were considered indicative of significant arteriovenous shunt vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Although there were no significant differences in skin-temperature gradients, core temperatures in the untreated patients decreased significantly more (1.2 +/- 0.4 degrees C) than in those given phenylephrine (0.5 +/- 0.2 degree C, P < 0.001). These data suggest that maintaining precapillary vasoconstriction of blood vessels, not in the arteriovenous shunt reduces the magnitude of redistribution hypothermia. IMPLICATIONS: Core hypothermia immediately after induction of general anesthesia results largely from core-to-peripheral redistribution of body heat. Core temperature reduction during the first hour of anesthesia decreased less in patients given phenylephrine than in untreated controls. These data suggest that maintaining precapillary vasoconstriction possibly reduces the magnitude of redistribution hypothermia.

Adrenergic alpha-Agonists↗

Treatment of hypotension after hyperbaric tetracaine spinal anesthesia. A randomized, double-blind, cross-over comparison of phenylephrine and epinephrine.

BACKGROUND: Despite many advantages, spinal anesthesia often is followed by undesirable decreases in blood pressure, for which the ideal treatment remains controversial. Because spinal anesthesia-induced sympathectomy and management with a pure alpha-adrenergic agonist can separately lead to bradycardia, the authors hypothesized that epinephrine, a mixed alpha- and beta-adrenergic agonist, would more effectively restore arterial blood pressure and cardiac output after spinal anesthesia than phenylephrine, a pure alpha-adrenergic agonist. METHODS: Using a prospective, double-blind, randomized, cross-over study design, 13 patients received sequential infusions of epinephrine and phenylephrine to manage hypotension after hyperbaric tetracaine (10 mg) spinal anesthesia. Blood pressure, heart rate, and stroke volume (measured by Doppler echocardiography using the transmitral time-velocity integral) were recorded at baseline, 5 min after injection of tetracaine, and before and after management of hypotension with epinephrine and phenylephrine. Cardiac output was calculated by multiplying stroke volume x heart rate. RESULTS: Five min after placement of a hyperbaric tetracaine spinal anesthesia, significant decrease in systolic (from 143 +/- 6 mmHg to 125 +/- 5 mmHg; P < 0.001), diastolic (from 81 +/- 3 to 71 +/- 3; P < 0.001), and mean (from 102 +/- 4 to 89 +/- 3; P < 0.001) arterial pressures occurred. Heart rate (75 +/- 4 beats/min to 76 +/- 4 beat/min; P = 0.9), stroke volume (115 +/- 17 to 113 +/- 13; P = 0.9), and cardiac output (8.0 +/- 1 l/m to 8.0 +/- 1l/m; P = 0.8) did not change significantly after spinal anesthesia. Phenylephrine was effective at restoring systolic blood pressure after spinal anesthesia (120 +/- 6 mmHg to 144 +/- 5 mmHg; P < 0.001) but was associated with a decrease in heart rate from 80 +/- 5 beats/min to 60 +/- 4 beats/min (P < 0.001) and in cardiac output from 8.6 +/- 0.7 l/m to 6.2 +/- 0.7 l/m (P < 0.003). Epinephrine was effective at restoring systolic blood pressure after spinal anesthesia (119 +/- 5 mmHg to 139 +/- 6 mmHg; P < 0.001) and was associated with an increase in stroke volume from 114 +/- 12 ml to 142 +/- 17 (P < 0.001) and cardiac output from 7.8 +/- 0.6 l/m to 10.8 +/- 1.1 l/m (P < 0.001). CONCLUSIONS: Epinephrine management of tetracaine spinal-induced hypotension increases heart rate and cardiac output and restores systolic arterial pressure but does not restore mean and diastolic blood pressure. Phenylephrine management of tetracaine spinal-induced hypotension decreases heart rate and cardiac output while restoring systolic, mean, and diastolic blood pressure.

Adrenergic Agonists↗

The addition of phenylephrine contributes to the development of transient neurologic symptoms after spinal anesthesia with 0.5% tetracaine.

