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PubMed1996

Role of NO in the pulmonary artery hyporeactivity to phenylephrine in experimental biliary cirrhosis.

The aim of this study was to see whether increased activity of nitric oxide (NO) might account for decreased pulmonary vascular tone seen in the hyperdynamic circulation of cirrhosis. We compared the pulmonary vascular reactivity of isolated pulmonary arteries (PA) from control rats (n = 10), and rats with biliary cirrhosis (n = 10) induced by chronic bile duct ligation (4 weeks). The responses of PA rings to cumulative concentrations of phenylephrine, acetylcholine, and sodium nitroprusside were studied, and also the effects of inhibition of synthesis of NO by the L-arginine analogue, N omega-nitro-L-arginine (L-NOARG) in PA rings challenged with cumulative concentrations of phenylephrine and acetylcholine. The contractile response to phenylephrine was significantly reduced in cirrhotic PA rings as compared with controls. Pretreatment with L-NOARG (10(-4) M) significantly increased the contractile response to phenylephrine in PA rings from cirrhotic rats but not in control PA rings. Furthermore, L-NOARG restored the response to phenylephrine in cirrhotic PA rings back to normal. There was no difference in the relaxation of PA rings from both groups in response to acetylcholine and sodium nitroprusside. We conclude that in vitro pulmonary artery ring hyporeactivity to phenylephrine results from increased nitric oxide production in the pulmonary circulation of cirrhotic rats and might account for the hepatopulmonary syndrome.

Acetylcholine↗

PubMed2003

Ephedrine, but not phenylephrine, increases bispectral index values during combined general and epidural anesthesia.

Ephedrine and phenylephrine are used to treat hypotension during combined general and epidural anesthesia, and they may change anesthetic depth. In the current study, we evaluated the effects of ephedrine versus phenylephrine on bispectral index (BIS) during combined general and epidural anesthesia. After injection of ropivacaine through the epidural catheter, general anesthesia was induced with propofol and vecuronium, and was maintained with 0.75% sevoflurane. Approximately 10 min after the intubation, BIS was recorded as a baseline value. Patients with decreases in arterial blood pressure <30% of the preanesthetic values were defined as control group (n = 9). Patients who had to be treated for larger decreases in arterial blood pressure were randomly assigned to receive ephedrine 0.1 mg/kg (n = 17) or phenylephrine 2 micro g/kg (n = 17). BIS values were recorded at 1-min intervals for 10 min. BIS in the ephedrine group was significantly larger from 7 to 10 min than that in the control and phenylephrine groups (P < 0.05). Seven patients in the ephedrine group had BIS >60, whereas no patient in the control and phenylephrine groups had BIS >60 (P < 0.005). Ephedrine, but not phenylephrine, increased BIS during general anesthesia combined with epidural anesthesia.

Aged↗

PubMed2026

Comparison of a Modified Regimen of Prophylactic Phenylephrine Boluses Versus Variable Rate Infusion During Elective Cesarean Delivery Under Spinal Anesthesia: A Noninferiority Randomized Double-Blind Study.

