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PubMed1997

Role of the lipoxygenase pathway in phenylephrine-induced vascular smooth muscle cell proliferation and migration.

We studied the effects of phenylephrine-stimulated proliferation and migration of vascular smooth muscle cells and the role of 12-lipoxygenase-mediated pathways under normal as well as high glucose conditions. Phenylephrine-induced increases in cellular proliferation and migration were attenuated by the specific 12-lipoxygenase inhibitor baicalein. In contrast, neither of the cyclo-oxygenase inhibitors, indomethacin or ibuprofen, had any effect. Direct addition of the 12-lipoxygenase product, 12-S-hydroxyeicosatetraenoic acid (12-HETE), increased the proliferation and migration of vascular smooth muscle cells treated with both phenylephrine and nordihydroguaiaretic acid. Furthermore, we observed that phenylephrine induced greater increases in the proliferation and migration of vascular smooth muscle cells and also that the 12-lipoxygenase inhibitor prevented the enhancement of proliferation and migration of vascular smooth muscle cells induced by phenylephrine in the presence of high glucose (25 mmol/l). These results suggest that 12-lipoxygenase activation plays a key role in phenylephrine-induced responses of vascular smooth muscle cells under normal and hyperglycemic conditions. 12-lipoxygenase may be a good pharmacological target for treatment of vascular disease of hypertension and diabetes mellitus.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1987

Comparison of epinephrine and phenylephrine for resuscitation and neurologic outcome of cardiac arrest in dogs.

A study was done comparing resuscitability and 24-hour neurologic outcome in fibrillating dogs that were treated with either phenylephrine (a primary alpha agonist) or epinephrine. Ventricular fibrillation was induced electrically in 18 dogs. After three minutes, standard CPR was instituted using a mechanical resuscitator. Dogs were given phenylephrine or epinephrine at nine minutes and defibrillation was attempted at 12 minutes. Dogs underwent hemodynamic monitoring and pharmacologic support, if necessary, for an additional 90 minutes. At four, eight, 12, and 24 hours, a standard neurologic examination was performed and deficit scores were assigned by an observer blinded to the drug given. Fourteen of the 18 dogs were resuscitated. There were no statistically significant differences in the epinephrine- or phenylephrine-treated groups with regard to number of animals resuscitated, time and interventions required for resuscitation, initial cardiac rhythm post resuscitation, or occurrence of ventricular fibrillation during resuscitation. No differences were found in arterial, central venous, or myocardial perfusion pressures during CPR. Phenylephrine-treated dogs tended to have higher mean pressures in the critical care period (15 to 30 minutes), although this was not significant. Total neurologic deficit scores were 127.8 +/- 83.8 for the phenylephrine-treated group and 129.4 +/- 87.4 for the epinephrine group. No significant differences were found in the level of consciousness, cranial nerve function, motor skills, or general behavior scores. We conclude that there is no difference in neurologic or cardiovascular outcome when phenylephrine is compared to epinephrine in a canine model of cardiac arrest and cardiopulmonary resuscitation.

Animals↗

PubMed2002

Effect of phenylephrine injected into the nucleus tractus solitarius of Sprague-Dawley rats and spontaneously hypertensive rats.

In alpha-chloralose-anesthetized Sprague-Dawley (SD) rats with unilateral nucleus tractus solitarius (NTS) lesions, injection of the alpha(1)-adrenergic receptor agonist phenylephrine into the contralateral NTS dose-dependently increased arterial pressure (AP). Bunazosin (0.1 nmol) or prazosin (0.36 nmol), an alpha(1)-adrenergic receptor antagonist, also increased AP. When injected into the NTS, pre-treatment with phenylephrine (10 nmol) or both antagonists abolished the cardiovascular effects of glutamate and acetylcholine. In contrast, pre-treatment with prazosin or methylatropine did not alter the effect of phenylephrine. Phenylephrine (30 nmol) injected into the NTS abolished aortic depressor nerve (ADN) evoked-responses. The pressor effect of phenylephrine in the NTS was exaggerated in spontaneously hypertensive rats (SHR). These results suggest that when injected into the NTS, the effect of phenylephrine may be due to a baroreflex blockade resulting from direct modulatory actions or non-specific neuronal alterations rather than stimulating the alpha(1)-adrenergic receptor. Additionally, this effect is enhanced in SHR.

