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PubMed1998

Promotion by the alpha-adrenoceptor agonist phenylephrine, but not by the beta-adrenoceptor agonist isoproterenol, of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of prolonged administration of the alpha-adrenoceptor agonist phenylephrine and the beta-adrenoceptor agonist isoproterenol on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine and on the labeling index of gastric mucosa were compared in Wistar rats. Rats received subcutaneous injections of 3 or 6 mg/kg body weight of phenylephrine or 0.1 or 0.2 mg/kg body weight of isoproterenol every other day after 25 weeks of oral treatment with the carcinogen. Long-term administration of phenylephrine at a high dose, but not at a low dose, significantly increased the incidence of gastric cancers and the labeling index of antral epithelial cells at the end of the experiment in week 52. However, administration of isoproterenol at either dosage had no significant effect on the incidence of gastric cancers and the labeling index of antral epithelial cells. These findings indicate that increased activity of the sympathetic nervous system enhances gastric carcinogenesis through alpha-adrenoceptors.

Adrenergic alpha-Agonists↗

PubMed1997

Alpha 1-adrenoceptor subtype involved in the positive and negative inotropic responses to phenylephrine in rat papillary muscle.

1. In rat papillary muscle, stimulation of alpha 1-adrenoceptors results in a biphasic inotropic response: a transient negative inotropic phase and a subsequent sustained positive inotropic phase. This study was designed to determine whether the positive and negative inotropic effects in this tissue are mediated by different alpha 1-adrenoceptor subtypes. 2. After treatment with the tumor-promoting compound, phorbol 12, 13-dibutyrate, phenylephrine (in the presence of propranolol) produced only a positive inotropic effect. The selective alpha 1A-adrenoceptor antagonist, WB4101, significantly inhibited the positive inotropic effect. In contrast, inactivation of alpha 1B-adrenoceptors with chloroethylclonidine (CEC) did not alter the positive effect. 3. In the presence of the Ca2+ channel antagonist, nifedipine, phenylephrine induced only a sustained negative inotropic effect. The negative inotropic effect was significantly attenuated by WB4101, but was not affected by CEC. 4. We conclude that both the positive and negative inotropic responses of rat papillary muscle to phenylephrine are mediated exclusively by the WB4101-sensitive but CEC-resistant alpha 1-adrenoceptor subtype. The alpha 1-adrenoceptor subtype with such a property may correspond to the alpha 1A-subtype.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1999

The influence of phenylephrine outward potassium currents in single smooth muscle cells from the rabbit mesenteric artery.

In mesenteric artery smooth muscle cells, depolarizing voltage steps activated outward K+ currents whose amplitude was decreased by about 20% with phenylephrine (1-10 microM: n = 14 cells). Attenuation of outward current was only partly dependent on [Ca2+]i, because it persisted, although reduced, with 10 mM BAPTA in the patch pipette and was abolished in the presence of 3 mM 3,4-diaminopyridine (n = 13). In outside-out patches, phenylephrine did not exert any direct effect on the unitary current amplitude or open probability of large conductance K+ channels. Outward current was significantly increased (>100% in both cases) by 10 mM caffeine, presumably owing to the release of internal Ca2+ stores. With 10 mM BAPTA in the pipette, the only response to caffeine was a small decrease (9 +/- 3.7%, n = 10) in the K+ current. These observations show that a minor effect of phenylephrine is to reduce outward K+ current (probably Kv) in mesenteric cells.

4-Aminopyridine↗

PubMed2000

Quantitative analysis of chlorpheniramine maleate and phenylephrine hydrochloride in nasal drops by differential-derivative spectrophotometric, zero-crossing first derivative UV spectrophotometric and absorbance ratio methods.

Three simple, rapid and accurate methods are described for the simultaneous determination of chlorpheniramine maleate and phenylephrine hydrochloride in two component mixtures. The first method comprised of measurement of difference absorptivities derivatized in first order of a nasal drops in 0.1 N NaOH relative to that of an equimolar solution in methanol at wavelengths of 271.6 and 250.2 nm, respectively. The second method, zero-crossing derivative spectrophotometry, is based on recording the first derivative curves and determining each component using the zero-crossing technique. Using first derivative spectrophotometry, the amplitudes in the first derivative spectra at 246.5 and 238.6 nm were selected to simultaneously determine chlorpheniramine maleate and phenylephrine hydrochloride in the mixture. The presence of identical zero-crossing points for pure drugs and nasal drop solutions established the non-interference of the excipients in the absorption at these wavelengths. Absorbance ratio method was also developed for a comparison method. The proposed procedures were successfully applied to the determination of chlorpheniramine maleate and phenylephrine hydrochloride in nasal drops, with a high percentage of recovery, good accuracy and precision.

