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At least 487 records · Page 27Linked to original sources

PubMed1989

Seasonal variation in responsiveness of human eccrine sweat glands to phenylephrine.

The responses of eccrine sweat glands to intradermally injected phenylephrine were studied in six healthy male volunteers in two experiments carried out in February and June. Phenylephrine (10(-7)-10(-2) M, 50 microliters) had no consistent effect on sweat gland activity during February, but evoked dose-related increases in sweat gland activity during June. Responsiveness to phenylephrine could be antagonized by prazosin (10(-5) and 10(-4) M) added to the injection solution.

Adult↗

PubMed1992

Role of vagal activity in the cardiovascular responses to phenylephrine in man.

The effects of phenylephrine on blood pressure (BP), left ventricular function and total peripheral resistance (TPR) were evaluated in six normotensive male volunteers before and after vagal blockade with atropine. Before atropine, phenylephrine dose-related increased TPR, systolic and diastolic BP and decreased cardiac output by decreases in both stroke volume and heart rate. Post-atropine, the BP (but not TPR) responses to phenylephrine were markedly potentiated, related to an increase in stroke volume despite the higher afterload. Thus vagal tone may regulate cardiac output via effects on both heart rate and venous return.

Adult↗

PubMed1985

Serum concentrations and urinary excretion of lidocaine and its two desethylated metabolites after spinal anaesthesia using lidocaine or lidocaine with phenylephrine.

In 13 patients undergoing transurethral prostatic resection under spinal anaesthesia with heavy lidocaine or with heavy lidocaine plus phenylephrine hydrochloride, the serum concentrations of lidocaine, monoethylglycinexylidide and glycinexylidide and their renal excretion were measured with a HPLC method. Seven patients were given lidocaine alone 1.25 mg/kg and six lidocaine 1.25 mg/kg mixed with phenylephrine hydrochloride 3 mg. There was no significant difference between the two groups either in the serum levels of lidocaine or in the renal excretion rate of lidocaine and its metabolites. This finding gives support to the opinion that phenylephrine in low doses has no prolonging effect on spinal anaesthesia performed with heavy lidocaine.

Aged↗

PubMed1991

Effects of caffeine, halothane, succinylcholine, phenylephrine and isoproterenol on myocardial force of contraction of malignant hyperthermia susceptible swine.

The effects of caffeine, halothane, succinylcholine, phenylephrine and isoproterenol on force of contraction were studied in electrically driven (0.2 Hz) trabeculae isolated from the right ventricles of the hearts of malignant hyperthermia susceptible (MHS) and healthy control (nMHS) swine. Caffeine (0.1-10 mmol/l) had positive inotropic effects, amounting to 275 +/- 35% of control in nMHS and 268 +/- 34% in MHS (n = 16). Halothane (0.25-4 vol%) decreased the force of contraction maximally to 52 +/- 4% in nMHS and 51 +/- 5% of control in MHS (n = 16). Propranolol did not change these effects. Succinylcholine (0.1-10000 mumol/l) had a small positive inotropic effect in both groups, which was blocked by propranolol. Phenylephrine (0.1-300 mumol/l) increased the force of contraction maximally to 188 +/- 24% of control in nMHS and to 193 +/- 23% in MHS (n = 16). The inotropic effect was blocked by prazosin but not by succinylcholine (1 mmol/l). Isoproterenol (0.01-10 mumol/l) had a positive inotropic effect of maximally 275 +/- 21% of control in nMHS and 396 +/- 31% in MHS (n = 17) (P less than 0.05). Succinylcholine potentiated this effect, and propranolol shifted the concentration-response curves to the right. We conclude that caffeine, halothane, succinylcholine and phenylephrine have similar inotropic effects in the hearts of nMHS and MHS, whereas isoproterenol has a significantly greater effect in MHS than in nMHS.

Animals↗

PubMedDate not supplied

Hepatic sinusoidal responses to intraportal injections of phenylephrine and isoprenaline in the rat.