BACKGROUND: Prophylactic phenylephrine boluses have been found to be as effective as variable rate infusions during elective cesarean delivery but require a higher number of physician interventions to maintain blood pressure near baseline values. Therefore, there is a need to find a feasible regimen of bolus administration that is equally efficacious to the infusion regimen while at the same time requires a comparable number of physician interventions and is thus non-inferior to the infusion regimen. METHODS: Healthy pregnant women with term, uncomplicated, singleton pregnancies undergoing elective cesarean delivery under spinal anesthesia were randomly divided into two groups. The Bolus group received a phenylephrine bolus 100 μg immediately after spinal anesthesia and then at every systolic blood pressure value <90% of the baseline. The infusion group received a prophylactic variable-rate infusion of phenylephrine beginning at 50 μg/min and titrated to maintain systolic blood pressure at 90-99% of baseline. The primary outcome was the number of physician interventions needed to maintain the target systolic blood pressure; the secondary outcomes included phenylephrine requirements, incidence of hypotension/hypertension/bradycardia, umbilical arterial and venous blood gas analysis, Apgar scores, and maternal complications. The primary outcome was analyzed in terms of non-inferiority using a non-inferiority margin of two interventions. RESULTS: Eighty patients were included in the study. The median (interquartile range [IQR]) number of physician interventions was 6 (5-8) in the infusion group and 3 (2-4) in the bolus group (P < .001). The difference of medians (95% confidence interval [CI]) between the two groups was -3 (-4 to -2). Phenylephrine requirements were higher in the infusion group (630 [426-765] μg) compared to the bolus group (300 [200-400] μg; P < .001). Blood pressure was higher at certain time points in the infusion group, but overall accuracy of blood pressure control was not different between the groups. Incidence of hypotension, hypertension, and bradycardia, neonatal outcomes, and maternal complications did not differ between the groups. CONCLUSIONS: The modified regimen of prophylactic boluses is non-inferior to variable rate prophylactic phenylephrine infusion in terms of physician interventions needed to maintain systolic blood pressure within the target range and maternal and neonatal outcomes.

Humans↗

PubMed2004

Phenylephrine-induced vasoconstriction of the rat superior mesenteric artery is decreased after repeated swimming.

This study was performed to determine the effect of forced swimming on the vascular responsiveness of the rat superior mesenteric artery to phenylephrine, focusing on the involvement of locally produced substances. Repeated but not single sessions of forced swimming exercise reduced the vasoconstrictor potency of phenylephrine in the studied arteries, regardless of the presence of intact endothelium. No significant changes were observed in the maximal response to phenylephrine. Treatment with indomethacin (1 microM) did not affect the exercise-induced reduction in vascular responsiveness to phenylephrine. However, the reduction of vascular reactivity to phenylephrine due to repeated exercise was no longer observed after treatment with N(G)-monomethyl-L-arginine (L-NMMA, 100 microM). The results suggest that repeated exercise reduces vasomotor responses to phenylephrine in rat superior mesenteric arteries through a non-endothelial nitric oxide (NO)-related mechanism.

Animals↗

PubMed1985

Effect of prostaglandin F2 alpha, phenylephrine and ergonovine on uterine contractions in the ewe.

Two experiments were conducted to determine the effect of prostaglandin F2 alpha (PGF2 alpha), phenylephrine and ergonovine on uterine contractions. In the first experiment, ewes were bilaterally ovariectomized, and a strain gauge force transducer was sutured to the serosa of one uterine horn. Each ewe was treated sc with 2 micrograms of estradiol-17 beta daily to prevent regression of the uterus. Beginning at least 5 d after ovariectomy, four dose levels of PGF2 alpha, phenylephrine and methoxamine were given by im injection and ergonovine was given by im or iv injection. Phenylephrine, methoxamine and ergonovine are alpha-adrenoceptor agonists. Uterine activity was recorded by physiograph for 30 min before and 90 min after treatment. Tracing were analyzed for 20-min periods before treatment and 4 to 24 min and 50 to 70 min after treatment. In Exp. 2, transducers were attached to uteri of intact ewes at d 10 to 12 of an estrous cycle. During subsequent estrus, one or two dose levels of PGF2 alpha, phenylephrine and ergonovine were given by im injection and uterine activity recorded. In Exp. 1, PGF2 alpha and phenylephrine increased (P less than .05 or .01) the number of amplitude of contractions at both 4 to 24 and 50 to 70 min. Ergonovine given im increased the number of contractions. In intact estrous ewes, PGF2 alpha increased the number and amplitude of contractions at 4 to 24 min, phenylephrine increased the number and amplitude at both 4 to 24 and 50 to 70 min, and ergonovine increased the number slightly but significantly at 4 to 24 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

A mechanistic study on the enhancement of corneal penetration of phenylephrine by flurbiprofen in the rabbit.