BACKGROUND: Recent reports indicate that transient neurologic symptoms commonly occur after single-injection spinal anesthesia with lidocaine. Information regarding tetracaine has been limited to a single case report. In addition, little is known about the cause of these symptoms or the cofactors that affect their occurrence. The present study sought to determine whether the presence of phenylephrine or the concentration of glucose in the anesthetic solution affects the incidence of transient neurologic symptoms after spinal anesthesia with 0.5% tetracaine. METHODS: One-hundred sixty patients classified as American Society of Anesthesiologists physical status I or II who were scheduled for elective surgery on a lower limb or perineum were sequentially assigned to one of four equal groups to receive intrathecal 0.5% tetracaine in 7.5% or 0.75% glucose, with or without 0.125% phenylephrine. Patients were evaluated on postoperative day one for the presence of pain, dysesthesia, or both in the legs or buttocks by an investigator unaware of the drug given. RESULTS: Symptoms were present in 10 patients (12.5%) receiving a spinal anesthetic containing phenylephrine, but in only one patient (1.3%) receiving spinal anesthesia without phenylephrine. There was no significant difference in the incidence of symptoms between groups receiving 7.5% glucose and those receiving 0.75% glucose (8.8% and 5% of patients, respectively). CONCLUSIONS: These results suggest that adding phenylephrine to tetracaine for spinal anesthesia increases the potential for transient neurologic symptoms, but that the concentration of glucose does not affect their occurrence.

Adult↗

Effects of sodium nitroprusside and phenylephrine on blood flow in free musculocutaneous flaps during general anesthesia.

BACKGROUND: Hypoperfusion and necrosis in free flaps used to correct tissue defects remain important clinical problems. The authors studied the effects of two vasoactive drugs, sodium nitroprusside and phenylephrine, which are used frequently in anesthetic practice, on total blood flow and microcirculatory flow in free musculocutaneous flaps during general anesthesia. METHODS: In a porcine model (n = 9) in which clinical conditions for anesthesia and microvascular surgery were simulated, latissimus dorsi free flaps were transferred to the lower extremity. Total blood flow in the flaps was measured using ultrasound flowmetry and microcirculatory flow was measured using laser Doppler flowmetry. The effects of sodium nitroprusside and phenylephrine were studied during local infusion through the feeding artery of the flap and during systemic administration. RESULTS: Systemic sodium nitroprusside caused a 30% decrease in mean arterial pressure, but cardiac output did not change. The total flow in the flap decreased by 40% (P < 0.01), and microcirculatory flow decreased by 23% in the skin (P < 0.01) and by 30% in the muscle (P < 0.01) of the flap. Sodium nitroprusside infused locally into the flap artery increased the total flap flow by 20% (P < 0.01). Systemic phenylephrine caused a 30% increase in mean arterial pressure, whereas heart rate, cardiac output, and flap blood flow did not change. Local phenylephrine caused a 30% decrease (P < 0.01) in the total flap flow. CONCLUSIONS: Systemic phenylephrine in a dose increasing the systemic vascular resistance and arterial pressure by 30% appears to have no adverse effects on blood flow in free musculocutaneous flaps. Sodium nitroprusside, however, in a dose causing a 30% decrease in systemic vascular resistance and arterial pressure, causes a severe reduction in free flap blood flow despite maintaining cardiac output.

Anesthesia, General↗

Effect of halothane on phenylephrine-induced vascular smooth muscle contractions in endotoxin-exposed rat aortic rings.

