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 379 records · Page 21Linked to original sources

PubMed2002

Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans.

To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ~0.5 degrees C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P < 0.005) but did not change mean arterial blood pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [DeltaMAP 8.4 +/- 1.2 mmHg; DeltaTPR 0.96 +/- 0.85 peripheral resistance units (PRU)] compared with normothermia (DeltaMAP 15.4 +/- 1.4 mmHg, DeltaTPR 7.13 +/- 1.18 PRU; all P < 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P > 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate.

Adult↗

PubMed1998

Liposomal VIP attenuates phenylephrine- and ANG II-induced vasoconstriction in vivo.

The purpose of this study was to determine whether vasoactive intestinal peptide (VIP) modulates vasoconstriction elicited by phenylephrine and ANG II in vivo and, if so, to begin to elucidate the mechanisms underlying this phenomenon. Using intravital microscopy, we found that suffusion of phenylephrine and ANG II elicits significant vasoconstriction in the in situ hamster cheek pouch that is potentiated by VIP-(10-28), a VIP receptor antagonist, but not by VIP-(1-12) (P < 0.05). Aqueous VIP has no significant effects on phenylephrine- and ANG II-induced vasoconstriction. However, VIP on sterically stabilized liposomes (SSL), a formulation where VIP assumes a predominantly alpha-helix conformation, significantly attenuates this response. Maximal effect is observed within 30 min and is no longer seen after 60 min. Empty SSL are inactive. Indomethacin has no significant effects on responses induced by VIP on SSL. The vasodilators ACh, nitroglycerin, calcium ionophore A-23187, 8-bromo-cAMP, and isoproterenol have no significant effects on phenylephrine- and ANG II-induced vasoconstriction. Collectively, these data suggest that vasoconstriction modulates VIP release in the in situ hamster cheek pouch and that alpha-helix VIP opposes alpha-adrenergic- and ANG II-induced vasoconstriction in this organ in a reversible, prostaglandin-, NO-, cGMP-, and cAMP-independent fashion.

Acetylcholine↗

PubMed1989

Effect of endothelium on phenylephrine-induced contraction in the rat isolated aortic strips.

Phenylephrine tested on the isolated endothelium intact rat aortic strips elicited an enhanced response in the second assay when compared with the response obtained in the first trial. Removal of the endothelium and the pretreatment of the strips in the endothelium with methylene blue almost completely prevented the enhanced response to phenylephrine in the second assay. Pretreatment of the strips with lysine acetyl salicylate failed to abolish the potentiated response to phenylephrine in the second test. These data were taken as an evidence that the basal production or release of endothelium-derived relaxing factor(s) but not cyclooxygenase products of arachidonic acid from the endothelium of the rat aorta can influence the contractile effect of phenylephrine and the enhanced response to this alpha-adrenoceptor agonist in the second assay is probably due to the recuded production or release of these endogenously occurring endothelium-originated substance(s).

Animals↗

PubMed1998

Comparison between noninvasive indices of baroreceptor sensitivity and the phenylephrine method in post-myocardial infarction patients.

BACKGROUND: Depressed baroreflex sensitivity obtained by means of a phenylephrine test plays a prognostic role in patients with a previous myocardial infarction. Our purpose was to evaluate the correlation and agreement between the baroreflex sensitivity obtained with phenylephrine and that obtained by two noninvasive methods: the alpha-index and sequence analysis. METHODS AND RESULTS: The alpha-index was measured by means of the spectral analysis of RR and systolic blood pressure variabilities in both the high- and low-frequency bands; sequences were identified from simultaneously recorded time series in which the RR and systolic blood pressure concurrently increased or decreased. Noninvasive baroreflex sensitivity tests were performed during both spontaneous and controlled respiration. Fifty-two consecutive patients with recent myocardial infarction underwent the analyses. Although the correlations between phenylephrine and either of the noninvasive methods were always significant, those found during controlled respiration had the highest r values (r=.70). However, the limits of agreement calculated by means of the Bland and Altman method were wide for both noninvasive methods. CONCLUSIONS: The results obtained by means of noninvasive baroreflex sensitivity assessments should not be used in clinical practice as an alternative to those obtained by the phenylephrine method.

