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 685 records · Page 38Linked to original sources

PubMedDate not supplied

[Prevention of phenylephrine-induced acute experimental pulmonary edema in the rat using furosemide].

The intravenous, intraperitoneal or oral administration of furosemide before intravenous infusion of phenylephrin protects rats, the highest doses and the longest the time between administration of the diuretic drug and the beginning of injection, inducing the best protection. The diuretic effects of furosemide do not seem to be the only ones involved because rehydrated animals by isotonic saline solution are still protected. Moreover other diuretic drugs as acetazolamide are useless and on the other hand ethacrynic acid, without any diuretic activity in the Rat, can protect that animal from the edematous effects of phenylephrin.

Acute Disease↗

PubMedDate not supplied

Allergic contact blepharoconjunctivitis due to phenylephrine eye drops.

We present two cases of sensitization to phenylephrine hydrochloride with clinical manifestation of blepharoconjunctivitis in the course of an ophthalmologic examination. Patch testing with available commercial preparations containing phenylephrine hydrochloride was positive in both patients. The other eye drops tested during the ophthalmologic examination were negative for both cases.

Aged↗

PubMed1999

4-Aminopyridine induces positive lusitropic effects and prevents the negative inotropic action of phenylephrine in the rat cardiac tissue subjected to ischaemia.

The effects of 4-aminopyridine (4-AP) at concentration of 1 mM on the contractility of rat isolated papillary muscle subjected to simulated ischaemia has been evaluated. Additionally, the effects of 4-AP on the phenylephrine inotropic action (a selective agonist of alpha1-adrenergic receptor) on rat isolated cardiac tissue underwent simulated ischaemia and reperfusion was studied. Experiments were performed on rat isolated papillary muscles obtained from left ventricle. The following parameters have been measured: force of contraction (Fc), velocity of contraction (+dF/dt), velocity of relaxation (-dF/dt) and the ratio between time to peak contraction (ttp) and relaxation time at the level of 10% of total contraction amplitude (tt10) as an index of lusitropic effects. Simulated ischaemia lasting 45 min was induced by replacement of standard normoxic solution by no-substrat one gassing with 95% N2/5%CO2. Although 4-AP exerted a slight, but significant positive inotropic action itself, pretreatment with 1 mM of this compound significantly depressed a recovery of Fc and +dF/dt, but improves recovery of -dF/dt in the rat papillary muscle during reperfusion as compared with control group of preparations. Moreover, the paradoxical negative inotropic action of phenylephrine observed in rat stunned papillary muscle was prevented in preparations previously treated by 4-AP. These findings suggest that an inhibition of outward K+ current (probably transient outward and rapid component of delayed rectifying currents at 1 mM of 4-AP) aggravates ischaemia-induced failure in contractility but prevents changes in alpha1-adrenergic receptor signaling pathway occuring during ischaemia.

4-Aminopyridine↗

PubMed1975

Mydriatic effects using low concentrations of phenylephrine hydrochloride.

The dose response relationship of different concentrations of phenylephrine with and without prior application of topical anesthetic was measured to determine the minimum concentration which produced maximum mydriasis. As little as 0.125% phenylephrine caused mydriasis in some subjects and maximum mydriasis was achieved with 2%. Concentrations greater than 2% produced very little additional mydriasis. A therapeutically effective dose could be as low as 1% with prior installation of a topical anesthetic.

Administration, Topical↗

PubMed2001

Phenylephrine induced aortic vasoconstriction is attenuated in hyperthyroid rats.