OBJECTIVES: a) To determine the response of endotoxin-exposed vascular smooth muscle to exogenous vasoconstrictors during concomitant exposure to an inhaled anesthetic (halothane); and b) to determine if excess nitric oxide production is responsible for any altered response. DESIGN: In vitro, prospective, repeated-measures, dose-response study. SETTING: University/medical school experimental physiology laboratory. SUBJECTS: Adult male Sprague-Dawley rats, whose aortae were studied in an in vitro preparation. INTERVENTIONS: Thoracic aortae were excised from anesthetized animals and cut into 3-mm rings. After incubation in aerated organ baths containing a modified essential medium with or without Escherichia coli lipopolysaccharide (100 micrograms/mL) at 37 degrees C for 5 hrs, the rings were removed and suspended in separate baths for isometric tension recording. Phenylephrine dose-response data (10(-10) to 10(-5) M) were determined for lipopolysaccharide- and nonlipopolysaccharide-treated rings. After washout and equilibration, two vessels (one each lipopolysaccharide- and nonlipopolysaccharide-treated) were additionally exposed to 2% halothane and phenylephrine dose-response determinations were repeated for all vessels. This procedure was repeated for 1% halothane in a separate experiment. In some experiments, the nitric oxide synthase inhibitor, N omega-nitro-L-arginine (3 x 10(-4) M), was added to the bath after the washout from the second phenylephrine dose-response determination. Then, a third phenylephrine dose-response determination was performed, with and without 2% halothane. MEASUREMENTS AND MAIN RESULTS: Dose-response curves were evaluated using a logistic regression analysis. In addition, absolute and percentage changes in tension were compared between the first and second contractions. Exposure to lipopolysaccharide resulted in a decrease in the maximum tension from 2.07 +/- 0.03 (controls) to 1.24 +/- 0.04 g/mg of vessel dry weight and an increase in the dose at which the contraction is 50% of maximum (ED50) from 3.78 x 10(-8) to 2.05 x 10(-7) M (p < .05). Exposure to 2% halothane produced significant reductions in the maximum tensions in both groups. The lipopolysaccharide-treated vessels showed not only a proportionately larger decrease (-51 +/- 5% vs. -18 +/- 2% in the control plus halothane group), but also a significantly greater absolute decrease (0.59 +/- 0.09 vs. 0.34 +/- 0.04 g/mg in the control plus halothane group). The addition of 1% halothane produced less pronounced decreases in tension, with only an additive effect in the lipopolysaccharide-treated vessels. The addition of N omega-nitro-L-arginine resulted in a reversal of the lipopolysaccharide-induced decrease in tension. However, 2% halothane still had a significantly greater effect on the lipopolysaccharide-exposed rings. CONCLUSIONS: Exposure of rat aortic rings to lipopolysaccharide in vitro decreased the contractile response to phenylephrine. The addition of 2% halothane resulted in a more than additive decrease in tension in the lipopolysaccharide-treated vessels. Patients in septic or endotoxic shock are sensitive to most anesthetic regimens, and some of this sensitivity may be due to an altered vasoconstrictive response induced by lipopolysaccharide exposure. The inability of nitric oxide synthase inhibition to reverse this response completely suggests that induction of nitric oxide synthase and increased production of nitric oxide are not solely responsible for this finding.

Anesthetics, Inhalation↗

Cerebral hemodynamic effects of phenylephrine and L-arginine after cortical impact injury.