Adult↗

PubMed1989

Phenylephrine-induced hypertension reduces ischemia following middle cerebral artery occlusion in rats.

We studied the influence of phenylephrine-induced hypertension on the area of ischemia during brief middle cerebral artery occlusion. Rats were anesthetized with 1.2 minimal alveolar concentration (MAC) isoflurane, and the middle cerebral artery was occluded via a subtemporal craniectomy. Immediately thereafter, in one group (n = 9) arterial blood pressure was increased 30-35 mm Hg above the preocclusion level by intravenous infusion of phenylephrine. In a second, control, group (n = 10) there was no manipulation of blood pressure. Local cerebral blood flow was determined autoradiographically 15 minutes after occlusion. The areas (expressed as a percentage of the total coronal cross-sectional area) in which local cerebral blood flow decreased to three ranges (0-6 ml/100 g/min [rapid neuronal death probable], 6-15 ml/100 g/min [delayed neuronal death probable], and 15-23 ml/100 g/min [electrophysiologic dysfunction with prolonged survival probable]) were measured. The areas in which local cerebral blood flow decreased to the two more severely ischemic ranges were smaller in the phenylephrine group than in the control group. For example, in the coronal section in the center of the middle cerebral artery distribution, local cerebral blood flow was 0-6 ml/100 g/min in 6.7 +/- 1.4% of the section in normotensive rats but was in that range in only 1.7 +/- 0.6% of the section during phenylephrine-induced hypertension (p less than 0.05). For the 6-15 ml/100 g/min range, the areas were 6.8 +/- 0.8% and 3.8 +/- 0.7%, respectively (p less than 0.05). For the 15-23 ml/100 g/min range, there were no differences between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Safety of hypertensive hypervolemic therapy with phenylephrine in the treatment of delayed ischemic deficits after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Hypertensive hypervolemic therapy has been shown to reverse delayed ischemic deficits after aneurysmal subarachnoid hemorrhage. Concern has been raised about systemic complications of therapy, including pulmonary edema and myocardial ischemia, especially when high doses of vasopressors are used. Patients in whom delayed ischemic deficits were treated with hypervolemia and phenylephrine were prospectively evaluated for signs of systemic toxicity. METHODS: Twenty-four consecutive patients treated with hypertensive hypervolemic therapy after aneurysmal subarachnoid hemorrhage were studied. Sixty-seven percent had underlying cardiac disease, vascular disease, or hypertension. No patient was excluded because of age or preexisting cardiac disease. Patients were closely monitored for signs of congestive heart failure (physical examination, chest x-ray films, arterial blood gases, cardiac index, pulmonary artery wedge pressure, and oxygen requirement). Indicators of cardiac ischemia and other extracerebral toxicity that were monitored included cardiac enzymes, electrocardiograms, serum creatinine, electrolyte and lactic acid levels, gastrointestinal motility, and urine output. RESULTS: Volume expansion and phenylephrine infusion produced an increase in several hemodynamic parameters including pulmonary artery wedge pressure, which rose 28% (13 +/- 3.6 to 16 +/- 1.9 mm Hg), mean arterial blood pressure, which rose 25% (99 +/- 12.5 to 123 +/- 11.4 mm Hg), and systemic vascular resistance, which rose 46% (1234 +/- 294 to 1739 +/- 315 dyne.s-1.cm-5); however, there was no change in cardiac index (3.9 +/- 0.9 to 4.0 +/- 0.6 L.min-1.m-2). There were no clinically significant episodes of pulmonary edema requiring a change in vasopressor therapy and no myocardial infarctions. Phenylephrine was stopped in only one patient (incidence, 4%; 95% confidence interval, 0% to 12%), who developed an exacerbation of his preexisting bradycardia. There was no evidence of noncardiac organ system toxicity. Eighty-eight percent of the patients exhibited neurological improvement. CONCLUSIONS: Hypertensive hypervolemic therapy with the use of high-dose phenylephrine can be administered with acceptable systemic toxicity, even in patients with previous cardiac disease, provided that close monitoring is performed. To minimize risk, aggressive treatment should probably be reserved for patients with signs of delayed ischemia rather than administered prophylactically.