Adrenergic alpha-1 Receptor Agonists↗

PubMed2000

Effect of phenylephrine on focal atrial fibrillation originating in the pulmonary veins and superior vena cava.

OBJECTIVES: This study was aimed at evaluating the effects of phenylephrine infusion on the occurrence of focal atrial fibrillation (AF). BACKGROUND: Paroxysmal AF can be initiated by ectopic atrial beats originating in the pulmonary vein (PV) or superior vena cava (SVC). The effect of change in autonomic tone on this focal AF is unknown. METHODS: This study included 12 patients with frequent bursts of AF documented by 24-h Holter monitoring. The number and coupling interval of spontaneous ectopic activity and bursts of AF were evaluated for 1 min before and after phenylephrine (2 to 3 microg/kg) injection. RESULTS: After detailed mapping, four patients had a focus located in the left superior PV, six in the right superior PV and two in the SVC. In 10 patients with AF foci originating in the PVs, the frequency of ectopic activity (19.5 +/- 27.4 vs. 11.4 +/- 22.9 beats/min, p = 0.059) was reduced as well as AF bursts (14 +/- 3 vs. 1.8 +/- 2.7 bursts/min, p = 0.005) before versus after phenylephrine injection; the minimal coupling interval of ectopic activity and AF bursts became longer compared with baseline. The maximal percent increase in sinus cycle length after phenylephrine injection was significantly greater in patients with complete suppression of AF compared with those with partial suppression (43 +/- 19 vs. 14 +/- 5%, p = 0.01). However, no significant effect of phenylephrine on AF originating in the SVC was found. CONCLUSIONS: Change in autonomic tone induced by phenylephrine injection was effective in suppressing focal AF originating in the PVs but not in the SVC.

Aged↗

PubMed2001

Stimulatory effect of phenylephrine on the secretion of beta-endorphin from rat adrenal medulla in vitro.

In an attempt to investigate the role of alpha1-adrenoceptors in the regulation of opioid secretion from adrenal gland, phenylephrine was employed to investigate the effect on secretion of beta-endorphin-like immunoreactivity (BER) from adrenal medulla of rat in vitro. Phenylephrine enhanced the BER from isolated adrenal medulla in a concentration-dependent manner and this action was abolished by the antagonists of alpha1-adrenoceptors, prazosin and tamsulosin. Investigations of signal pathway further support that an activation of alpha1-adrenoceptors is responsible for the stimulatory effect of phenylephrine on BER secretion from adrenal medulla. In the presence of U73312, the specific inhibitor of phospholipase C (PLC), phenylephrine-induced change of BER was reduced in a concentration-dependent manner but it was not affected by U73343, the negative control of U73312. Moreover, chelerythrine and GF 109203X diminished the action of phenylephrine at concentration sufficient to inhibit protein kinase C (PKC). In conclusion, our results suggest that an activation of alpha1-adrenoceptors in adrenal medulla by phenylephrine may enhance the secretion of opioids from adrenal gland of rat via signals of PLC-PKC pathway.

Adrenal Medulla↗

PubMed2002

Angiotensin-(1-7) is involved in the endothelium-dependent modulation of phenylephrine-induced contraction in the aorta of mRen-2 transgenic rats.

1. The contribution of the local vascular production of angiotensin-(1-7) [Ang-(1-7)] to the control of alpha-adrenergic-induced contractions in the aorta of Sprague-Dawley (SD) and TGR(mRen-2)27 [mRen-2] rats was studied. 2. In mRen-2 rats, contractile responses to phenylephrine were diminished as compared to control SD rats in endothelium containing but not in endothelium-denuded vessels. L-NAME increased contractile responses to phenylephrine in mRen-2 rats and, after nitric oxide synthase blockade, responses to phenylephrine became comparable in both strains. 3. Inhibition of angiotensin-converting enzyme (ACE) by captopril potentiated contractile responses in mRen-2 rats and diminished contractile responses in SD rats, both effects being dependent on the presence of a functional endothelium. The effect of captopril in mRen-2 rats was abolished in vessels pre-incubated with Ang-(1-7). 4. Blockade of Ang-(1-7) and bradykinin (BK) receptors by A-779 and HOE 140 respectively, increased phenylephrine-induced contraction in mRen-2, but not in SD rats. This effect was seen only in endothelium-containing vessels. 5. Angiotensin II AT(1) and AT(2) receptor blockade by CV 11974 and PD 123319 did not affect the contractile responses to phenylephrine in aortas of transgenic animals but diminished the response in SD rats. This effect was only seen in the presence of a functional endothelium. 6. It is concluded that the decreased contractile responses to phenylephrine in aortas of mRen-2 rats was dependent on an intact endothelium, the local release and action of Ang-(1-7) and bradykinin.