Anti-Allergic Agents↗

PubMed2002

Validation of a HPLC quantification of acetaminophen, phenylephrine and chlorpheniramine in pharmaceutical formulations: capsules and sachets.

Acetaminophen, phenylephrine and chlorpheniramine are frequently associated in pharmaceutical formulations against the common cold. Their quantification presents several problems. A HPLC method for the simultaneous determination of these compounds in pharmaceutical formulations such as capsules and sachets, including the separation of impurities and excipients has been developed and validated. The selectivity of the method was also tested to be used if phenylpropanolamine hydrochloride were employed instead of phenylephrine. Final chromatographic conditions were a gradient elution, being solvent A: phosphate buffer 40 mM at pH 6.0 and solvent B: acetonitrile. At t=0, the mobile phase consisted of 92% A and 8% B and it changed with a linear gradient during 8 min to 75% A and 25% B. At min 8, it changed to 30% A and 70% B for 5 min and at t=15 min, it returns to the initial conditions (92% A and 8% B) during 1 min remaining at this composition until t=20 min. UV detection was performed at 215 nm for phenylephrine and chlorpheniramine, because at this wavelength sensitivity was higher than in other more characteristic wavelengths and it was necessary for the detection of minor compounds. For acetaminophen 280 nm was employed. Validation parameters permit to consider the method adequate.

Acetaminophen↗

PubMed1999

Support of mean arterial pressure during tepid cardiopulmonary bypass: effects of phenylephrine and pump flow on systemic oxygen supply and demand.

OBJECTIVE: To examine the effects of phenylephrine infusion and increases in pump flow on systemic oxygen supply and demand when they are used to support mean arterial pressure (MAP) during cardiopulmonary bypass (CPB). DESIGN: Prospective, unblinded study. SETTING: The animal cardiopulmonary laboratory at the Mayo Foundation (Rochester, MN). PARTICIPANTS: Twelve pigs. INTERVENTIONS: Twelve pigs had systemic oxygen delivery (DO2) and consumption (VO2) measured before CPB and then underwent CPB at 35 degrees C. During CPB, measurements of DO2 and VO2 were obtained at an MAP of approximately 50 mmHg and a pump flow of 2.2 L/min/m2. Thereafter, MAP was elevated to 70 mmHg either by increases in pump flow or by a phenylephrine infusion, and the balance between systemic oxygen supply and demand was reassessed. MEASUREMENTS AND MAIN RESULTS: Before CPB, DO2 was 375 +/- 83 mL/min/m2 and decreased with the onset of CPB mainly because of the effects of hemodilution. During CPB, with a pump flow of 2.2 L/min/m2 and an MAP of 53 mmHg, DO2 was 218 +/- 40 mL/min/m2. Increasing perfusion pressure to an MAP of 72 mmHg with phenylephrine and maintaining pump flow constant (2.2 L/min/m2) did not change DO2 (222 +/- 37 mL/min/m2), and the oxygen extraction ratio (OER) was increased relative to pre-CPB levels. In contrast, increasing MAP to 71 mmHg by increasing pump flow to 3.2 L/min/m2 resulted in a significantly greater DO2, and the OER normalized to the pre-CPB value. CONCLUSIONS: During CPB with conventional flow rates, DO2 is decreased. Supporting MAP with increases in pump flow better maintains DO2 than the administration of an alpha-agonist.

Adrenergic alpha-Agonists↗

PubMed2006

The effect of ephedrine and phenylephrine on BIS values during propofol anaesthesia.

BACKGROUND: The purpose of this study was to evaluate the effect of ephedrine and phenylephrine on propofol concentrations and bispectral index during propofol anesthesia. METHODS: General anaesthesia was induced with propofol and was maintained with propofol (4 mg kg-1 h-1) and fentanyl. Vecuronium was used to facilitate the artificial ventilation of the lungs. Patients with systolic blood pressure > 90 mmHg were defined as the control group (n = 16). Patients who had to be treated for larger decreases in arterial blood pressure (systolic blood pressure 60, whereas no patient in the control or phenylephrine groups had bispectral index >60. There were no significant differences in propofol concentrations or cardiac output relative to baseline at 3 or 10 min after the administration of ephedrine or phenylephrine. CONCLUSIONS: Ephedrine increases bispectral index values without decreasing propofol concentrations during general anesthesia.