The effect of flurbiprofen on the corneal penetration of phenylephrine was investigated using isolated albino rabbit corneas mounted in the Ussing diffusion chamber. The corneal penetration of phenylephrine was increased 5-11 times by 4-16 mM flurbiprofen. Such an increase in the corneal penetration of phenylephrine by flurbiprofen appeared to correlate with the increase in the lipophilicity of phenylephrine by flurbiprofen due to ion pair formation. The magnitude of increase at 16 mM flurbiprofen was 2.4 times less than that afforded by 0.5% EDTA and 16.3 times less than that afforded by deepithelizing the cornea. Since flurbiprofen also increased the corneal penetration of benzoic acid and sorbitol with which it cannot form ion pairs, increased lipophilicity of phenylephrine due to ion pair formation with flurbiprofen was unlikely to be the only mechanism that enhanced corneal penetration. An additional mechanism under our experimental conditions of prolonged exposure of the cornea to the phenylephrine-flurbiprofen combination was lowering of the barrier function of the corneal epithelium by concentrations of flurbiprofen greater than that used therapeutically.

Animals↗

PubMed2006

The effect of phenylephrine and cyclopentolate on objective wavefront measurements.

PURPOSE: To investigate the impact of phenylephrine and cyclopentolate on wavefront refraction and fourth order spherical aberration C12. METHODS: This cohort study comprised 151 eyes with sphere up to -10.00 diopters (D) and cylinder -3.75 D. Aberrometry was performed using the ALLEGRO WAVE (WaveLight Laser Technologies AG, Erlangen, Germany) after instillation of phenylephrine 5% yielding objective phenylephrine refraction in accommodated steady-state, as well as after cyclopentolate 0.5% providing objective cyclopentolate refraction in non-accommodated state. Accommodation target fogging was turned off. Wavefront aberrations were expressed by Zernike expansion up to the sixth order, and paraxial curvature matching with Taylor series was used to calculate objective wavefront sphere. RESULTS: Objective wavefront sphere was not influenced by pupil size. Eyes showed substantial accommodation after phenylephrine with a myopic shift of -0.66 D comparing objective to subjective manifest sphere (r=0.942, P<.001). Cycloplegic eyes behaved like a model eye, with a difference of -0.08 D between objective and subjective cycloplegic sphere (r=0.976, P<.001). C12 increased ten-fold from 4.0- to 7.0-mm pupil size, keeping the same sign. Comparing cyclopentolate with phenylephrine, the sign of C12 changed in a positive direction by an average +0.124 +/- 0.109 microm (range: -0.052 to +0.632 microm) at 7.0 mm, whereas the total higher order aberrations changed very little. A good correlation was found between C12 and the change in objective wavefront sphere between cyclopentolate and phenylephrine (r=0.75, P<.001). CONCLUSIONS: Fogging of the accommodation target should be used for wavefront measurements. Weaker cycloplegic agents, such as tropicamide, may be used to ensure relaxed but not completely paralyzed accommodation, which would yield "manifest" aberration values close to the natural resting state.

Accommodation, Ocular↗

PubMed1999

Comparison between spectral analysis and the phenylephrine method for the assessment of baroreflex sensitivity in chronic heart failure.

Baroreflex sensitivity assessed by means of the phenylephrine test plays a prognostic role in patients with previous myocardial infarction, but the need for drug injection limits the use of this technique. Recently, several non-invasive methods based on spectral analysis of systolic arterial pressure and heart period have been proposed, but their agreement with the phenylephrine test has not been investigated in patients with heart failure. The two methods (phenylephrine test and spectral analysis) were compared in a group of 49 patients with chronic congestive heart failure both at rest and during controlled breathing. The linear correlation and the limits of agreement between the phenylephrine test slope and the alpha-index [alpha(c); corrected by the coherence function between the interbeat interval (RR interval) and systolic arterial pressure] were evaluated. Only 16 patients had a measurable alpha-index at rest in both the low-frequency (LF) and high-frequency (HF) bands; the alpha(c)-index allowed measurements in all patients. It correlated moderately with the phenylephrine test slope at rest (r=0. 71 and P<0.001 in LF; r=0.57 and P<0.001 in HF) and during controlled breathing (r=0.51 and P<0.001 in LF; r=0.63 and P<0.001 in HF). Multivariate regression analysis showed that only alpha(c)LF during rest and alpha(c)HF during controlled breathing contributed significantly to baroreflex gain estimation. However, the agreement between methods was weak; the normalized limits of agreement and bias were -162 to 243% (0.46 ms/mmHg) for alpha(c)LF and -185 to 151% (-0.99 ms/mmHg) for alpha(c)HF. Thus the comparison between baroreflex sensitivity measurements obtained by the phenylephrine test and spectral analysis showed a moderate correlation between the two methods; however, despite the linear association, a consistent lack of agreement between the two techniques was found. Because both systematic and random factors contribute to the difference, these two techniques cannot be considered as alternatives for the assessment of heart failure.