Analysis of Variance↗

PubMed2000

Phenylephrine protects neonatal rat cardiomyocytes from hypoxia and serum deprivation-induced apoptosis.

Previous studies have shown that alpha-adrenergic activation reduces myocardial damages caused by ischemia/reperfusion. However, the molecular mechanisms of how alpha-adrenergic activation protects the myocardium are not completely understood. The objective of this study was to test the hypothesis that alpha-adrenergic activation protects the myocardium by, at least in part, inhibiting apoptosis in cardiomyocytes. The current data has shown that apoptosis in neonatal rat cardiomyocytes, induced by 24 h treatment with hypoxia (95% N2 and 5% CO2) and serum deprivation, was inhibited by co-treatment with phenylephrine. Pre-treatment with phenylephrine for 24 h also protected cardiomyocytes against subsequent 24 h treatment with hypoxia and serum deprivation. Exposure of cardiomyocytes to phenylephrine for up to 9 days under normoxic conditions did not cause apoptosis. The phenylephrine-mediated cytoprotection was blocked by an alpha-adrenergic antagonist, phentolamine. beta-adrenergic activation with isoproterenol did not protect cardiomyocytes against hypoxia and serum deprivation-induced apoptosis. Under hypoxic conditions, phenylephrine prevented the down-regulation of Bcl-2 and Bcl-X mRNA/protein and induced hypertrophic growth. Phenylephrine-mediated protection was abrogated by the phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin and was mimicked by the caspase-9 peptidic inhibitor LEHD-fmk. These results suggest that alpha-adrenergic activation protects cardiomyocytes against hypoxia and serum deprivation-induced apoptosis through regulating the expression of mitochondrion-associated apoptosis regulatory genes, preventing activation of mitochondrial damage-induced apoptosis pathway (cytochrome C-caspase-9), and activating hypertrophic growth.

Actinin↗

PubMed1991

Arginine vasopressin attenuates phenylephrine-induced forearm vasoconstriction in men.

1. The aim of this study was to examine whether arginine vasopressin modulates the vasoconstricting action of phenylephrine in human forearms. 2. In seven healthy subjects, we determined the percentage increases in forearm vascular resistance evoked by intra-arterial infusion of phenylephrine at graded doses during simultaneous intra-arterial infusion of saline or arginine vasopressin at two doses. Similarly, in another seven subjects, we examined the effects of intra-arterial infusions of saline or angiotensin II on the vasoconstricting action of intra-arterial phenylephrine. 3. Arginine vasopressin and angiotensin II caused small, but insignificant, increases in baseline forearm vascular resistance. Arginine vasopressin at the two doses significantly attenuated the percentage increases in forearm vascular resistance evoked with phenylephrine at graded doses. Angiotensin II did not alter the forearm vascular responses to phenylephrine. 4. Intra-arterial infusion of arginine vasopressin at doses of 0.6 and 1.8 ng/min raised the plasma arginine vasopressin concentration in the venous effluents from 1.6 +/- 0.3 (control) to 4.0 +/- 0.9 and to 16.4 +/- 6.9 pg/ml, respectively. 5. These results suggest that arginine vasopressin at physiological concentrations with a minimal direct effect on resistance arteries attenuates the vasoconstricting action of phenylephrine in human forearms.

Adolescent↗

PubMed1997

Bisoprolol attenuates noradrenaline- and phenylephrine-evoked venoconstriction in man in vivo.