BACKGROUND: Abnormal vascular responsiveness to vasoconstrictors may play an important role in peripheral vascular resistance in hyperthyroidism. The aim of the present study was to evaluate whether the vascular response to potassium chloride and phenylephrine is abnormal in a rat model of thyroxine-induced cardiac hypertrophy. METHODS: Left ventricular hypertrophy was induced in Wistar rats by subcutaneous administration of L-thyroxine for two weeks ("THYR"), n=17. Animals treated with normal saline served as controls, ("NORM"), n=20. The thoracic aorta was dissected and cut into rings that were suspended in an isolated organ bath with Krebs-Henseleit buffer. Maximal tension, Tmax, in g was measured in response to KCl and PE at the highest concentration in rings with endothelium (+E) and without endothelium (-E) in both groups. Relaxation response (Relax percent) to acetylcholine administration was expressed as percent of the maximal tension induced by phenylephrine. RESULTS: Left ventricular weight was 0.9 (SEM, 0.04) g for THYR group vs 0.7 (0.02) g for the NORM group, p<0.05. With KCl, Tmax was not different between the THYR and NORM groups with and without endothelium. With PE, there was a difference in Tmax between THYR+E and NORM+E, 1.2 (0.05) g vs 1.5 (0.09) g, p<0.05. Tmax was also different between THYR-E and NORM-E, 1.5 (0.08) g vs 1.7 (0.07) g, p<0.05. Relax percent was not significantly different between THYR+E and NORM+E (45.9 percent vs 42.8 percent, p>0.05). CONCLUSIONS: We conclude that: a) Vascular tension of the thoracic aorta in response to PE is lower in thyroxine-treated rats as compared to controls, probably due to enhanced PE-induced vasorelaxation at high concentration. b) Relaxation response of the thoracic aorta to acetylcholine is not different between THYR and NORM groups.

Acetylcholine↗

PubMed1992

Effect of acute footshock stress on the responsiveness of the isolated rat tail artery to phenylephrine and epinephrine.

The effects of acute footshock stress on the sensitivity of the isolated rat tail artery were studied. Footshock stress applied to male Wistar rats (200-300 g) causes subsensitivity to the vasoconstrictor effects of phenylephrine and epinephrine. No significant changes in the pA2 values of prazosin were detected, using epinephrine as the agonist. Footshock stress-induced subsensitivity to epinephrine was not affected by the calcium entry blocker nifedipine. However, nifedipine significantly depressed the maximum response to epinephrine in tail arteries isolated from acute footshock-stressed rats. The present results suggest that acute footshock stress-induced reduced sensitivity to phenylephrine and epinephrine may not be only related to events at the alpha-adrenoceptor level. The nifedipine-induced depression of the maximum response to epinephrine suggests a role for the calcium mobilization processes in the vascular responsiveness during acute stress.

Animals↗

PubMed2004

[Synthesis of BODIPY-FL-labeled phenylephrine and the determination of its biological activity].

OBJECTIVE: To synthesize BODIPY-FL-labeled phenylephrine (BODIPY-FL-PE) and determine its biological activity. METHODS: Condensation of BODIPY-FL (green fluorescence dye) and phenylephrine (alpha1-adrenoceptor agonist) was performed by adding dicyclohexylcarbodiimide (DCC) in the presence of absolute tetrahydrofuran(THF). The reaction occurred in absolutely oxygen and water condition at room temperature. The crude product was separated and purified by thin-layer chromatography (TLC). The structure of BODIPY-FL-PE was characterized by TLC and mass spectrometry (MS). Its pharmabiological activity was determined by Western blot. RESULTS: BODIPY-FL-PE,the target molecule, was synthesized and its structure was identified by using ultra-violet spectrometry (UV) and MS. The result of Western blot indicated that alpha1-adrenoceptor (alpha1-AR) induced ERK phosphorylation was confirmed in both BODIPY-FL-PE and PE treated groups. CONCLUSION: The synthesized BODIPY-FL-PE has pharmacological activity that could activate alpha1-AR. Visualization of AR behaviors could be achieved by tracing the trajectories of BODIPY-FL-PE labeled AR. It might be a promising tool for investigating dynamic behaviors of AR in living cells.

Adrenergic alpha-1 Receptor Agonists↗

PubMed2003

Accelerated acetylcholine metabolism in the lung after infusion of phenylephrine in dogs.

We investigated whether continuous administration of an a-adrenergic agonist, phenylephrine, could affect acetylcholine metabolism within the pulmonary circulation in anesthetized dogs. Infusions of phenylephrine at 3 microg/kg/min for 120 min shifted the dose-response curve for the depressor responses produced by acetylcholine (0.03-10 micro g/kg) injected into the right atrium to the right by about 30-fold. In contrast, the magnitude of the rightward shift in the dose-response curve for the depressor responses produced by acetylcholine injected into the left ventricle was only 3-fold. These results suggest that continuous administration of alpha-adrenergic agonists accelerate acetylcholine metabolism within the pulmonary circulation.

