Effects Of Phenylephrine Research Articles

The effect of the intravenous phenylephrine on the level of spinal anesthesia

BackgroundSpinal anesthesia causes hypotension and bradycardia due to sympathetic nerve block and it is difficult to predict the level of sensory block and the duration of blockade. Recent studies have reported that intravenous phenylephrine can reduce the rostral spread of spinal anesthesia in pregnant women. We think a phenylephrine infusion will be useful for maintaining the baseline blood pressure by reducing the rostral spread of spinal anesthesia during the elective surgery of non-obstetric patients.MethodsSixty patients who were undergoing urologic surgery were randomized into two groups: Group C (the control group without phenylephrine) and Group P (with the addition of phenylephrine). After a bolus infusion of 50 µg phenylephrine following the spinal injection, phenylephrine was continuously infused at the rate of 200 µg/hr. We compared the dermatomal spreads of spinal anesthesia, the hemodynamic parameters (blood pressure, heart rate) and the incidences of hypotension between the two groups.ResultsAt 20 minutes, the level of the upper dermatome blocked against cold sensation was a median of T8 (interquartile range: T8-T10) for the phenylephrine group, as compared with T4 (interquartile range: T4-T6) for the control group (P < 0.001).ConclusionsIntravenous phenylephrine can decrease the rostral spread of spinal anesthesia during urologic surgery.

The Dose-Dependent Effects of Phenylephrine for Elective Cesarean Delivery Under Spinal Anesthesia

The Dose-Dependent Effects of Phenylephrine for Elective Cesarean Delivery Under Spinal Anesthesia

Phenylephrine Tumescence in Split-Thickness Skin Graft Donor Sites in Surgery for Burn Injury— A Concentration Finding Study

The purpose of this study is to determine the lowest concentration of subcutaneous phenylephrine (neosynephrine) required for effective vasoconstriction in skin graft donor sites. Surgery for burn injury is associated with blood loss. Tourniquet use and tumescence with epinephrine have decreased blood loss. However, absorption of epinephrine has been reported with systemic effects. Phenylephrine, an α1-adrenergic receptor agonist, has vasoconstrictive properties similar to epinephrine's without other α-adrenergic or β-adrenergic activity. The aim of this study is to determine the lowest effective concentration of phenylephrine that will provide vasoconstriction in split-thickness graft donor sites. By using intensive care unit equivalency tables, the authors estimated a concentration of phenylephrine on the basis of current epinephrine tumescence. This concentration was titrated up or down according to an algorithm established a priori, determining the minimum concentration that achieved vasoconstriction in three consecutive patients. The primary outcome was local vasoconstriction. Secondary outcomes measured were pre-, intra-, and postoperative mean arterial pressure, systolic pressure and heart rate, graft take, and donor site healing. The subjects were six otherwise healthy adult patients (five men and one woman) with a mean age of 36 years. The average TBSA was 737.5 cm². Vasoconstriction was achieved at 5 μg/ml. No significant alterations in hemodynamic measures were observed. The optimal concentration of phenylephrine for prevention of bleeding in donor sites appears to be 5 μg/ml. Participants will be able to identify the effects of phenylephrine and epinephrine tumescence. They will also identify the concentration at which phenylephrine will be effective in donor sites.

The Dose-Dependent Effects of Phenylephrine for Elective Cesarean Delivery Under Spinal Anesthesia

Hypotension is the most common serious side effect of spinal anesthesia for cesarean delivery. There has been a move recently toward the use of phenylephrine as a vasopressor infusion to improve maternal cardiovascular stability and fetal outcome. Although it seems safe in the elective setting, there have been concerns about its propensity for causing an increase in afterload and a baroreceptor-mediated bradycardia in the mother, with a consequent reduction in maternal cardiac output (CO). Using a noninvasive measure of CO, our aim was to investigate whether there were any dose-dependent effects of phenylephrine on maternal cardiovascular stability and, if so, any impact on fetal outcome. In this randomized, double-blind study, 75 women scheduled for elective cesarean delivery were allocated to receive a phenylephrine infusion at 25 μg/min, 50 μg/min, or 100 μg/min. This infusion was titrated to maintain maternal baseline systolic blood pressure (SBP), from induction of spinal anesthesia until delivery. The maternal cardiovascular variables recorded included heart rate (HR) and SBP. A suprasternal Doppler monitor measured CO and stroke volume, as well as measures of venous return (corrected flow time) and contractility, at baseline, and then every 5 minutes for 20 minutes after initiation of spinal anesthesia. Apgar scores and umbilical cord blood gases were recorded. SBP control was satisfactory in all groups; however, the group receiving phenylephrine 100 μg/min required significantly higher doses to achieve arterial blood pressure control compared with the lower infusion rates. There were no significant differences in the number of times SBP decreased below 80% of baseline, or the numbers of boluses of ephedrine or phenylephrine required to maintain SBP above 80% of baseline. There were significant time and dose-dependent reductions in HR and CO with phenylephrine, such that HR and CO were seen to decrease with time in each group, and also with increasing concentrations of phenylephrine. Stroke volume remained stable throughout. Apgar scores and umbilical cord blood gases were similar among groups. By infusing a higher concentration (100 μg/min), we subject the mother and fetus to a much higher dose of phenylephrine, with significant effects on maternal HR and CO (up to a 20% reduction). Future investigation is required to determine whether this reduction in maternal CO has detrimental effects when providing anesthesia for an emergency cesarean delivery for a compromised fetus.