OBJECTIVE: To determine the effects of a pressor agent (phenylephrine and L-arginine) on the abnormal cerebral hemodynamics and on neurologic outcome after a severe cortical impact injury in rats. DESIGN: Prospective, randomized study. SETTING: University laboratory. SUBJECTS: Male Long-Evans rats, weighing 300 to 400 g, fasted overnight. INTERVENTIONS: The animals were anesthetized with isoflurane, and a severe cortical impact injury (velocity, 5 m/sec; deformation, 3 mm) was produced in the right parietal cortex. Five minutes after impact injury, one of the following three treatments were infused: 1 mL saline intravenously for 10 mins, 300 mg/kg L-arginine in 1 mL saline intravenously for 10 mins, or 0.3 microg/kg/min phenylephrine intravenously for 3 hrs. Mean arterial pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and laser Doppler flow (LDF) at the impact site and in the contralateral parietal cortex were monitored for 3 hrs after the impact injury. Histologic examination of the brain was performed at 2 wks after injury in a separate group of L-arginine- and saline-treated animals. MEASUREMENTS AND MAIN RESULTS: The immediate response to the impact injury was an increase in ICP, and a decrease in mean arterial pressure, CPP, and LDF. In the saline-treated animals, LDF decreased to <25% of the baseline values at the impact site and stayed at that level for the entire 3-hr monitoring period. On the contralateral side, LDF decreased initially and recovered gradually to approximately 50% of the preimpact baseline value. Infusion of both phenylephrine and L-arginine increased LDF back to near-baseline levels. However, phenylephrine increased ICP significantly, whereas ICP with L-arginine did not change. L-arginine treatment reduced the contusion volume from a median value of 5.28 mm3 to 0.63 mm3. CONCLUSIONS: Phenylephrine increased cerebral blood flow (CBF) by increasing CPP. L-arginine, however, increased CBF without changing CPP. The improvement in CBF was accompanied by a decrease in neurologic injury. Although the pressor agents are used currently to increase CBF after traumatic brain injury, other strategies may also increase CBF without the potential adverse effects of induced hypertension.

Animals↗

Implications of altered inotropic effects of phenylephrine in pressure-overloaded cat ventricular muscle.

The positive inotropic action of phenylephrine in cardiac muscle is mediated by alpha- and beta-adrenoceptors. Data suggest the responsiveness of myocardium to inotropic agents is altered in cardiac disease. We evaluated the actions of phenylephrine on isometric contraction and K+-induced contracture in isolated cat right ventricular muscle from normal hearts and hearts with partial pulmonary artery ligation-induced pressure overload of 5-11 days in duration. Peak contractile force (Po) and rate of force development (dP/dt) were lower (p less than or equal to 0.005) in pressure-overloaded (0.59 +/- 0.2 g/mm2 and 4.6 +/- 1.7 g/s/mm2, respectively) than in normal (1.33 +/- 0.2 g/mm2 and 10.5 +/- 1.6 g/s/mm2, respectively) muscle. Phenylephrine (10(-6), 5 X 10(-6), and 10(-5) M) significantly (p less than or equal to 0.01) increased Po and dP/dt in normal but not in pressure-overloaded muscle. Phenylephrine (5 X 10(-6) M) reduced peak K+-induced contracture force (Pc) similarly in normal (-30 +/- 8%) and pressure-overloaded (-36 +/- 11%) muscles. beta-Adrenergic blockade (nadolol, 10(-4) M) reduced, but did not abolish, the "relaxant" action of the drug on Pc in both muscle groups. The lack of a positive inotropic effect of phenylephrine in pressure-overloaded muscle suggests a derangement in both alpha- and beta-adrenoceptor function in this model of cardiac disease.

Animals↗

Effect of ketanserin on phenylephrine-dependent changes in splanchnic hemodynamics and systemic blood pressure in healthy subjects.

We studied the effect of ketanserin on basal status and phenylephrine-dependent changes in arterial blood pressure and splanchnic hemodynamics in seven healthy subjects. The drug was administered as an intravenous bolus of 10 mg followed by infusion of 4 mg/h. After a basal period of saline or ketanserin infusion, phenylephrine was infused at a constant rate in a fixed dose sequence of 1, 2, and 3 micrograms/kg/min. Blood pressure was measured intraarterially. Splanchnic blood flow, mean wedged hepatic blood pressure, and splanchnic vascular resistance were assessed by means of the hepatic venous catheter technique using indocyanine green dye. At steady-state plasma concentrations, basal arterial pressure and heart rate were not altered in this small group of normal subjects, whereas mean wedged hepatic venous pressure was lowered by ketanserin. During saline infusion, phenylephrine provoked a dose-dependent rise in arterial and wedged hepatic blood pressure; these effects were attenuated by ketanserin. Phenylephrine induced a significant, but not dose-dependent, decrease in estimated splanchnic blood flow. Ketanserin did not relevantly influence basal or phenylephrine-dependent splanchnic blood flow. We suggest that the hypotensive action of ketanserin is in part related to an interaction at alpha 1-adrenoceptors. Moreover, a dissociation of effects on vascular alpha-receptors seems to exist in the splanchnic and systemic circulations.