AIMS: The aim of this study was to examine the effects of bisoprolol (BIS), a selective beta1-adrenoceptor antagonist without partial agonistic activity, on noradrenaline- and phenylephrine-evoked venoconstriction in man using the dorsal hand vein compliance technique. METHODS: Twelve healthy male volunteers participated in three weekly experimental sessions. Subjects were allocated to treatments and sessions on a double-blind basis. In each session either BIS 5 mg (BIS5), or BIS 10 mg (BIS10), or placebo was administered orally, and noradrenaline acid tartrate (0.1-33.33 ng min (-1) followed by phenylephrine hydrochloride (0.033-10 microg min(-l)) was infused into the dorsal hand vein. Systolic and diastolic blood pressure and heart rate were also measured. RESULTS: Both noradrenaline and phenylephrine produced dose-dependent venoconstriction: the geometric mean ED50 for noradrenaline was 3.21 ng min(-1) and for phenylephrine 135.04 ng min(-1); the potency ratio (noradrenaline/phenylephrine) was 42. Both BIS5 and BIS10 significantly decreased the venoconstriction to noradrenaline (ANOVA; P<0.005), and to phenylephrine (ANOVA; P<0.001). The antagonism of the venoconstrictor responses was also reflected in a significant increase in logED50 values for both noradrenaline (ANOVA; P<0.005), and phenylephrine (ANOVA; P<0.0025) in the presence of both doses of BIS. Both doses of BIS significantly decreased heart rate (ANOVA; P<0.0001), and systolic blood pressure (ANOVA; P<0.0025). CONCLUSIONS: Bisoprolol can antagonize alpha1-adrenoceptor mediated venoconstriction in the human dorsal hand vein in vivo through a mechanism which remains to be elucidated.

Adolescent↗

PubMed2003

Effect of phenylephrine provocation on dispersion of repolarization in congenital long QT syndrome.

INTRODUCTION: Syncope and sudden death are associated with sympathetic stimulation in LQT1 while LQT2 patients are more susceptible to arrhythmias during nonexertional states. Abnormal spatial (QTd)- and transmural (TDR)-dispersion of repolarization may indicate increased arrhythmogenicity. This study compares the effect of phenylephrine on QTd and TDR in genotyped LQTS to control (C). METHODS AND RESULTS: Seventeen LQT1, 12 LQT2, and 18 age- and sex-matched normal controls received 2 mcg/kg of phenylephrine intravenously. At baseline and peak phenylephrine effect, BP, QT, RR, Bazett's QTc, precordial QTd (QTmax-QTmin), and T-peak to T-end (Tp-e) intervals were determined blinded to the patient's clinical and genotype status. Baseline QT intervals and QTc were significantly longer in LQT1 and LQT2 compared to C. Baseline QTd and Tp-e were greater in LQT2 than either LQT1 or C: QTd=79+/-29 ms (LQT2), 53+/-26 (LQT1), and 45+/-15 (C) and Tp-e=120+/-30 ms (LQT2), 99+/-20 (LQT1), and 90+/-11 (C). Overall, phenylephrine exerted no significant effect on either QTd or Tp-e except with subgroup analysis of symptomatic LQTS where LQT1 and LQT2 patients had a divergent response with TDR. CONCLUSIONS: Phenylephrine-induced bradycardia decreased TDR in symptomatic LQT1 but increased TDR in symptomatic LQT2. The observed effects of phenylephrine are consistent with the protective effect of beta-blocker in LQT1 and the increased arrhythmogenicity noted during nonexertional states in LQT2.

Adolescent↗

PubMed1986

Uterine motor responses to an alpha-adrenergic agonist (phenylephrine) in the ewe during oestrus and at the end of gestation.