Adult↗

PubMed2001

Contractile responses of diabetic rat aorta to phenylephrine at different stages of diabetic duration.

AIM: To investigate the time-dependent changes in contractile responses of aorta to phenylephrine (Phe) in diabetic rats and age-matched control, and its possible mechanism. METHODS: At stages of 2-, 6-, and 12-week diabetic duration, aortic rings were studied for contractile responses to agonists in vitro. RESULTS: At the stage of 2-week diabetic duration, contractile responses to lower concentrations of phenylephrine were increased (P < 0.05), but the maximal contraction of phenylephrine did not change. At the stage of 6-week diabetic duration, contractile responses to phenylephrine were increased (P < 0.01) at each concentration, and the maximal contraction was increased by approximately 40 %. However, at the stage of 12-week diabetic duration: 1) the maximal contractile response to Phe 10 micromol . L-1 was decreased (P < 0.05), 2) in Ca2+ free edetic acid medium, Phe 10 micromol . L-1-induced transient contraction was also decreased (P < 0.05), 3) in Ca2+ free edetic acid medium, in the presence of nifedipine 10 micromol . L-1 and Phe 10 micromol . L-1, the Ca2+ repletion-caused contraction was not different from control, 4) in normal medium, cyclopiazonic acid (CPA) 10 micromol . L-1-induced contraction was decreased (P < 0.01). CONCLUSION: The results suggested that contractile responses to phenylephrine in diabetic rat aorta changed with the development of diabetes, and the changes of functional Ca2+ store sizes and Ca2+ entry mainly through voltage-dependent Ca2+ channels were responsible for the alterations of contractile responses to phenylephrine in diabetes.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Discriminative stimulus effect of phenylephrine.

Rats were trained to discriminate phenylephrine in a two-lever, food-motivated operant task by increasing the i.p. administered training dose from 0.8 to 2 mg/kg. Stable discrimination to 2 mg/kg phenylephrine was established and testing of 0.5-2.5 mg/kg was shown to be dose-responsive and allowed for a calculated ED50 value of 0.87 mg/kg. Administration of methoxamine (0.5-6 mg/kg), another alpha 1-adrenoceptor agonist, produced a dose-responsive generalization, whereas only the lowest (0.04 mg/kg) and highest (0.12 mg/kg) doses of the alpha 2-adrenoceptor agonist clonidine produced generalization in the phenylephrine-trained rats. Likewise, yohimbine (2.5-4.5 mg/kg) generalized, whereas pretreatment with prazosin (0.1-0.4 mg/kg), the alpha 1-adrenoceptor antagonist, dose-responsively decreased phenylephrine discrimination. The results would indicate that phenylephrine is capable of controlling differential responding in a drug discrimination paradigm and would suggest that this effect is centrally mediated. The possibility that peripheral administration of phenylephrine (Neosynephrine) affects the brain in chronic users of nasal decongestants is discussed.

Adrenergic alpha-Agonists↗

PubMed1991

On the mechanism of the positive inotropic action of the alpha adrenoceptor agonist, phenylephrine, in isolated rat left atria.