1. Specific alpha- and beta-adrenoreceptor agonists, phenylephrine and isoprenaline, were injected intraportally into the intact rat liver under direct microscopic observation by an in vivo transillumination technique. 2. The diameter of a hepatic sinusoid and the intra-sinusoidal erythrocyte velocity were quantitatively measured, and the sinusoidal volume flow was calculated from these two parameters. 3. Results show that phenylephrine causes a sinusoidal constriction and an increased sinusoidal blood flow, whereas isoprenaline causes the opposite effects on the sinusoids. 4. All the sinusoidal responses to phenylephrine and isoprenaline were dose-dependent and were possibly related to the direct effect of these drugs on the sinusoids.

Animals↗

PubMedDate not supplied

Effects of a non-vasoconstrictor dose of phenylephrine on prostaglandin E2 and renin release in anaesthetized dogs.

Phenylephrine (1 microgram/min) was infused into the renal artery of pentobarbitone anaesthetized dogs. Systemic blood pressure and renal blood flow were monitored. Arterial and renal venous blood samples were collected before and 10 min after the start of the infusion. Plasma prostaglandin E2 concentration and plasma renin activity were measured by radioimmunoassay. This dose of phenylephrine did not affect systemic blood pressure and renal blood flow. However, both prostaglandin E2 and renin secretion rates were increased by the infusion of phenylephrine. These results suggest that renal alpha-adrenoceptors participate in prostaglandin and renin release independent of the changes in systemic blood pressure and renal blood flow.

Anesthesia↗

PubMed1987

Responses of isolated canine and simian femoral arteries and veins to phenylephrine, xylazine and KCl after removal of endothelium.

Using the cannula inserting method, vasoconstrictor responses to phenylephrine (an alpha 1-adrenoreceptor agonist), xylazine (an alpha 2-adrenoreceptor agonist) and KCl after removal of the endothelium by intraluminal treatment with saponin were investigated in isolated and perfused canine and simian femoral arteries and veins. In arteries, vasoconstrictor responses to KCl were markedly potentiated by removal of the endothelium in both species. KCl-induced vasoconstrictions were not modified by treatment with an alpha 1-adrenoreceptor antagonist, bunazosin, which blocked noradrenaline-induced constrictions. The phenylephrine-induced constriction was significantly potentiated by removal of the endothelium in simian arteries but not in canine arteries. In both arteries, responses to xylazine were not influenced by removal of the endothelium. In femoral veins of both species, responses to phenylephrine, xylazine and KCl were not significantly modified by a relatively small dose of saponin but were moderately depressed by a large dose. It is suggested that the endothelium may play an important role for inducing alpha 1-adrenoreceptor-mediated constrictor responses in simian femoral arteries, but not in canine arteries or in either vein tested.

Animals↗

PubMed1992

Effect of the optical isomers of YM-12617 on increased intra-urethral pressure induced by phenylephrine in anaesthetized dogs.

1. Effects of the individual optical isomers of YM-12617 (R, S 5-[2-[[2-(o-ethoxyphenoxy)ethyl]-amino]propyl]-2- methoxybenzenesulphonamide HCl, (+/-)-YM), a potent selective alpha 1-adrenoceptor antagonist, on the increase in intraurethral pressure (IUP) and diastolic blood pressure (DBP) induced by phenylephrine were evaluated in pentobarbital-anaesthetized female dogs. 2. Phenylephrine (0.1-30 micrograms kg-1 i.v.), an alpha 1-adrenoceptor agonist, dose-dependently increased IUP and DBP. 3. alpha-adrenoceptor antagonists (i.v.) dose-dependently antagonized the increase in IUP and DBP induced by phenylephrine, with a potency ranking of R(-)-YM greater than (+/-)-YM greater than prazosin greater than phentolamine greater than S(+)-YM greater than yohimbine. 4. These results suggest that the alpha 1-adrenoceptor mediates the increase in IUP as well as DBP in anaesthetized dogs, and that alpha 1-adrenoceptors in the urethra and arteries show a stereochemical preference for R(-)-YM.

Adrenergic alpha-Agonists↗

PubMed1972

The effect of cold storage on the inhibitory action of isoprenaline, phenylephrine and nicotine on the mechanical and membranal activities of guinea-pig taenia caecum.