Adult↗

PubMed2006

Effects of phenylephrine on transplanted submandibular gland.

Autotransplantation of the submandibular gland is a potential treatment for severe kerato-conjunctivitis sicca. However, one of the major barriers to this procedure is that secretions from the transplanted gland decrease shortly after the operation, which may lead to obstruction of Wharton's duct, or even to transplantation failure. Using a rabbit model, we investigated whether phenylephrine could improve the secretion from the transplanted gland. We found that phenylephrine treatment significantly reversed the decrease in salivary secretion after transplantation, enhanced the expressions of alpha1A-, alpha1B-, and alpha1D-adrenoceptor mRNA, and ameliorated atrophy of acinar cells. Furthermore, phenylephrine also induced translocation of aquaporin-5 from the cytoplasm to the apical membrane, and increased the levels of phospho-ERK1/2, ERK1/2, phospho-PKCzeta, and PKCzeta in the transplanted gland. These results indicate that phenylephrine treatment moderates structural injury and improves secretory function in the transplanted submandibular gland through promoting alpha1-adrenoceptor expression and post-receptor signal transduction.

Adrenergic alpha-Agonists↗

PubMed1990

Epinephrine and phenylephrine increase cardiorespiratory toxicity of intravenously administered bupivacaine in rats.

We studied the effects of epinephrine and phenylephrine on the cardiorespiratory toxicity of intravenously injected bupivacaine in Sprague-Dawley rats. Our data show that both epinephrine and phenylephrine significantly increased cardiorespiratory toxicity of intravenously injected bupivacaine (P less than 0.007, X2 analyses with Yates' correction). Our data suggest that epinephrine or phenylephrine added to bupivacaine may be more toxic to cardiorespiratory systems than plain bupivacaine or epinephrine alone or phenylephrine alone when injected intravenously in rats.

Animals↗

PubMed1992

Computerized electroencephalographic monitoring and selective shunting: influence on intraoperative administration of phenylephrine and myocardial infarction after general anesthesia for carotid endarterectomy.

During carotid endarterectomy (CEA), phenylephrine infusions are commonly used to induce hypertension during carotid clamping in an attempt to increase collateral cerebral blood flow and prevent cerebral ischemia. Although this practice appears to increase the incidence of intraoperative myocardial ischemia during CEA when general anesthesia is employed, whether the limited use of phenylephrine infusions in specific instances of cerebral ischemia, as shown on an electro-encephalogram, results in low perioperative rates of both myocardial infarction (MI) and cerebral infarction remains unclear. We studied 171 CEAs done under general anesthesia performed with selective shunting based on the identification of cerebral ischemia by a two-channel computerized electroencephalographic monitor. The use of a phenylephrine infusion was restricted to the following instances of cerebral ischemia: 1) ischemia associated with hypotension that did not resolve within 2 minutes of decreases in anesthetic administration and treatment with fluid and/or colloid; 2) ischemia poorly or slowly responsive to shunt placement, accompanied by either hypo- or normotension; and 3) ischemia poorly or slowly responsive to removal of the carotid clamp, accompanied by either hypo- or normotension. Two non-Q wave MIs (1.2%) occurred, both nonfatal. There were two cerebral infarctions (1.2%) and three deaths not related to MI (1.8%). Based on these findings, in order to decrease the incidence of both MI and cerebral infarction after general anesthesia for CEA, we recommend the restrictive use of phenylephrine-induced hypertension for specific instances of slowly or poorly reversible cerebral ischemia, as shown on the electroencephalogram.

Adult↗

PubMed2006

[Duration of action of silodosin (KMD-3213) against phenylephrine-induced increase in intraurethral pressure in rats].