Adult↗

Acute pressor actions of ouabain do not enhance the actions of phenylephrine or norepinephrine in anesthetized rats.

The inhibition of high-affinity isoforms of the Na+,K+-ATPase by nanomolar levels of ouabain has been proposed to enhance the actions of vasoconstrictor agents that act via a Ca+2-dependent mechanism. The present study tested this hypothesis by evaluating the effects of ouabain (6 and 18 microg/kg, i.v.) on the vasopressor actions of phenylephrine and norepinephrine in anesthetized, reflex-blocked rats. In separate groups of animals, dose-response curves for increases in diastolic pressure produced by phenylephrine were generated after the administration of saline (control), ouabain (18 microg/kg), L-omega-N-nitro arginine methyl ester (L-NAME, 3 micromol/kg) and angiotensin II (15 ng/kg per min). Treatment with ouabain (18 microg/kg) produced an increase in diastolic pressure of 19+/-3 mm Hg but did not significantly alter the potency or maximal response produced by phenylephrine. In contrast, treatment with angiotensin II and L-NAME, agents known to enhance the actions of alpha-adrenoceptor agonists, increased the potency of phenylephrine. In animals in which the pressor actions of norepinephrine were evaluated before and after the administration of ouabain (6 microg/kg), ouabain did not alter the pressor response to norepinephrine. Blockade of alpha-adrenoceptors with phentolamine was found to attenuate as well as partially reverse the increase in diastolic pressure produced by ouabain. These observations suggest that ouabain produces a pressor response by actions on sympathetic nerve endings as well as on vascular smooth muscle and that these actions do not alter the sensitivity to phenylephrine or norepinephrine.

Angiotensin II↗

Effects of topical anesthetics on phenylephrine-induced mydriasis.

Pupil responses to phenylephrine alone and to phenylephrine preceded by a topical anesthetic were recorded by means of an infrared pupillometer. In response to phenylephrine, pupils dilated more in eyes with pale irides. Dilation was greater if a topical anesthetic was applied before the mydriatic. Benoxinate, proparacaine, and tetracaine produced approximately equal degrees of enhancement of the mydriasis. One drop of 1% phenylephrine had only a small dilating effect on an eye when the fellow eye received the phenylephrine preceded by 0.5% proparacaine.

Administration, Topical↗

Comparison of adrenaline and phenylephrine in out-of-hospital cardiopulmonary resuscitation. A double-blind study.

Phenylephrine, a strong alpha-adrenergic receptor-stimulating agent, was compared with adrenaline in 65 patients with out-of-hospital cardiac arrest, in a double-blind study. The resuscitation was performed by the physician-staffed Prehospital Emergency Care Unit of Helsinki University Central Hospital. The patients received either 1.0 mg of phenylephrine or 0.5 mg of adrenaline i.v. in the treatment of fine ventricular fibrillation, asystole or electromechanical dissociation. If two doses of either drug did not restore circulation, 0.5 mg of known 0.01% adrenaline was given i.v., maximally twice. In the adrenaline group, which consisted of 36 patients with a mean age of 61 years, 10 patients (28%) were successfully resuscitated. The phenylephrine group consisted of 29 patients with a mean age of 62 years. In this group nine patients (31%) were successfully resuscitated. The two groups were comparable regarding their apnoea-times, and there was no difference in the need for extra adrenaline between the groups. No adverse effects, such as hypertension or bradycardia, were noted in the patients treated with either adrenaline or phenylephrine, nor did the overall rate of successful resuscitation fall during the test period. It is concluded that phenylephrine seems as effective as adrenaline in the treatment of cardiac arrest, but further studies seem warranted.