1. The effects of prolonged cold storage on the mechanical and membranal responses to stimulation of alpha- and beta-adrenoceptors by phenylephrine and isoprenaline, respectively, were studied on the guinea-pig taenia caecum.2. Cold storage invariably caused a decrease in the resting membrane potential, and this effect was enhanced as the duration of treatment was prolonged.3. After cold storage (18 days) the tissue potassium ion content (89.7 +/- 1.7 mmol/kg wet wt.) was decreased to 30.5 +/- 1.9 mmol/kg wet wt. whereas that for sodium (69.2 +/- 1.4 mmol/kg wet wt.) increased to 134.0 +/- 2.3 mmol/kg wet wt.4. In the fresh preparations, phenylephrine (1 and 2 muM) caused a cessation of spontaneous action potentials, accompanied by hyperpolarization of the membrane and relaxation of the muscle. These effects were markedly diminished after 18 days of cold storage. Isoprenaline (1 and 2 muM) also blocked the action potentials and caused a concomitant muscle relaxation, but in most cases the hyperpolarization was not observed. After 14 days of cold storage these mechanical and membranal changes associated with isoprenaline treatment were not demonstrable in most preparations.5. Nicotine (5 muM and 50 muM) produced a biphasic effect, cessation of the action potential, hyperpolarization and subsequent relaxation followed by a long lasting depolarization, an accelerated discharge of action potentials and an increase in muscle tension. After a few days of cold storage the hyperpolarization effect disappeared but the intensity of the long-lasting depolarization as well as the contractile effects were increased. After cold storage for more than 7 days, nicotine did not affect mechanical or electrical activity.6. Dibutyryl 3'5' cyclic AMP (1 muM to 500 muM) failed to affect the mechanical and electrical activities of taenia caecum.7. Phenylephrine and isoprenaline had no effect on the high potassiumdepolarized taenia.8. These observations suggest that the electro-mechanical effect of an alpha-adrenoceptor stimulant on the guinea-pig taenia caecum is more resistant to cold treatment than that of a beta-adrenoceptor stimulant. This inhibitory system of stimulation of both a- and 8-receptors of guinea-pig taenia caecum may react by different mechanisms. The results also demonstrate that cold storage itself changes the membrane permeability to ions and the tissue ion content (Na+ and K+) of smooth muscle of guinea-pig taenia caecum.

Action Potentials↗

PubMed1977

Effect of isoprenaline and phenylephrine on the adenosine 3',5'-monophosphate content and mechanical activity of cold-stored and fresh taenia caecum from the guinea-pig.

1. Cold storage treatment of the guinea-pig taenia caecum had a greater inhibitory effect on the isoprenaline-induced relaxation than that induced by phenylephrine. Prolonged cold storage (12-14 days) almost abolished the effect of isoprenaline but only reduced the phenylephrine effect. The ED50 of cyclic adenosine 3',5'-monophosphate (cyclic AMP) that elicited muscle relaxation was not altered by the prolonged cold storage. 2. After cold storage treatment, tissue cyclic AMP content was decreased; however, isoprenaline still caused a dose-dependent increase in the cyclic AMP level. The threshold dose of isoprenaline for cyclic AMP accumulation was the same in fresh and cold-stored preparations. 3. In the fresh preparation, the onset of the isoprenaline (10(-6)M)-induced relaxation preceded the increase in tissue cyclic AMP. 4. Isoprenaline, phenylephrine, adrenaline and noradrenaline at doses (ED50) sufficient to induce muscle relaxation did not always increase the cyclic AMP level. 5. Similarly, the responses to papaverine and nitroglycerine were not accompanied by an increase in cyclic AMP. 6. The adenylate cyclase and phosphodiesterase (low and high Km) activities of taenia caecum were not attenuated by the prolonged cold storage. 7. Propranolol inhibited both the isoprenaline-induced relazation and cyclic AMP accumulation; however, the pA2 values were significantly different for the two events. 8. Based on these results, both the relaxation and cyclic AMP accumulation caused by isoprenaline are mediated by activation of beta-adrenoceptors but are independent phenomena.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1989

Comparative effects of the alpha-adrenoceptor agonists noradrenaline, phenylephrine and clonidine in the human saphenous vein in vivo and in vitro.