Phenylephrine enhanced swelling-activated chloride current in human atrial myocytes

Objective To study the function of phenylephrine, an α1-adrenoceptor agonists, in the regulation of swelling-activated chloride current ( ICl.swell) in human atrial myocytes by a whole-cell patch-clamp technique. Methods Atrial myocytes were isolated from specimens of right atrial appendage obtained from patients undergoing coronary artery bypass and enzymatically dissociated. The myocytes were perfused with isotonic bath solution (1.0T) or hyposmotic bath solution (0. 6-times isosmotic, 0. 6 T),and exposured to phenylephrine, 4,4'-diisothiocyanostilbene-2,2' disulfonicacid (DIDS), or prazosin, an α1-adrenoceptor antagonis respectively. The currents under different conditions were compared. Results ICl.swell evoked by hyposmotic bath solution was recorded. After approaching steady state values, subsequent exposure to 100 μmol/L phenylephrine caused enhancement of ICl.swell. The current was increased from (-1.11±0.55) pA/pF to ( - 1.56 ±0.69) pA/pF at -90 mV (P<0.05,n=7) and from (3.24±2.04) pA/pF to (4.64±2.61) pA/pF at +40 mV (P<0. 01,n=7) respectively. This effect was concentration-dependent, and could be reversed by DIDS or after exposure to the isotonic solution. Application of 1 μmol/L prazosin could attenuate the effect of phenylephrine. Conclusion Phenylephrine can enhance ICl.swell in human atrial myocytes, which is distinct from the reports in other species, indicating distinguished species-dependent variations in the modulation of ICl.swell, in atrial myocytes by phenylephrine. Key words: Chloride current; Phenylephrine; α1-adrenoceptor agonist; Atrial myocyte

Placental Transfer and Fetal Metabolic Effects of Phenylephrine and Ephedrine During Spinal Anesthesia for Cesarean Delivery

Placental Transfer and Fetal Metabolic Effects of Phenylephrine and Ephedrine During Spinal Anesthesia for Cesarean Delivery

Effect of 1-acyl-5,6-dimethoxy / diethoxy-2-methylthiobenzimidazoles on APD90 and isometric contraction in guinea pig atrium and aortic preparations activated by carbachol and phenylephrine

Studies have shown that 1-acyl-5,6-diethoxy-2-methylthiobenzimidazole derivatives 3-pyridyl-(1); 2-pyridyl- (2); 4-thiazolyl- (3); 4-pyridyl- (4); methyl- (5); 2-thienyl- (6) and 1-acetyl-5,6-dimethoxy-2-methylthiobenzimidazole (7) exhibit positive inotropic properties. The goal of the study was to investigate the effects of the above-mentioned compounds in restoring a decreased isometric contraction and APD90 induced by carbachol in an isolated guinea pig atrium, and to relax the aortic rings precontracted by phenylephrine. Isometric contraction and APD90 were recorded by using a force transducer and standard microelectrode technique (stimulation rate 1 Hz). Carbachol (1 μM) caused a decrease of the isometric contraction and APD90 on an overage by 63.2% and 49.6%, respectively. Compounds 1–5 used in a dose-dependent fashion (10–500 μM) abolished the action of carbachol and restored the contraction force and APD90 in the electrically driven atrium significantly; compound 2 reversed the APD90 to the baseline. Compounds 2 and 7 antagonized the contraction of aortic rings evoked by phenylephrine (10–4 M) and caused their relaxation by 24.4% and 17% at a dose of 10–4 M and by 76.2% and 72.5% at a dose of 5 × 10–4 M in groups 2 and 7, respectively. Conclusion. The results presented in the study have shown that some 1-acyl-5,6-dimethoxy / diethoxy-2-methylthiobenzimidazoles are able to abolish the effects of carbachol and phenylephrine on the AP duration and isometric contraction in guinea pig atrium and blood vessels. These data will contribute to the synthesis of targeted compounds with positive inotropic and blood-vessel relaxing characteristics among benzimidazole derivatives, which could be useful in clinical practice. Keywords: 1-acyl-2-methylthio-5,6-dimethoxy / diethoxybenzimidazoles, guinea pig atrium, blood vessel, phenylephrine hydrochloride, carbamylcholine chloride