The alpha-adrenergic activity of the myometrium was studied by recording the electromyographic activity (EMG) of the uterus in 4 conscious cyclic ewes during oestrus and in 8 conscious pregnant ewes during the last 6 days of gestation. In the cyclic ewes, changes in intra-uterine pressure were recorded at the same time as the EMG. Motor responses to perfusions of phenylephrine, a specific alpha-adrenergic agonist, were studied at three uterine sites. In the ewes in oestrus, uterine activity was stimulated at the three sites by perfusions with phenylephrine (0.6, 2.5, 5 or 10 micrograms/kg/min). The whole uterine horn was alpha-adrenergic-responsive. The effect of the drug was dose-dependent in that the uterine response increased with the dose and reached a plateau at 5 micrograms/kg/min. In the late pregnant ewes, the motor responses to the perfusion of phenylephrine at 10 micrograms/kg/min were studied at three uterine sites once a day during the last 6 days of gestation. Plasma levels of progesterone and total oestrogens were measured at the same time. Up to 48 h before parturition, the effect of phenylephrine depended on the uterine site. The drug had no or little effect at the tubal end of the horn. Phenylephrine stimulated uterine activity at the cervical end of the horn in at least 50% of the ewes. Thus, during this part of gestation, the alpha-adrenergic sensitivity of the myometrium was greater at the cervical than at the tubal end of the uterine horn. Forty-eight hours before parturition, phenylephrine stimulated uterine activity at all three uterine sites in all the ewes. Thus, alpha-adrenergic sensitivity developed over the uterine horn beginning 48 h before parturition at the same time that the oestrogen level increased.

Animals↗

PubMed2001

Effects of stretch or distention on phenylephrine-induced constriction of human coronary artery bypass grafts.

OBJECTIVE: To determine the effects of grafting saphenous veins into the arterial circulation and to compare the responsiveness of saphenous veins and mammary arteries to vasoconstrictors (phenylephrine or potassium) and a vasodilator (the calcium antagonist isradipine). DESIGN: Prospective, controlled, in vitro study. SETTING: Laboratory facility in a university teaching hospital. PARTICIPANTS: Small excess segments of internal mammary arteries or saphenous veins obtained from patients undergoing coronary artery bypass graft surgery. INTERVENTIONS: Vessel segments were cut into rings to measure isometric tension development in isolated tissue chambers. The law of LaPlace for a cylinder was applied to determine tensions in vitro corresponding with arterial or venous tensions in vivo or distending pressures ex vivo. MEASUREMENTS AND MAIN RESULTS: Stretching saphenous vein rings from venous to arterial tensions reduced maximal phenylephrine-induced constriction but did not alter their dose response to phenylephrine, potassium, or isradipine. At arterial tensions, potassium, but not phenylephrine, was more potent in constricting mammary artery than saphenous vein; isradipine was more potent as a vasodilator of potassium-constricted mammary artery than saphenous vein. Maximal phenylephrine-induced or potassium-induced constriction was no different for either vessel at arterial tensions; however, prior distention of veins to tensions corresponding with pressures of 200 or 300 mmHg significantly (p < 0.01, Dunnett's test) reduced subsequent constriction. CONCLUSION: Phenylephrine may be more likely to constrict native internal mammary arteries than distended autogenous saphenous vein grafts in vivo because high-pressure distention of veins markedly inhibits their vasoreactivity.

Coronary Artery Bypass↗

PubMed1999

[Perioperative circulatory side effects of topical 5% phenylephrine for mydriasis].

PURPOSE: To study the systemic effects of topically applied 5% phenylephrine. To investigate intraoperative injection of epinephrine in the anterior chamber as an alternative. METHOD: 75 patients undergoing cataract surgery were randomized into three groups. In group 1, the pupil was dilated using topically 5% phenylephrine and 1% cyclopentolate, the patients blocked the lacrimal drainage system themselves by digital compression. Group 2 received the same drops, digital compression was performed by one of the investigators. In Group 3, no preoperative phenylephrine was used--instead, epinephrine 1:25,000 was injected in the anterior chamber at the beginning of surgery. Retrobulbar anesthesia was performed in a short narcosis with ketamine and propofol. RESULTS: Mean preoperative blood pressure values were higher than the day before. They fell during narcosis, to increase significantly after the injection of the local anesthetics. At the beginning of surgery they were back to prenarcotic values. Intraoperative blood pressure remained stable. Preoperative day values were found two hours postop. There was no significant difference in the circulatory behavior between the three groups. For mydriasis, intraoperative intracameral epinephrine was not as effective as preoperative phenylephrine. CONCLUSION: In normotonic or medically treated arterial hypertensive patients, preoperative mydriasis using 5% phenylephrine is safe--proceeding the way described above. Compression of the lacrimal drainage system can be performed by the patients effectively. Intraoperative intracameral epinephrine does not replace preoperative phenylephrine.