Acetylcholine↗

PubMed2005

Effects of isoliensinine on proliferation of porcine coronary arterial smooth muscle cells induced by phenylephrine.

AIM: To investigate the inhibitory effects and mechanism of action of isoliensinine (IL) on the proliferation of porcine coronary arterial smooth muscle cells (CASMCs) induced by phenylephrine (Phen) and its mechanisms of action. METHODS: MTT assay, immunohistochemical method and Western blotting were adopted. RESULTS: IL (0.03 - 3 micromol x L(-1)) could inhibit the CASMCs proliferation induced by Phen (0.1 micromol x L(-1)) in a concentration-dependent manner. IL (0.1 micromol x L(-1)) antagonized Phen-induced overexpression of PDGF-beta and bFGF from 0.545 +/- 0.026 and 0.47 +/- 0.03 to 0.458 +/- 0.019 and 0.376 +/- 0.017 (P < 0.01 , P < 0.01). IL (0.1 micromol x L(-1)) also decreased c-fos, c-myc and hsp70 overexpression induced by Phen from 0.57 +/- 0.04, 0.44 +/- 0.04 and (173 +/- 36)% to 0.46 +/- 0.05, 0.372 +/- 0.021 and (115 +/- 35)% respectively (P < 0.01, P < 0.01, P < 0.01). CONCLUSION: IL exerted antiproliferative effect on CASMCs induced by phenylephrine, and its mechanisms were related to decrease the overexpression of growth factors (PDGF-beta, bFGF), protooncogene (c-fos, c-myc) and hsp70.

Animals↗

PubMedDate not supplied

Differences in the responses of the canine basilar and dorsal pedal artery to phenylephrine, clonidine and serotonin.

The effects of phenylephrine, clonidine and serotonin were studied on isolated preparations of the canine basilar and dorsal pedal artery. Differences were mainly observed in the responses of the two types of arterial preparations to clonidine and phenylephrine. While in the dorsal pedal artery, alpha 1- and alpha 2-receptors were involved in the response to alpha-agonists, in the basilar artery contractions induced by alpha 2-receptor stimulation prevailed. Moreover, in the latter artery the contractile responses induced by each of the agonists used were more dependent on the presence of extracellular calcium than those in the dorsal pedal artery.

Animals↗

PubMed1975

Relationship between cyclic AMP metabolism and inotropic response of perfused rat hearts to phenylephrine and other adrenergic amines.

A positive correlation between inotropic response and increment of cyclic AMP levels and labeling (from 14-C-adenine in the perfusate) was found after isoprenaline, dopamine, and phenylephrine alone, and after isoprenaline in the presence of chlorpromazine. 2. a lack of correlation between contractile activity and cyclic AMP levels and labeling was found when the hearts were exposed to phenylephrine in the presence of propranolol. The contractile activity increased, but the parameters for cyclic AMP did not change. These resuls together with findings by other workers indicate that the inotropic response to beta-stimulation always is associated with cyclic AMP accumulation, while the inotropic response to alpha-stimulation (when present) is not correlated to cyclic AMP elevation. Other differences between alpha- and beta-adrenergic effects on heart (course of development of the inotropic response, effect of theophylline on the response, effects on relaxing processes, action potential, and on refractory period) also indicate different mechanisms of action. On the basis of the available data we suggest as a conclusion that the inotropic response after alpha-adrenergic stimulation does not involve cyclic AMP as a mediator whereas beta-adrenergic effects are mediated by cyclic AMP. This means that the naturally occurring adrenergic amines norepinephrine and epinephrine, both of which are able to stimulate both alpha and beta myocardial receptors (twenzel and Su, 1966), elicit the inotropic response through two different mechanisms. Usually the beta-adrenergic effect on the heart is the more important. The contribution from alpha-stimulation, however, may increase under certain conditions: hypothyroidism or proplythiouracil treatment per se (Nakashima et al., 1971) or hypothermia (Kunos and Szentiványi, 1968; Buckley and Jordan. 1970; Benfey et al., 1973; Kunos, Yong, and Nickerson, 1973; Nickerson, 1973). Thus a single physiologic response may be mediated by more than one mechanism. Multiple mechanisms of action for one agent might have more general biologic significance; e.g., they may serve to maintain the responsiveness of a tissue under various conditions.