The duration of action of Silodosin (KMD-3213) against the phenylephrine-induced increase in intraurethral pressure in urethane-anesthetized rats was compared with that of tamsulosin hydrochloride. Silodosin, tamsulosin, or vehicle was orally administered to fasted male rats. Then, under urethane anesthesia, a cannula was inserted into the prostatic urethra. Phenylephrine, at a dose of 30 microg/kg, was infused (infusion rate: 36 ml/h; infusion time: 100 s/kg) via the femoral vein at 12 h, 18 h, or 24 h after administration of the study drug, and the intraurethral pressure in the prostate region was measured. Although the plasma silodosin concentration would have resolved within a few hours, silodosin significantly inhibited the phenylephrine-induced increase in intraurethral pressure (versus the vehicle-treated group) at 12 h, 18 h, and 24 h after its oral administration (at doses of 100 microg/kg and above, 1000 microg/kg and above, and 3000 microg/kg, respectively). On the other hand, tamsulosin hydrochloride showed no inhibitory action at 24 h after its oral administration at doses up to 3000 microg/kg. Thus, silodosin inhibits the phenylephrine-induced increase in intraurethral pressure for a longer time than tamsulosin hydrochloride.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1998

Proliferation of adult rat hepatocytes in primary cultures induced by platelet-derived growth factor is potentiated by phenylephrine.

We investigated whether or not proliferation of adult rat hepatocytes induced by platelet-derived growth factor (PDGF) is affected by alpha1-adrenoceptor agonists such as phenylephrine during the early and late phases of primary culture. Adult rat hepatocytes underwent significant DNA synthesis after culture with 10 ng/ml of PDGF for 2 hr at a low cell density (3.3 x 10(4) cells/cm2). Under these culture conditions, the number of nuclei increased significantly during the 3.5-hr culture period. Hepatocyte DNA synthesis and proliferation induced by 10 ng/ml of PDGF decreased slightly as a result of increasing the initial plating density. An alpha1-adrenoceptor agonist, phenylephrine (10(-6) and 10(-5) M), alone did not affect hepatocyte DNA synthesis and proliferation, but markedly potentiated PDGF-induced hepatocyte DNA synthesis and proliferation. The phenylephrine effect was mimicked by phorbol myristate acetate (10(-7) M), but not by ionomycin (10(-5) M). The mitogenic effects of PDGF were almost completely blocked by treating hepatocytes with genistein (5 x 10(-6) M), U-73122 (3 x 10(-6) M), sphingosine (10(-5) M), wortmannin (10(-7) M) and rapamycin (10 ng/ml). These results demonstrate that PDGF can induce the proliferation of adult rat hepatocytes rapidly in primary culture, regardless of the initial plating density. The present results also suggest that following stimulation with PDGF, activation of tyrosine kinase, phospholipase C, phosphatidylinositol 3-kinase, protein kinase C (PKC) and p70 ribosomal protein S6 kinase is essential for the proliferation of adult rat hepatocytes. The co-mitogenic effects of phenylephrine may involve PKC activation.

Adrenergic alpha-Antagonists↗

PubMed1999

Effects of phenylephrine and prazosin on axial movement of the rat incisor and arterial blood pressure.

We investigated the dose-response effects of phenylephrine and antagonistic effects of prazosin on axial movement of the rat incisor and arterial blood pressure. Phenylephrine caused a temporal extrusive tooth movement and an increase in blood pressure at all doses. With increasing phenylephrine doses, the maximum extrusive tooth movement and maximum increase in blood pressure were enhanced. The maximum extrusive tooth movement and increase in blood pressure induced by phenylephrine were markedly suppressed after pretreatment with prazosin. These results suggested that extrusive tooth movement is closely related to the rise in blood pressure due to stimulation of vascular alpha1-receptors.

Adrenergic alpha-Agonists↗

PubMed1982

Inhibition by trifluoperazine of glycogenolytic effects of phenylephrine, vasopressin, and angiotensin II.