Administration, Topical↗

PubMed1975

Reduction in myocardial ischemia with nitroglycerin or nitroglycerin plus phenylephrine administered during acute myocardial infarction.

Nitroglycerin reduces ischemic injury during acute myocardial infarction (AMI) in dogs--an effect that is potentiated when drug-induced hypotension and tachycardia are prevented with phenylephrine. To determine the effectiveness of nitroglycerin, alone or with phenylephrine, during AMI in man, 12 patients (five or whom had left heart failure) were evaluated by summing ST-segment abnormalities (sigmaST) from 35 precordial electrodes. The seven patients without heart failure did not benefit consistently from nitroglycerin alone; however, addition of phenylephrine to abolish nitroglycerin-induced arterial pressure reduction uniformly diminished sigmaST (4.9 to 3.2 mv; P less than 0.05). In patients with heart failure, nitroglycerin alone consistently reduced ischemia (5.8 to 4.4 mv, P less than 0.05); addition of phenylephrine often partially reversed this effect. Thus, administration of nitroglycerin, alone or with phenylephrine, can reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends on the presence or absence of left ventricular failure before treatment.

Acute Disease↗

PubMed1996

Randomized trial of bolus phenylephrine or ephedrine for maintenance of arterial pressure during spinal anaesthesia for Caesarean section.

Thirty-eight healthy women undergoing elective Caesarean section under spinal anaesthesia at term were allocated randomly to receive boluses of either phenylephrine 100 micrograms or ephedrine 5 mg for maintenance of maternal arterial pressure. The indication for administration of vasopressor was a reduction in systolic pressure to < or = 90% of baseline values. Maternal arterial pressure (BP) and heart rate (HR) were measured every minute by automated oscillometry. Cardiac output (CO) was measured by cross-sectional and Doppler echocardiography before and after preloading with 1500 ml Ringer lactate solution and then every 2 min after administration of bupivacaine. Umbilical artery pulsatility index (PI) was measured using Doppler before and after spinal anaesthesia. The median (range) number of boluses of phenylephrine and ephedrine was similar; 6 (1-10) vs 4 (1-8) respectively. Maternal systolic BP and CO changes were similar in both groups, but the mean [95% CI] maximum percentage change in maternal HR was larger in the phenylephrine group (-28.5 [-24.2, -32.9]%) than in the ephedrine group (-14.4 [-10.6, -18.2]%). As a consequence atropine was required in 11/19 women in the phenylephrine group compared with 2/19 in the ephedrine group (P < 0.01). Mean umbilical artery pH [95% CI] was higher in the phenylephrine group (7.29 [7.28-7.30]) than in the ephedrine group (7.27 [7.25-7.28]). The results of the present study support the use of phenylephrine for maintenance of maternal arterial pressure during spinal anaesthesia for elective Caesarean section.

Adult↗

PubMed2001

Evaluation of pre-emptive intramuscular phenylephrine and ephedrine for reduction of spinal anaesthesia-induced hypotension during Caesarean section.

Pre-emptive intramuscular (i.m.) vasopressors were evaluated in 108 patients undergoing elective Caesarean section under spinal anaesthesia, assigned to four groups in a randomized, double-blind, placebo-controlled study. Group 1 received pre-emptive phenylephrine 4 mg i.m., group 2 received phenylephrine 2 mg i.m., group 3 received ephedrine 45 mg i.m., while controls received an i.m. injection of saline, all given immediately after induction of spinal anaesthesia. Hypotension was defined as a 25% decrease in mean arterial pressure (MAP). Rescue intravenous (i.v.) boluses of ephedrine were given if the patient was hypotensive or reported nausea, vomiting or dizziness. The incidence of hypotension was 33% in the phenylephrine 4 mg group compared with 70% in the control and phenylephrine 2 mg groups (P=0.03), and 48% in the ephedrine 45 mg group. The phenylephrine 4 mg and ephedrine 45 mg groups had a significantly lower percentage reduction in MAP (-21 (SD 14)% and -22 (14)%) compared with controls (-32 (18)%, P=0.04). They also had a lower total dose of rescue i.v. ephedrine (15.7 (15.7) mg and 15.8 (15.6) mg) compared with controls (28.8 (20.6) mg, P=0.02). We conclude that pre-emptive i.m. phenylephrine 4 mg and ephedrine 45 mg reduce the severity of hypotension and the total dose of rescue i.v. ephedrine during spinal anaesthesia for Caesarean section.