Animals↗

PubMed1991

[The treatment of prolonged erections using phenylephrine].

Phenylephrine was used intracavernously to treat prolonged erections in 38 cases. A rapid detumescence was obtained in every case. Phenylephrine seems to be superior to all other adrenergic drugs in reason of its rapid action and its lack of side effects.

Adult↗

PubMed1977

The role of beta-adrenoceptors in the responses of the hepatic arterial vascular bed of the dog to phenylephrine, isoprenaline, noradrenaline and adrenaline.

1 The sympathetically-innervated hepatic arterial vascular bed of the dog was perfused from a femoral artery. Hepatic arterial blood flow and perfusion pressure were recorded continuously, and the hepatic arterial vascular resistance (HAVR) calculated from these measurements.2 Intra-arterial injections of phenylephrine caused dose-dependent rises in HAVR, indicating hepatic arterial vasoconstriction, at all doses above threshold. No secondary reductions in HAVR followed these responses.3 Intra-arterial injections of isoprenaline caused only dose-dependent reductions in HAVR at doses above threshold.4 Intra-arterial injections of noradrenaline typically caused an initial increase in HAVR which was followed at all but the highest doses by a secondary, delayed, reduction in HAVR.5 Intra-arterial injections of adrenaline, like those of noradrenaline, resulted in hepatic arterial vasoconstriction followed by hepatic arterial vasodilatation.6 On a molar basis, the most potent hepatic arterial vasoconstrictor was noradrenaline, followed by adrenaline and phenylephrine.7 The maximum reductions in HAVR caused by adrenaline (mean reduction = 21.9%) and noradrenaline (16.9%) were significantly smaller than those due to isoprenaline ((P) < 0.001).8 Propranolol attenuated the hepatic arterial vasodilator responses due to isoprenaline, and the secondary falls in HAVR following intra-arterial adrenaline and noradrenaline.9 Propranolol did not modify the vasoconstrictor responses to phenylephrine.10 Both adrenaline and noradrenaline were more potent hepatic arterial vasoconstrictors after propranolol than in the absence of beta-adrenoceptor blockade. The potentiation of the vasoconstrictor effects of adrenaline was statistically significant.11 After propranolol, adrenaline was a more potent hepatic arterial vasoconstrictor than noradrenaline.12 Since the beta-adrenoceptors in the hepatic arterial vasculature were not blocked by atenolol, but were stimulated by salbutamol, it is concluded that they are predominantly of the beta(2)-type.13 The vasoconstrictor actions of phenylephrine, noradrenaline and adrenaline were all antagonized by the systemic administration of phentolamine, all three dose-response curves being shifted to the right.14 The results are discussed with regard to the possible control of the hepatic arterial vasculature by naturally-occurring catecholamines.

Albuterol↗

PubMed1990

Topical 2.5% and 5% phenylephrine: comparison of effects on heart rate and blood pressure.

We compared the effects of 2.5% and 5% concentrations of topical ocular phenylephrine hydrochloride on blood pressure and heart rate in 200 adult patients undergoing extracapsular cataract surgery under either general or neuroleptic anesthesia. Although there was little initial change in mean systolic or diastolic blood pressure in either group, once anesthesia was induced there was a rise of 1 to 5 mm Hg in the lower-dose group, compared with 17 to 26 mm Hg in the higher-dose group. A slight decrease in mean heart rate of 5 to 6 beats/min was noted immediately after the instillation of either the 2.5% or 5% solution. The results suggest that lower doses of topical phenylephrine are safer than higher doses when used preoperatively. This may be particularly significant in hypertensive patients, who have higher baseline blood pressure.

Administration, Topical↗

PubMed1987

Cyanosis and cardiovascular depression in a neonate: complications of halothane anesthesia or phenylephrine eyedrops?