Alpha adrenoceptor agonists have been reported to increase contractile force and to stimulate Na+/H+ exchange in the heart. We studied the influence of hexamethylamiloride (HMA), a selective inhibitor of Na+/H+ exchange, on the positive inotropic action of phenylephrine in isolated, paced rat left atria (3 microM propranolol). HMA (10 microM) blocked the ouabain-induced contracture, an event dependent on Na+ uptake via the Na+/H+ exchanger. The same concentration of HMA prevented 50% of the positive inotropic effect of phenylephrine (10 microM), but had no effect on base-line developed force. HMA reduced the maximal effect (234 +/- 19 vs. 117 +/- 20% increase of base-line), but not the EC50 (4.4 +/- 1.0 vs. 3.6 +/- 2 microM) of phenylephrine. Phenylephrine (100 microM) caused both a leftward and upward shift of the Ca++ concentration-effect curve, but only a leftward shift, in the additional presence of HMA (3 microM). It is known that lithium, but not choline, will exchange for H+ via the Na+/H+ exchanger: phenylephrine's (100 microM) positive inotropic effect in choline-substituted solutions averaged 37% of that in lithium-substituted solutions. The positive inotropic effect of phenylephrine was amplified by ouabain (200 microM). These results are consistent with the hypothesis that alpha adrenoceptor agonists produce their positive inotropic effects, in part, via stimulation of Na+/H+ exchange. Such stimulation could cause an intracellular alkalinization and (in the presence of ouabain), elevated intracellular Na+.

Amiloride↗

PubMed1975

The influence of temperature increase, elevation of extracellular h+-concentration, and of triiodothyronine on the actions of phenylephrine, histamine, and beta-sympathomimetic drugs on rabbit aortic strips.

In the isolated preparation from the rabbit thoracic aorta, the affinities of the vasoconstrictor agents phenylephrine and histamine, as well as of the vasodilator beta-sympathomimetic drugs isoprenaline, fenoterol (TH 1165a), terbutaline, and salbutamol under the conditions of temperature increase, triiodothyronine and decrease of extracellular pH were investigated. It was observed that (1) a temperature increase from 25 degrees to 42 degrees C significantly indreased the maximal tension evoked by histamine, whereas that induced by the alpha-sympathomimetic drug phenylephrine was not altered significantly; the maximal relaxation caused by beta-sympathomimetic drugs either at 25 degrees or at 42 degrees C did not differ from one another; (2) the affinities of histamine, phenylephrine and of the beta-sympathomimetic drugs isoprenaline, fenoterol, terbutaline, and salbutamol each were comparable at either 25 degrees or 42 degrees C; the rank order of efficacy of the beta-sympathomimetic drugs is isoprenaline greater than fenoterol greater than salbutamol greater than terbutaline; (3) a decrease of the pH from 7.37 to 7.15 diminished the affinities of histamine and of the beta sympathomimetic drugs whereas that of the alpha-adrenergic drug phenylephrine was not altered. A further decrease of the pH to 6.8 diminished additionally the affinity of histamine and of isoprenaline, and especially that of the other beta-sympathomimetic drugs to such an extent that in the latter case complete dose-response curves could not be determined any more; (4) pretreatment of the animals with 0.4 mg/kg of triiodothyronine (T3) for two days, which strongly depressed the tension induced by either histamine or phenylephrine, did not alter the affinity of both drugs; T3 in vitro (10(-6) M) only diminished the affinity of histamine but left that of phenylephrine unaltered; pretreatment for two days with 0.2 mg/kg of T3 yielded a significant diminution of the pD2-values for two beta-sympathomimetic drugs investigated, namely isoprenaline and fenoterol; also the administration of T3 in vitro in a final concentration of 10(-6) M resulted in a diminution of the affinity of both beta-sympathomimetic drugs; (5) the results obtained show that also on the aorta beta-adrenoceptor stimulants are dependent on the metabolic state while alpha-adrenoceptor stimulants are not.

Adrenergic beta-Agonists↗

PubMed1990

Improved ocular: systemic absorption ratio of timolol by viscous vehicle and phenylephrine.