Anesthesia, Intravenous↗

PubMed1993

Physicochemical characterization of high- and low-melting phenylephrine oxazolidines.

Phenylephrine oxazolidine is a new prodrug of phenylephrine developed for improving ocular absorption and reducing systemic side effects. In the present study, high- and low-melting phenylephrine oxazolidines (HMP and LMP) were characterized in terms of their stereochemistry and crystal properties. It was found that the molecular configuration of the prodrug in the crystals of either HMP or LMP is identical (5R/2R). The two crystals were shown to have the same IR spectra and X-ray diffraction patterns but different crystal habits, thermal properties, solubilities and intrinsic dissolution rates. Single crystal X-ray structure analysis indicates that crystals of both HMP and LMP are orthorhombic and belong to the P2(1)2(1)2(1) space group with four molecules in a unit cell (a = 20.697 A, b = 7.065 A, and c = 9.304 A). The molecules in the crystal are held together by an intermolecular hydrogen bonding interaction between N(3) and O(13). The different physical properties observed for LMP result from crystal imperfections caused by the presence of trace amounts (often at levels < 0.5%) of an unidentified, structurally related synthetic impurity which can be dispersed in the prodrug. It was observed that both HMP and LMP can sustain thermal and mechanical treatment in the solid state. However, LMP was partially converted to HMP when suspended in certain solvents.

Calorimetry, Differential Scanning↗

PubMed2002

Nitric oxide synthase/guanylate cyclase pathway modulates the rat vas deferens contractility induced by phenylephrine.

The involvement of the nitric oxide synthase/soluble guanylate cyclase pathway on the modulation of phenylephrine-induced contractility in the rat vas deferens was investigated. Phenlylephrine-concentration response curves were obtained in absence and in presence of inhibitors, N(G)-Nitro-L-arginine (L-NOARG), NG-Nitro-L-arginine methyl esther (L-NAME) or N(G)-monomethyl-L-arginine (L-NMMA) or GC inhibitior, 1H-(1,2,4)-oxadiaziol-(4,3-a)quinoxalin-1-one (ODQ) or nitric oxide donor, 3-morpholinosydnonimine hydrochloride (SIN-1) alone or together with L-NMMA or ODQ. Both nitric oxide synthase and GC inhibitors reduced the Phe-Emax. SIN-1 alone did not change phenylephrine-induced responses and it could reverse the L-NMMA effect but not ODQ effect. The reduction of the phenylephrine-induced contractility obtained in consequence of the inhibition of the nitric oxide/GC pathway suggest that, in the rat vas deferens, despite its well identified relaxant properties, nitric oxide potentiates the contractility induced by adrenergic stimulation.

Animals↗

PubMed1979

The effect of phenylephrine on excretion of fluid and electrolytes by the parotid and mandibular glands of the rat.

The effect has been investigated of the alpha-adrenergic agonist, phenylephrine, on excretion of water and electrolytes (Na, K, and HCO3) by the parotid and mandibular glands of the rat. In the mandibular glands the agonist was as effective as acetylcholine (or parasympathetic nerve stimulation) in stimulating secretion, and the electrolyte excretory patterns seen in the two modes of stimulation were similar. In the parotid gland, phenylephrine was only one-fifth as potent as acetylcholine (or parasympathetic nerve stimulation) in evoking a secretory response but, when due allowance for flow rate differences is made, the electrolyte excretion patterns were similar. In both glands the secretory response to phenylephrine was totally different, in magnitude and in electrolyte excretion pattern, to that evoked by the beta-adrenergic agonist, isoprenaline. It is concluded, as has already been established for secretion of exportable protein, that alpha-adrenergic agonists have very similar effects to muscarinic agonists both on endpiece and on duct cells and that these actions are completely different from those evoked by activation of beta-adrenergic receptors.

Animals↗

PubMed1997

Reduced responsiveness of rat mesenteric resistance artery smooth muscle to phenylephrine and calcium following myocardial infarction.