The alpha-adrenoceptor-mediated contractile effects of noradrenaline (alpha 1 + alpha 2), phenylephrine (alpha 1) and clonidine (alpha 2) on human saphenous veins were investigated in vivo and in vitro. By infusion (0.3 ml min-1) of the drugs (increasing concentrations in the infused solution) into distended (40 mmHg) saphenous veins in six healthy subjects, local vasoconstriction was induced, measured by a photo-electric device. The drugs induced dose-dependent contractions in all subjects, and dose-response curves were constructed. These were compared with concentration-response curves based on in-vitro results. Macroscopically normal saphenous veins, taken at saphenousectomies, were used, and the preparations were contracted isometrically in organ baths by the agonists. From the curves obtained in vivo and in vitro, the relative potencies of phenylephrine and clonidine (in relation to noradrenaline) were calculated and compared. The relative potencies of phenylephrine in vivo (76%) and in vitro (82%) did not differ significantly. However, the relative potency of clonidine was significantly (P less than 0.05) lower in vivo (90%) than in vitro (99%). Thus, it is concluded that there are differences between the results obtained in vivo and in vitro, stressing the importance of comparative in vivo-in vitro studies.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Hemodynamic effects of atropine, dobutamine, nitroprusside, phenylephrine, and propranolol in conscious horses.

The authors investigated the cardiovascular effects of low doses of nitroprusside, dobutamine, and phenylephrine and a beta-adrenergic blocking dose of propranolol in conscious, healthy horses with and without prior atropine administration. A parasympathetic blocking dose of atropine produced significant increases in heart rate and arterial pressures, and decreased stroke volume, ejection fraction, pulse pressure, and right-ventricular end-diastolic pressure and volume. Cardiac output was not changed by atropine administration. Nitroprusside reduced arterial pressures to a greater extent in atropinized horses but increased heart rate in both atropinized and non-atropinized horses. Dobutamine increased mean arterial pressure in both non-atropinized and atropinized horses but increased heart rate, diastolic arterial pressure, and systemic vascular resistance only in atropinized horses. Propranolol did not affect any of the hemodynamic variables that were measured. Phenylephrine, in the presence of beta-adrenergic blockade, increased mean arterial pressure and reduced cardiac output. This study showed that low doses of nitroprusside, dobutamine, and phenylephrine produce significant hemodynamic effects in conscious, healthy horses and that these effects are modified by prevailing parasympathetic tone.

Animals↗

PubMed1992

Effect on cardiac sympathetic nerve activity of phenylephrine microinjected into the cat intermediolateral cell column.

1. In anaesthetized cats the effect of the alpha 1-adrenoceptor agonist phenylephrine, microinjected into the left intermediolateral cell column of the spinal cord at the third thoracic level, was studied on left inferior cardiac nerve activity. 2. Microinjection of 100 nl of 10 or 40 mM-phenylephrine caused increases in inferior cardiac nerve activity in fifteen out of seventeen experiments. 3. The microinjection of the alpha 1-adrenoceptor antagonist alfuzosin (100 nl of 10 mM) into the intermediolateral cell column antagonized the excitatory response elicited by phenylephrine. 4. Increases in inferior cardiac nerve activity produced by glutamate and 5-hydroxytryptamine microinjected into the intermediolateral cell column were not antagonized by alfuzosin. 5. It is concluded that activation of alpha 1-adrenoceptors in the region of the intermediolateral cell column can cause an increase in the firing rate of sympathetic preganglionic neurones which innervate postganglionic neurones projecting into the inferior cardiac nerve.

Adrenergic alpha-Antagonists↗

PubMed1991

Effect on mydriasis of modifying the volume of phenylephrine drops.

The cardiovascular effects of topically administered phenylephrine 10% are well known and can be minimised by reducing the concentration of drops administered. By modifying the dimensions of the dropper tip we reduced the volume of the drops administered, and therefore the total dose of phenylephrine, without altering the concentration. No difference in the mydriasis produced by drops of small and normal volume could be detected. Since a smaller dose of phenylephrine is administered with smaller drops, the risk of systemic side effects could be reduced by modifying the tips of eyedroppers.

Dose-Response Relationship, Drug↗

PubMed2001

Topical phenylephrine increases anal canal resting pressure in patients with faecal incontinence.