Adult↗

Effects of ephedrine and phenylephrine on maternal and fetal atrial natriuretic peptide levels during elective cesarean section.

The effects of ephedrine and phenylephrine on fetal and maternal plasma atrial natriuretic peptide (ANP) concentrations were studied during 30 elective cesarean sections. After induction of spinal anesthesia, reductions from baseline maternal blood pressure were corrected with one of these pressor agents administered in a double-blinded, randomized manner. Immediately following delivery, umbilical artery (UA) ANP concentrations were significantly higher than umbilical vein (UV) concentrations (pg/ml) for both groups (ephedrine, 120.8 +/- 64.0 vs. 86.8 +/- 40.8, phenylephrine, 125.0 +/- 54.2 vs. 72.4 +/- 31.7), but there were no differences between groups for UA and UV ANP levels. Postpartum maternal ANP concentrations were significantly higher than baseline values in both groups, but again there were no differences between groups. Correlations between total doses of ephedrine or phenylephrine and UA or UV ANP levels did not reach significance. Postpartum maternal (MV2), UA, and UV blood gas variables (pH, PCO2, and PO2) were also not different between groups. These data suggest that effects of pressor doses of ephedrine (beta and alpha agonist) and phenylephrine (alpha agonist) on maternal and fetal ANP levels are not different. Therefore, 1) assuming these pressor drugs stimulate ANP release, this stimulation is not solely mediated by beta receptors and 2) to the extent that fetal ANP influences feto-placental circulatory homeostasis, the effects of ephedrine and phenylephrine on this regulatory mechanism do not appear to be different.

Adult↗

Effects of isoprenaline and phenylephrine on energy-rich phosphate compounds and glucose-6-phosphate in smooth and cardiac muscle.

1. Tension changes produced by phenylephrine and isoprenaline have been examined in four tissues-the guinea-pig taenia coli, the longitudinal muscle strip of rabbit duodenum, the abdominal aorta of the rabbit and the rat heart.2. Changes in the amounts of adenosine triphosphate (ATP), creatine phosphate (CP) and glucose-6-phosphate (G-6-P) associated with the addition of phenylephrine and isoprenaline have been measured in the four tissues using enzymatic fluorimetric analysis.3. An alpha-adrenoceptor-mediated increase in tension (phenylephrine; rabbit aorta) was associated with no change in the amounts of ATP, CP or G-6-P.4. An alpha-adrenoceptor-mediated decrease in tension (phenylephrine; guineapig taenia coli and rabbit duodenum) was associated with no change in the amounts of ATP, CP or G-6-P.5. A beta-adrenoceptor-mediated increase in force of contraction (phenylephrine and isoprenaline; rat heart) was associated with a reduction in the amounts of ATP and CP and an increase in the amount of G-6-P.6. A beta-adrenoceptor-mediated decrease in tension (isoprenaline; guinea-pig taenia coli and rabbit duodenum) was associated with an increase in the amounts of ATP and CP and no change in the amount of G-6-P.7. beta-Adrenoceptor-mediated metabolic changes were antagonized by propranolol.

Adenosine Triphosphate↗

Theophylline and phenylephrine effects on cardiac relaxation.

In the driven isolated left atrium of the rabbit theophylline shortened relaxation time in a similar manner to isoprenaline and histamine. 2 Phenylephrine lengthened relaxation time in a similar manner to calcium. 3 Theophylline caused phenylephrine to shorten relaxation time, which was inhibited by a beta-adrenoceptor blocking drug, but theophylline did not potentiate the effect of phenylephrine on peak tension. 4 Theophylline separated drug effects on cardiac relaxation and contraction: in the presence of theophylline at a low calcium concentration, phenylephrine shortened relaxation time by beta-adrenoceptor stimulation and increased peak tension by alpha-adrenoceptor stimulation. At a high calcium concentration, theophylline potentiated the effect of isoprenaline, histamine and phenylephrine on relaxation time but inhibited the effect on peak tension.

Animals↗