1. We evaluated responses of peripheral resistance arterial smooth muscle to alpha 1-adrenoceptor stimulation in a rat model of heart failure in relation to neurohumoral changes, wall structure, receptor density and cellular calcium handling. 2. Plasma samples and third order mesenteric artery side-branches were obtained from Wistar rats after induction of left ventricular infarction (M1) or sham surgery. Vessels were denuded of endothelium, sympathectomized, depleted of neuropeptides, and mounted in a myograph for recording of isometric force development in response to calcium, agonist and high potassium. Also, the morphology of these preparations was determined. Separate vessel segments were used in radioligand binding assays with [1H]-prazosin. 3. At 1 week after MI, circulating plasma levels of adrenaline, angiotensin II, atrial natriuretic factor (ANF) and vasopressin were significantly elevated. At 5 weeks only a significant elevation of ANF persisted. 4. At 5 weeks after MI, the structure of the vessels and responsiveness to high potassium or Bay K 8466 (10(6) mol l-1) were not modified. Yet, at this stage, sensitivity to phenylephrine was increased (pD2: 6.24 +/- 0.04 vs 5.98 +/- 0.04 for controls) while maximal contractile responses to phenylephrine in the presence of 2.5 mmol l-1 calcium (2.26 +/- 0.28 vs 3.53 +/- 0.34 N m-1) and the sensitivity to calcium in the presence of phenylephrine (pD2: 2.81 +/- 0.22 vs 3.74 +/- 0.16) were reduced. Responses to the agonist in calcium-free solution and the calcium sensitivity in the presence of 125 mmol l-1 potassium or of phorbol myristate acetate (PMA, 10(-6) mol l-1) were not altered. 5. At 5 weeks after MI, the density of prazosin binding sites was not reduced (4.04 +/- 1.40 vs 2.29 +/- 0.21 fmol microgram-1 DNA in controls). 6. In conclusion, myocardial infarction leads in the rat to a reduction of contractile responses of mesenteric resistance arterial smooth muscle to alpha 1-adrenoceptor stimulation. This seems to involve impaired agonist-stimulated calcium influx.

Animals↗

PubMed1997

Characterization of alpha1-adrenoceptor subtypes mediating contractions to phenylephrine in rat thoracic aorta, mesenteric artery and pulmonary artery.

1. The subtype of alpha1-adrenoceptor mediating contractions to phenylephrine of the rat thoracic aorta, mesenteric artery and pulmonary artery were investigated by use of antagonists which show selectivity between the cloned alpha1-adrenoceptor subtypes in binding studies. 2. Cumulative concentration-contraction curves for phenylephrine were competitively antagonized in the rat thoracic aorta by prazosin (pA2 9.9), WB4101 (pA2 9.6), 5-methylurapidil (pA2 8.1), benoxathian (pA2 9.2) and indoramin (pA2 7.4). These compounds were also competitive antagonists in the mesenteric and pulmonary arteries (except for 5-methylurapidil in the pulmonary artery), (prazosin pA2 9.9 and 9.7; WB4101 pA2 9.8 and 9.6; 5-methylurapidil pA2 7.9 and pK(B) estimate 8.0; benoxathian pA2 8.8 and 9.3; indoramin pA2 7.2 and 7.5, respectively). 3. RS 17053 was not a competitive antagonist in any blood vessel as Schild plot slopes were greater than unity. The pK(B) estimates for RS 17053 were 7.1 in aorta, 7.0 in the mesenteric artery and 7.7 in the pulmonary artery. 4. The alpha1D-subtype selective antagonist BMY 7378 appeared to be non-competitive with shallow Schild plot slopes. The data were better fitted with two lines in all tissues, with Schild plot slopes that were no longer different from unity, except in the pulmonary artery. The higher affinity site for BMY 7378 in the aorta had a pA2 of 9.0, while it was 8.8 and 8.9 in the mesenteric and pulmonary arteries, respectively. 5. MDL73005EF acted in a non-competitive manner in all three blood vessels, with shallow Schild plot slopes. The pK(B) estimates for MDL73005EF were 8.4 in aorta, 7.5 in the mesenteric artery and 8.0 in the pulmonary artery. 6. In all three blood vessels the functionally determined antagonist affinity estimates correlated best with published pKi values for their displacement of [3H]-prazosin binding on membranes expressing cloned alpha1d-adrenoceptors compared with alpha1a- or alpha1b-adrenoceptors. The antagonist affinity estimates in the aorta, mesenteric and pulmonary arteries correlated highly with their previously published pA2 values in rat aorta (alpha1D) and less well with those for alpha1A- and alpha1B-adrenoceptors mediating contraction of the rat epididymal vas deferens and rat spleen, respectively. 7. The results of this study suggest that the contraction to phenylephrine of the rat thoracic aorta, mesenteric artery and pulmonary artery are mediated in part via the alpha1D-subtype of adrenoceptor. The data for both BMY 7378 and MDL73005EF in all three blood vessels are consistent with receptor heterogeneity. However, the identity of the second site is unclear.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed2002

Alterations in phenylephrine-induced contractions and the vascular expression of Na+,K+-ATPase in ouabain-induced hypertension.