The effects of trifluoperazine on the activation of glycogenolysis by various hormones were studied in perfused rat liver. Trifluoperazine significantly inhibited glycogenolytic effect of phenylephrine and angiotensin II by lowering maximal response, and that of vasopressin by shifting the dose-response curve to the right, while alpha-antagonist phentolamine was inhibitory only to phenylephrine. Phosphorylase activation of phenylephrine was inhibited by trifluoperazine in parallel with glycogenolytic response. The increase in 45Ca2+ efflux induced by phenylephrine, angiotensin II, and vasopressin was also inhibited by the agent. These inhibitory effects of trifluoperazine were not related to the change in tissue cyclic AMP or cyclic GMP levels. On the other hand, neither the glycogenolytic effect of glucagon, cyclic AMP, and N6,O2-dibutyryl cyclic AMP nor phosphorylase activation by glucagon was affected by trifluoperazine. Thus, trifluoperazine specifically inhibits the activation of glycogenolysis by Ca2+-dependent hormones.

Angiotensin II↗

PubMed1995

Protective effects of calcium channel blockers on acute bromobenzene toxicity to isolated rat hepatocytes. Inhibition of phenylephrine-induced calcium oscillations.

BACKGROUND AND METHODS: Protective effects of verapamil, nifedipine, diltiazem, and ethylene glycol tetraacetic acid (EGTA) on acute bromobenzene (BB) toxicity to rat hepatocytes were evaluated, and cytosolic [Ca2+]i was monitored in single BB-exposed rat hepatocytes. Additionally, the effect of nifedipine on phenylephrine-stimulated calcium oscillations was investigated. RESULTS: BB at 0.8-2.4 mM increased the lactate dehydrogenase (LDH) leakage rate dose-dependently. Pretreatment with verapamil (25-35 microM), nifedipine (35-45 microM), diltiazem (25 microM), or EGTA (1.5-5 mM) markedly attenuated the BB-induced (1.6 mM) LDH leakage rate during 2 h of incubations. BB did not cause any detectable acute change in [Ca2+]i. BB interfered with phenylephrine-stimulated calcium oscillations, by blocking the oscillations in 58% of the cells and reducing the oscillation frequency in the rest. Nifedipine (100 and 200 microM) blocked the phenylephrine-induced calcium oscillations completely in 55% and 88% of the cells, respectively. CONCLUSIONS: The findings demonstrate that verapamil, nifedipine, diltiazem, and EGTA significantly protect rat hepatocytes against BB toxicity. BB interferes with phenylephrine-stimulated calcium oscillations. Nifedipine inhibits the oscillations at doses higher than those exerting a protective effect.

Animals↗

PubMed1995

[The experimental evaluation of the difference in closing dynamics of internal urethral ostium on the urinary continence and on the ejaculation induced by an administration of phenylephrine].

BACKGROUND: The internal urethral ostium is usually closed both on the ejaculation and on the urine collection, although the difference of the closing characteristics have not been known. METHODS: The difference in closing style of bladder neck (internal urethral ostium) between on the phenylephrine administration corresponding state to the ejaculation and on the filling of urinary bladder corresponding state to the urinary continence was evaluated by Stereo-UPP method using mongrel dogs. RESULTS: On phenylephrine administration, the length between verumontanum and bladder neck was lengthened, and a remarkable pressure increase was observed in the area. On the urinary continence filling physiological saline in the bladder, the length of the urethra on the UPP curve of the anterior wall of urethra was lengthened (10%) and the base of bladder was gradually become flat. The pressure in the bladder neck was not relatively increased. CONCLUSIONS: The internal urethral ostium was closed both on the phenylephrine administration and on the urine collection, although the closing characteristics of each was very different. It was demonstrated that on the phenylephrine administration the area between the verumontanum and the bladder neck was lengthened, together with the rise of pressure in the area, whereas on the urine collection bladder neck was closed in low pressure by flattening the base of bladder.

Adrenergic alpha-Agonists↗

PubMed1999

Variability in phenylephrine response and essential hypertension: a search for human alpha(1B)-adrenergic receptor polymorphisms.