Increasing the ocular absorption of timolol relative to its systemic absorption is important clinically because ophthalmic timolol may cause serious respiratory, cardiac, and central nervous system side effects. The authors evaluated the effects of phenylephrine coadministration and solution viscosity on the aqueous humor:plasma and iris ciliary body:plasma ratios of peak timolol concentrations after ocular application. Timolol eye drops (5 mg/ml, 25 microliters) were administered to the eyes of pigmented rabbits. Coadministered phenylephrine (0.8-8.2 mg/ml) decreased the systemic peak concentrations of timolol significantly. Since ocular absorption of timolol was not affected by phenylephrine, the ocular:systemic concentration ratios were improved four- to fivefold. Phenylephrine slows down the systemic absorption of timolol by constricting the conjunctival and nasal capillaries. The ratios of the aqueous humor:plasma and iris ciliary body:plasma peak concentration of timolol were improved three- to ninefold in the presence of sodium carboxymethylcellulose compared with nonviscous eye drops. The improved ocular penetration is probably due to the longer corneal contact, and the decreased rate of systemic absorption may be caused by the slower spreading of the solution on the nasal mucosa. Compared with timolol eye drops, the ratio of the eye:plasma peak timolol concentrations was improved tenfold by using viscous eye drops with phenylephrine. Systemic concentrations of ophthalmic timolol and possibly related side effects can be decreased when timolol is instilled in a viscous vehicle with a low phenylephrine concentration.

Absorption↗

PubMed1988

Effects of prolonged phenylephrine infusion on cardiac adrenoceptors and calcium channels.

Effects of prolonged in vivo infusion of phenylephrine upon receptor binding and cardiac contractility were studied in Sprague-Dawley rats. A 1-hr i.v. infusion of phenylephrine (3 mg/kg/hr) resulted in a sustained 50% increase in diastolic blood pressure and 5% increase in heart rate. Chronic (6-day) infusion (3 mg/kg/hr) utilizing Alzet mini-osmotic pumps maintained plasma concentrations of phenylephrine at 1.0 microgram/ml, depleted myocardial norepinephrine stores 8-fold and resulted in a modest cardiac hypertrophy. Density and affinity of myocardial adrenoceptors and calcium channels were quantified by analyzing saturation isotherms of radioligand binding. [3H]Prazosin, [3H]dihydroalprenolol and [3H]nitrendipine bound specifically and with high affinity to cardiac alpha-1 and beta adrenoceptors and calcium channels, respectively. As measured by Scatchard analyses, phenylephrine infusion significantly decreased the maximum number (Bmax) of specific [3H]prazosin binding sites by 39% (430 +/- 20 vs. 263 +/- 16 fmol/mg of protein; P less than .05). Chronic phenylephrine treatment also decreased the Bmax for [3H]dihydroalprenolol binding by 31% (124 +/- 3.3 vs. 86 +/- 6.6 fmol/mg of protein; P less than .05) and the Bmax for [3H]nitrendipine binding by 32% (342 +/- 8.8 vs. 235 +/- 6.7 fmol/mg of protein; P less than .05). Binding affinities (Kd) of [3H]prazosin, [3H]dihydroalprenolol and [3H]nitrendipine remained unchanged. Administration of vehicle alone or surgical manipulation due to osmotic pump implantation did not affect either the density or affinity of [3H]prazosin, [3H]dihydroalprenolol or [3H]nitrendipine binding. Contractile responses to phenylephrine were studied in isolated ventricular strips to determine the functional significance of alpha-1 adrenoceptor down-regulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Effect of topical phenylephrine on the equine pupil.