Hypertension development, phenylephrine-induced contraction and Na(+),K(+)-ATPase functional activity and protein expression in aorta (AO), tail (TA) and superior mesenteric (SMA) arteries from ouabain- (25 microg day(-1), s.c., 5 weeks) and vehicle-treated rats were evaluated. Ouabain treatment increased systolic blood pressure (127+/-1 vs 160+/-2 mmHg, n=24, 35; P<0.001) while the maximum response to phenylephrine was reduced (P<0.01) in AO (102.8+/-3.9 vs 67.1+/-10.1% of KCl response, n=12, 9) and SMA (82.5+/-7.5 vs 52.2+/-5.8%, n=12, 9). Endothelium removal potentiated the phenylephrine response to a greater extent in segments from ouabain-treated rats. Thus, differences of area under the concentration-response curves (dAUC) in endothelium-denuded and intact segments for control and ouabain-treated rats were, respectively: AO, 56.6+/-9.6 vs 198.3+/-18.3 (n=9, 7); SMA, 85.5+/-15.4 vs 165.4+/-24.8 (n=6, 6); TA, 13.0+/-6.1 vs 39.5+/-10.4% of the corresponding control AUC (n=6, 6); P<0.05. The relaxation to KCl (1 - 10 mM) was similar in segments from both groups. Compared to controls, the inhibition of 0.1 mM ouabain on KCl relaxation was greater in AO (dAUC: 64.8+/-4.6 vs 84.0+/-5.1%, n=11, 14; P<0.05), similar in SMA (dAUC: 39.1+/-3.9 vs 43.3+/-7.8%, n=6, 7; P>0.05) and smaller in TA (dAUC: 62.1+/-5.5 vs 41.4+/-8.2%, n=12, 13; P<0.05) in ouabain-treated rats. Protein expression of both alpha(1) and alpha(2) isoforms of Na(+),K(+)-ATPase was augmented in AO, unmodified in SMA and reduced in TA from ouabain-treated rats. These results suggest that chronic administration of ouabain induces hypertension and regional vascular alterations, the latter possibly as a consequence of the hypertension.

Animals↗

PubMed2005

Intracameral phenylephrine to prevent floppy iris syndrome during cataract surgery in patients on tamsulosin.

PURPOSE: To describe the use of intracameral phenylephrine to prevent the floppy iris syndrome seen in patients who are on the drug tamsulosin for benign prostatic hypertrophy, during cataract surgery. SETTING: Prince Charles Eye Unit, King Edward VII Hospital, Windsor, Berkshire, UK. METHOD: Seven patients who were on systemic tamsulosin for benign prostatic hypertrophy received intracameral phenylephrine before capsulorexhis during their cataract surgery. RESULTS: There was a significant reduction in the amount of mobility of the iris, reduction in the expected fluttering, and sustained papillary dilatation. ConclusionIntracameral phenylephrine is a simple and effective tool to prevent the effects of floppy iris syndrome in those patients undergoing cataract surgery who are on systemic tamsulosin.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1985

The Ca2+-mobilizing actions of vasopressin and angiotensin differ from those of the alpha-adrenergic agonist phenylephrine in the perfused rat liver.

A Ca2+-sensitive electrode was used to study net Ca2+-flux changes induced by the administration of phenylephrine, vasopressin and angiotensin to the perfused rat liver. The studies reveal that, although the Ca2+ responses induced by vasopressin and angiotensin are similar, they are quite different from the Ca2+ fluxes induced by phenylephrine. The administration of phenylephrine is accompanied by a stimulation of a net amount of Ca2+ efflux (140 nmol/g of liver). A re-uptake of a similar amount of Ca2+ occurs only after the hormone is removed. In contrast, the administration of vasopressin or angiotensin to livers perfused with 1.3 mM-Ca2+ induces the release of a relatively small amount of Ca2+ (approx. 40 nmol/g of liver) during the first 60 s. This is followed by a much larger amount of Ca2+ uptake (70-140 nmol/g of liver) after 1-2.5 min of hormone administration, and a slow efflux or loss of a similar amount of Ca2+ over a period of 6-8 min. At lower concentrations of perfusate Ca2+ (less than 600 microM) these hormones induce only a net efflux of the ion. These results suggest that at physiological concentrations of extracellular Ca2+ the mechanism by which alpha-adrenergic agonists mobilize cellular Ca2+ is different from that involving vasopressin and angiotensin. It seems that the hormones may have quite diverse effects on Ca2+ transport across the plasma membrane and perhaps organellar membranes in liver.