A 3-week-old patient underwent cataract extraction under halothane anesthesia. After induction of anesthesia and instillation of phenylephrine hydrochloride eyedrops, the patient experienced cyanosis and cardiovascular depression. Her condition improved over the next 10 minutes. The possible contributions of halothane and phenylephrine to this response are discussed.

Anesthesia↗

PubMed1978

Effect of estrogen on sensitivity of rabbit bladder and urethra to phenylephrine.

The sensitivity of alpha-adrenoceptors to phenylephrine as indicated by the ED50 of the rabbit bladder and urethra was compared for segments in vitro from control (estrous), ovariectomized, ovariectomized-estrogen-treated, and pregnant animals. In control animals there was a trend for urethral segments to be more sensitive to phenylephrine (lower ED50) than bladder segments. This difference was abolished by castration, which decreased the sensitivity of the anular urethral segment, and by pregnancy, which tended to enhance the sensitivity of the bladder. The tension generated by bladder segments was enhanced by pregnancy and tended to be decreased by castration. The effects of castration tended to be reversed by treatment with estrogen (1 microgram per kg of body weight per day for 14 days). These data indicate that estrogen can influence the response of the urethra and urinary bladder to alpha adrenergic stimulation.

Animals↗

PubMed1984

Renal alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction in dogs: comparison of phenylephrine, clonidine, and guanabenz.

The alpha 2-agonist, guanabenz, increases Na and water excretion with little change in renal blood flow, while clonidine has been reported to cause antinatriuresis proportional to renal vasoconstriction. We hypothesized that clonidine-mediated renal vasoconstriction involves alpha 1-receptors. Dose-response curves were constructed correlating decreases in renal blood flow with doses of phenylephrine, clonidine, and guanabenz injected as boluses into renal arteries of anesthetized dogs. Changes in renal blood flow before and after prazosin, yohimbine or verapamil were recorded. Guanabenz was a 10-fold weaker vasoconstrictor than clonidine, but was still effective when alpha 1-receptors were blocked. Tenfold differences were found between phenylephrine, clonidine, and guanabenz for dependence on alpha 1-receptors. Denervation did not significantly shift the curves. Verapamil markedly attenuated only clonidine and guanabenz, which supported their dependence on calcium channels for vascular smooth muscle contraction. Thus, postsynaptic alpha 2-adrenoceptors can contribute to renal vasoconstriction in the dog but the receptors are either less numerous on the vasculature or are less efficiently coupled to contractile elements than are alpha 1-receptors. Clonidine constricts the renal vasculature through both adrenoceptor subtypes.

Animals↗

PubMed1984

A suitable substitute for 4% cocaine before blind nasotracheal intubation: 3% lidocaine-0.25% phenylephrine nasal spray.

To assess the efficacy of potential substitutes for cocaine as a topical anesthetic before nasal intubation, the authors performed a double-blind study comparing the hemodynamic effects of blind nasotracheal intubation in 75 patients receiving one of three nasal sprays: 4% cocaine (C), a mixture of 3% lidocaine in 0.25% phenylephrine (L-P), and 0.25% phenylephrine alone (P). Three minutes after 0.5 ml of one of the solutions was sprayed into each nostril, anesthesia and paralysis were induced with thiopental (5 mg/kg) followed by succinylcholine (1 mg/kg); immediately after induction, mean arterial pressure (MAP) and heart rate (HR) were recorded. After blind nasotracheal intubation was accomplished, MAP and HR were recorded for 5 min while anesthesia was maintained with 70% N2O in O2. In patients receiving L-P, mean MAP during the 5 min after intubation decreased 2.3 +/- 2.2 mm Hg (mean +/- SEM); this was significantly different from the increase of 6.2 +/- 1.7 and 8.5 +/- 2.0 mm Hg in MAP after intubation of patients receiving C and P, respectively (P less than 0.005). Although mean HR decreased during the 5 min after intubation in all groups, this decrease was significantly greater (9.6 +/- 1.4 beats/min) in patients receiving L-P than in those receiving C (3.1 +/- 1.6 beats/min) or P (0.1 +/- 1.7 beats/min) (P less than 0.005). Changes in HR and MAP were similar in patients receiving C and P. There was no significant difference in the incidence or severity of epistaxis among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Local↗