The mydriatic effect of 10% phenylephrine was evaluated in 9 horses. Base-line pupillary size in mesopic conditions and during light stimulation was ascertained before application of pharmacologic agents. In study 1, 10% phenylephrine was applied to each eye (n = 5 horses). After 15 minutes, the pupillary size was determined in both lighting conditions. Phenylephrine was again applied to each eye, and after an additional 15 minutes, the pupillary size was determined. In study 2, 1% tropicamide was applied to each eye (n = 4 horses), and after 30 minutes, the pupillary size was determined in both lighting conditions. Tropicamide and phenylephrine were applied to each eye immediately after determination of pupillary size, and after an additional 30 minutes, the pupillary size was determined. There was no significant change (P greater than 0.9) in pupillary size when phenylephrine was used alone or when phenylephrine was used in an eye that had been dilated with tropicamide.

Animals↗

PubMed1979

Aerosol bronchodilator therapy: a comparison of the effects of bronkometer with isoetharine, isoproterenol and phenylephrine.

The bronchodilator action and cardiovascular toxicity of aerosols of (1) isoetharine, (2) isoetharine in combination with phenylephrine, (3) isoproterenol, and (4) phenylephrine were compared in a group of severe stable ambulatory asthmatics. All preparations except phenylephrine produced reduction in specific airway resistance and increased flow rates which peaked at 15 minutes. The action of isoproterenol and the two isoetharine preparations peaked at 15 minutes while the peak effect of isoetharine and isoetharine in combination with phenylephrine continued for 60 minutes. The difference between isoproterenol and isoetharine alone or in combination with phenylephrine was not statistically significant. None of the drugs produced any cardiovascular side effects. The authors conclude that isoetharine, though less potent than isoproterenol on a weight-for-weight basis, is an effective and safe bronchodilator. Addition of phenylephrine to isoetharine does not potentiate or prolong the action of the latter.

Adult↗

PubMed1995

Effect of anoxia on the urethral response to phenylephrine.

PURPOSE: Smooth muscle requires oxygen for proper contractile function. In addition, anoxia has been shown to inhibit the contractile response to various forms of stimulation. Continence, at least in part, depends upon active alpha-adrenergic tone, which provides intraurethral tension during bladder filling. The current study was designed to determine the effect of anoxia on the ability of the urethra to sustain tension. MATERIALS AND METHODS: Standard isolated urethral strip preparations were used to determine the effect of anoxia on the contractile response to phenylephrine; isolated whole urethra preparations were used to determine the effect of anoxia on the intraurethral pressure--flow characteristics. RESULTS: The peak tension responses of the female and male urethra to phenylephrine were significantly greater than the plateau tension. Anoxia induced an immediate decrease in phenylephrine-stimulated tonic tension to baseline tension. In the whole urethra preparation, phenylephrine increased opening pressure to a greater extent in the male urethra than in the female urethra. In both sexes, anoxia reduced the opening pressure and completely prevented phenylephrine stimulated increases in opening pressure. CONCLUSION: The tonic response to phenylephrine is lost virtually immediately upon the initiation of hypoxia. This suggests that hypoxia decreases the ability of the urethra to maintain a tonic response to alpha-adrenergic stimulation during bladder filling and may be a factor in incontinence, especially in females.

Adenosine Triphosphate↗

PubMed1993

Effects of the alpha 1-adrenoceptor agonist phenylephrine in pig heart. Study of the direct action on contractile proteins.

The effects of the alpha 1-adrenoceptor agonist phenylephrine (CAS 59-42-7) on Ca++ sensitivity of the contractile proteins and on force of contraction of the heart were studied in right ventricular preparations isolated from pigs. In contracting trabeculae phenylephrine (3-100 mumol/l) increased force of contraction in the presence of propranolol maximally by 91.8 +/- 36.2% (n = 5). The effect of phenylephrine was antagonized by prazosin, indicating an alpha-adrenoceptor-mediated positive inotropic effect. Glycerol- and Lubrol WX-extracted trabeculae ("chemically skinned") were activated by Ca(++)-concentrations between 0.01 and 47.7 mumol/l. Phenylephrine (0.1-100 mumol/l) did not affect the Ca++ activated force in these preparations. A direct intracellular action of phenylephrine on contractile proteins is thus rather unlikely to contribute to the positive inotropic effect of phenylephrine.

Adrenergic alpha-Agonists↗