Genetic polymorphisms in drug receptors, in particular adrenergic receptors, may contribute to intersubject differences in pharmacologic response. We tested patients and first-degree normotensive and hypertensive relatives of patients with essential hypertension and found substantial intersubject variability in blood pressure response to infusion of the alpha(1)-adrenergic agonist phenylephrine. Because response to phenylephrine depends upon interaction with alpha(1B)-adrenergic receptors, we tested whether polymorphisms in this receptor contribute to the variable responses. Accordingly, we developed a polymerase chain reaction-based method, generating four exon-spanning fragments, to identify polymorphisms in the coding sequence of the two exons of the human alpha(1B)-adrenergic receptor. We sequenced the entire coding sequence of exon 1 from 51 subjects and exon 2 from 16 of these 51 subjects. Compared with the published sequence for the alpha(1B)-adrenergic receptor, we found one amino acid addition in exon 2 at position 368 (Arg) and one substitution (Arg371Gly) in all subjects. We thus suggest we have defined the correct coding sequence of the human alpha(1B) receptor. We found two "silent" polymorphisms in exon 1, one of which occurred in 3 of 51 subjects. These polymorphisms were unrelated to blood pressure status or response to phenylephrine. The 95% confidence intervals for expression of polymorphisms in exons 1 and 2 were 0 to 11%. Our data reveal that although phenylephrine response varies in humans, frequent polymorphisms in the coding sequence of the human alpha(1B)-adrenergic receptor appear not to account for this variation or for the increased blood pressure in patients with essential hypertension.

Adult↗

PubMedDate not supplied

UV/VIS spectrophotometric methods for determination of caffeine and phenylephrine hydrochloride in complex pharmaceutical preparations. Validation of the methods.

The contents of active substances were determined in a preparation TP-4 (tablets) containing paracetamol, ascorbic acid, caffeine and phenylephrine hydrochloride. For determination of caffeine and phenylephrine hydrochloride, UV/VIS spectrophotometric method was used. The VIS spectrophotometric method based on the reaction of phenylephrine with ninhydrine in sulphuric acid (1.127 kg/l). Validation of methods performed for model mixtures proved those methods were accurate, precise, repeatable and linear in the range from 50% to 150% of the amount declared in the preparation. The content of caffeine and phenylephrine hydrochloride in TP-4, Thompyrin, Panadol Extra, Ring N satisfies the FP V demands.

Caffeine↗

PubMed2001

A prospective multicenter trial to determine the incidence of transient neurologic symptoms after spinal anesthesia with phenylephrine added to 0.5% tetracaine.

The addition of vasoconstrictors for spinal anesthesia is controversial, since an increase in the incidence of transient neurologic symptoms (TNS) has been reported. A multicenter, randomized, double-blind study was conducted to assess the effectiveness of spinal anesthesia with phenylephrine in addition to tetracaine as well as the incidence of neurological complications. We studied 64 patients with comparable demographic characteristics who were scheduled for elective surgery for a lower limb, or a gynecological or urological procedure. The patients were allocated randomly into 2 groups. Group P (n = 34) received 0.5% tetracaine in 10% glucose with 0.025% phenylephrine, while group C (n = 30) received 0.5% tetracaine in 10% glucose. Our results showed that only 2 patients (6.7%) in group C experienced TNS, and their symptoms disappeared within 72 hr after anesthesia, while none of the patients (0%) in group P complained of symptoms. The incidence of TNS was thus not significantly different between the two groups. Six hours after the sensory block, group P patients demonstrated sensory disturbance, with the median spinal dermatome corresponding to the L1 segment. Moreover, systolic blood pressure in group P was significantly higher than that in group C, 5 min, 15 min, and 20 min after injection. The incidence of TNS in the present study does not seem to be greater after surgery with spinal anesthesia using 0.5% hyperbaric tetracaine and 0.5 mg phenylephrine than without phenylephrine. Randomized, double-blind, cross-over trials with a larger sample size would be required in the future to obtain more reliable results.

Anesthesia, Spinal↗