Adolescent↗

PubMed2004

Comparison of phenylephrine infusion regimens for maintaining maternal blood pressure during spinal anaesthesia for Caesarean section.

BACKGROUND: During spinal anaesthesia for Caesarean section, the optimal phenylephrine regimen and the optimal blood pressure (BP) to which it should be titrated are undetermined. The ideal regimen would balance efficacy for maintaining uteroplacental perfusion pressure against potential for uteroplacental vasoconstriction, both of which may affect fetal acid-base status. We compared phenylephrine infusion regimens based on three different BP thresholds. METHODS: After intrathecal injection, we infused phenylephrine 100 microg min(-1) for 2 min. Then, until delivery, we infused phenylephrine whenever systolic BP (SBP), measured every 1 min, was below a randomly assigned percentage of baseline: 100% (Group 100, n=25), 90% (Group 90, n=25) or 80% (Group 80, n=24). We compared umbilical blood gases, Apgar scores and maternal haemodynamics and symptoms. RESULTS: Patients in Group 100 had fewer episodes [median 0 (range 0-8)] of hypotension (SBP <80% baseline) compared with Group 80 [5 (0-18)] and Group 90 [2 (0-7)] (P<0.001 in each instance). Total dose of phenylephrine was greater in Group 100 [median 1520 microg (interquartile range 1250-2130 microg)] compared with Group 90 [1070 (890-1360) microg] and Group 80 [790 (590-950) microg]. Umbilical arterial pH was greater in Group 100 [mean 7.32 (95% confidence interval 7.31-7.34)] than in Group 80 [7.30 (7.28-7.31)] (P=0.034). No patient had umbilical arterial pH <7.2. In Group 100, 1/24 (4%) patients had nausea or vomiting compared with 4/25 (16%) in Group 90 and 10/25 (40%) in Group 80 (P=0.006). CONCLUSIONS: For optimal management, phenylephrine should be titrated to maintain maternal BP at near-baseline values.

Adult↗

PubMed2004

Effects of ephedrine and phenylephrine on uterine and placental circulations and fetal outcome following fetal hypoxaemia and epidural-induced hypotension in a sheep model.

BACKGROUND: Recent studies support the use of alpha-agonists during regional anaesthesia in uncomplicated term pregnancies. We hypothesized that ephedrine and phenylephrine, administered for maternal hypotension following fetal hypoxaemia, are equal in respect of fetal outcome. METHODS: At 117-132 days gestation, chronically instrumented, anaesthetized and mechanically ventilated ewes were randomized to receive boluses of ephedrine (n=9) or phenylephrine (n=8) for maternal epidural-induced hypotension after a period of fetal hypoxaemia. Uterine (QUtA) and placental (QUA) volume blood flows were measured with perivascular transit-time ultrasonic flow probes, and uterine (RUtA) and placental (RUA) vascular resistances were computed from volume blood flows and maternal and fetal mean arterial pressures. Uterine (PIUtA) and umbilical artery (PIUA) pulsatility indices were obtained by Doppler ultrasonography. RESULTS: Ephedrine increased QUtA and decreased RUtA and PIUtA from a hypotensive to baseline level and had no significant effect on umbilical circulation. With phenylephrine, QUtA remained lower (P=0.011) and RUtA higher (P=0.043) than at baseline, although PIUtA decreased to baseline level. PIUA increased from baseline with phenylephrine (P=0.007), whereas QUA decreased (P=0.050). Maternal volume expansion with hydroxyethyl starch decreased RUtA significantly irrespective of the vasopressor used. There were no significant differences in fetal blood gas values or lactate concentrations between the ephedrine and phenylephrine groups. CONCLUSIONS: Despite the more favourable effects on uterine and placental circulations of ephedrine over phenylephrine, no significant differences in fetal acid-base status or lactate concentrations were observed.

Acid-Base Equilibrium↗