INTRODUCTION: The internal anal sphincter receives a stimulatory alpha(1) adrenergic innervation. Use of an adrenergic agonist may therefore have a role in treating patients with faecal incontinence. METHODS: Ten patients (seven females, median age 66 years) with passive faecal incontinence related to weak internal anal sphincter were studied. All patients had intact anal sphincters as assessed by endoanal ultrasound. Phenylephrine gel was applied in a double blind manner in concentrations of 0%, 10%, 20%, 30%, and 40% (Slaco Pharma (UK) Ltd, Watford, UK) on separate days. Maximum resting anal pressure (MRP), anodermal blood flow, blood pressure, and pulse rate were measured before, and one and two hours after application. RESULTS: All concentrations of phenylephrine gel increased median MRP (43, 48, 54, 65, and 70 cm H(2)O, for placebo, 10% (p=0.122), 20% (p=0.170), 30% (p=0.002), and 40% (p=0.004), respectively at one hour; comparisons with placebo). This was sustained at two hours. There was a clear dose-response relationship at one hour. Higher concentrations raised median MRP to within the normal range (> 60 cm H(2)O). At two hours, all concentrations greater than 20% increased the pressure to a similar degree, suggesting that the exact concentration may be important for the initial effect but given a certain threshold is less important after a period of time. Toxicity was rare. Two patients experienced transient perianal burning which settled within a few minutes. There was no significant effect on anodermal blood flow, blood pressure, or pulse rate. CONCLUSION: This study has demonstrated the feasibility of using topical phenylephrine to raise resting anal tone in patients with faecal incontinence. Randomised controlled trials are required to assess the efficacy of this agent.

Administration, Topical↗

PubMed1977

Cyclic AMP and the positive inotropic effect of norepinephrine and phenylephrine.

Time-response studies of the effects of norepinephrine and phenylephrine revealed that both agonists caused an increase in cyclic AMP levels before increases in contractile force in either the electrically stimulated left atria or spontaneously beating right atria of the rat. Norepinephrine caused a nearly sixfold increase in cyclic AMP, whereas phenylephrine produced only a 50% increase in the nucleotide. Pretreatment with reserpine did not affect the norepinephrine cyclic AMP response; however, the phenylephrine cyclic AMP response was abolished. Reserpine pretreatment did not significantly affect the contractile responses of either amine. In the presence of propranolol, norepinephrine was found to have the ability to produce an increace in contractile force in which cyclic AMP was apparently not involved. The time course of the contractile response induced by adrenergic amines was found to be remarkably influenced by the chronotropic response in spontaneously beating preparations while the cyclic AMP response was not greatly affected. This difference in the contractile response may be due to the ability of the chronotropic response to influence the flux of calcium through the cell membrane.

Animals↗

PubMed1979

Inhibition of the cardiac inotropic effect of phenylephrine by a tetramine disulfide with irreversible alpha-adrenoceptor blocking activity.

The newly synthesized alpha-adrenoceptor blocking drug BHC (N,N'-bis[6-(10-methoxybenzyl-amino)-a-hexyl]cystamine) was found to block irreversibly the positive inotropic effect of the sympathomimetic drug phenylephrine on the isolated rat left atrium. BHC was used to test the adrenoceptor interconversion hypothesis which claims that low temperature converts inotropic beta-adrenoceptors in rat atrium and frog ventricle to alpha-adrenoceptors. There was no evidence of adrenoceptor 'interconversion.' In the rat atrium low temperature did not increase the BHC antagonism of phenylephrine and did not cause BHC to inhibit the inotropic effect of noradrenaline or isoprenaline. In the perfused frog heart low temperature did not lead BHC to inhibit the inotropic effect of phenylephrine, adrenaline, or isoprenaline.

Adrenergic alpha-Antagonists↗

PubMed1991

Differences in alpha 1-adrenoceptor mechanisms for phenylephrine and tizanidine in rabbit thoracic aorta and common iliac artery.

Based on affinity for WB4101 and susceptibility to chloroethylclonidine, we evaluated the subtype of alpha 1-adrenoceptors activated by phenylephrine (a full agonist) and tizanidine (a partial agonist). The rabbit thoracic aorta and common iliac artery contain both alpha 1A- and alpha 1B-adrenoceptors, but the alpha 1B-subtype may be more predominantly in the common iliac artery than in the thoracic aorta. In rabbit thoracic aorta and common iliac artery, phenylephrine induced contraction through both alpha 1A- and alpha 1B-subtypes and tizanidine through only the alpha 1A-subtype. The subtype activated by phenylephrine may be partly different from that activated by tizanidine in the preparations used herein.

Animals↗