Angiotensin II↗

PubMed1990

Altered regulation of glycogen metabolism by vasopressin and phenylephrine in hepatocytes from insulin-resistant obese (fa/fa) rats. Role of protein kinase C.

The hormonal control of glycogen synthase and phosphorylase interconversion was investigated in hepatocytes isolated from lean and genetically obese (fa/fa) rats. In cells from obese animals, the inactivation of synthase by 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA), phospholipase C, vasopressin and the alpha 1-adrenergic agonist phenylephrine was markedly impaired, and the property of PMA to counteract phosphorylase activation by phenylephrine was attenuated. The maximal response of phosphorylase activation to phenylephrine and vasopressin was increased in obese-rat hepatocytes, but the sensitivity to these hormones was similar to that in lean-rat hepatocytes. These observations indicate that the defect in protein kinase C that we reported previously in heart of insulin-resistant fa/fa rats [van de Werve, Zaninetti, Lang, Vallotton & Jeanrenaud (1987) Diabetes 36, 310-319] is probably also expressed in liver.

Animals↗

PubMed2003

Randomized clinical trial of the efficacy and safety of tropicamide and phenylephrine in preoperative mydriasis for phacoemulsification.

PURPOSE: To compare the mydriatic effect and safety between different concentrations of tropicamide and phenyle-phrine in preoperative mydriasis for phaco-emulsification. METHODS: Two hundred and seventeen consecutive eyes in the same number of Chinese patients undergoing phaco-emulsification under local or topical anaesthesia in a university-based eye hospital were analyzed. Patients were randomized into two groups by cluster randomization, each group receiving a different preoperative mydriatic regimen. Regimen A consisted of tropicamide 1.0% with phenylephrine 2.5%, and Regimen B consisted of tropicamide 0.5% with phenylephrine 0.5%. The main outcome measures were horizontal pupillary diameter, systolic, diastolic and pulse pressure and pulse rate. RESULTS: The group who received Regimen A attained a mean horizontal pupillary diameter of 7.00 +/- 1.06 mm. Their pupils were significantly larger than those receiving Regimen B (6.61 +/- 1.03 mm, P = 0.007). No untoward cardiovascular effects were noted in either groups. CONCLUSION: Regimen A attained better preoperative mydriasis for phacoemulsification than Regimen B. Both regimens were safe with regard to their cardiovascular effects. The combination of tropicamide 1.0% and phenylephrine 2.5% is recommended as preoperative mydriatic for phacoemulsification in Chinese patients who have darkly pigmented irides.

Aged↗

PubMed2002

Vecuronium bromide, phenylephrine and atropine combinations as mydriatics in juvenile double-crested cormorants (Phalacrocorax auritus).

Topical vecuronium bromide (Norcuron) and combinations with atropine and phenylephrine, were evaluated as mydriatics in juvenile double-crested cormorants (Phalacrocorax auritus). Nine cormorants were treated with each of four protocols: 1% atropine; 4 mg/mL vecuronium bromide (total 0.16 mg/eye); atropine with vecuronium; and atropine, 2.5% phenylephrine, followed by vecuronium. Drugs were applied topically at 15-min intervals (0.01 mL/drop). Pupil diameter was measured manually every 15 min with a pupil gauge calibrated to the nearest 0.5 mm. No effect was observed with atropine alone. Average +/- SD peak pupil diameter for vecuronium, atropine/vecuronium, and atropine/phenylephrine/vecuronium were 5.4 +/- 1.1 mm, 5.7 +/- 0.8 mm and 6.2 +/- 0.4 mm, respectively; and duration of peak diameters were 38 +/- 28 min, 79 +/- 71 min and 103 +/- 58 min, respectively. The combined atropine, phenylephrine and vecuronium provided the most consistent dilation with larger average pupil size and longer average duration. No side-effects from vecuronium were observed in these birds.

Animals↗