Effect of Intravenous Phenylephrine or Ephedrine on the ED50 of Intrathecal Bupivacaine With Fentanyl for Cesarean Section

Effect of Intravenous Phenylephrine or Ephedrine on the ED50 of Intrathecal Bupivacaine With Fentanyl for Cesarean Section

Placental Transfer and Fetal Metabolic Effects of Phenylephrine and Ephedrine During Spinal Anesthesia for Cesarean Delivery

Placental Transfer and Fetal Metabolic Effects of Phenylephrine and Ephedrine During Spinal Anesthesia for Cesarean Delivery

Phenylephrine Induces Early and Late Cardioprotection Through Mitochondrial Permeability Transition Pore in the Isolated Rat Heart

The aim of this study was to investigate the role of mitochondrial permeability transition pore (mPTP) in cardioprotection afforded by phenylephrine pretreatment in early and late phases. Rat hearts were isolated and perfused with Krebs buffer in Langendorff preparation and subjected to 30 min regional ischemia followed by 60 min of reperfusion. Phenylephrine as a selective α1-adrenoceptor agonist and atractyloside as a specific opener of the mPTP were used. Seven groups (n = 6) of rats were randomly studied: (I) control: surgical procedure was performed with no ischemia/reperfusion, (II) ischemia/reperfusion: hearts underwent regional ischemia/reperfusion, (III) early phenylephrine: phenylephrine (50 μM) was perfused for 5 min prior to ischemia/reperfusion, (IV) late phenylephrine: rats were treated with phenylephrine (10 mg/kg, i.p) 24 h prior to ischemia/reperfusion, (V) early phenylephrine+atractyloside: hearts were perfused with phenylephrine as in group III and then atractyloside (20 mM) 5 min before reperfusion for 20 min, (VI) late phenylephrine+atractyloside: hearts were treated with phenylephrine as in group IV and then received atractyloside (20 mM), 5 min before reperfusion for 20 min, (VII) atractyloside-IR group: hearts were perfused with atractyloside (20 mM) 5 min before reperfusion for 20 min. Compared with ischemia/reperfusion group, perfusion of phenylephrine in early and late phases decreased myocardial infarct size (% of ischemia zone), reduced creatine kinase-MB (CK-MB) in the coronary effluent, and improved cardiac function. Administration of atractyloside abolished cardioprotective effects of phenylephrine in both early and late phases and returned infarct size, CK-MB and cardiac function to levels as seen in ischemia/reperfusion group. These results suggest that administration of atractyloside as a specific opener of the mPTP abolishes phenylephrine-induced early and late cardioprotection in the isolated rat hearts.

Activation of α1 and α2 noradrenergic receptors exert opposing effects on excitability of main olfactory bulb granule cells

The mammalian main olfactory bulb (MOB) receives a dense noradrenergic innervation from the pontine nucleus locus coeruleus that is important for neonatal odor preference learning and odor processing in mature animals. Modulation of GABAergic granule cells (GCs) is thought to play a key role in the net functional impact of norepinephrine (NE) release in the MOB, yet there are few direct studies of the influence of NE on these cells. In the present study we investigated noradrenergic modulation of GC excitability using electrophysiological approaches in rat MOB slices. A moderate concentration of NE (10 μM) and the α1 receptor agonist phenylephrine (10 μM) depolarized and increased spontaneous or current injection-evoked spiking in GCs. By contrast, low NE concentrations (0.1–1.0 μM) or the α2 receptor agonist clonidine (Clon, 10 μM) hyperpolarized and decreased the discharge of GCs. The effects of NE (10 μM) were blocked by antagonism of α1 and α2 receptors. Inhibitory effects of low NE concentrations were blocked or converted to excitatory responses by α2 receptor blockade, whereas excitatory effects of the moderate NE concentration were converted to inhibitory responses after α1 receptor blockade. NE (10 μM) and phenylephrine elicited inward currents that reversed near the potassium equilibrium potential. The effects of NE and phenylephrine were associated with increased membrane input resistance. Clonidine elicited an outward current associated with decreased membrane input resistance that reversed near the potassium equilibrium potential. These results indicate that α1 and α2 receptor activation exert opposing effects on GC excitability. Low concentrations of NE acting via α2 receptors suppress GC excitability, while higher concentrations of NE acting at α1 receptors increase GC excitability. These findings are consistent with recent findings that α1 and α2 receptor activation increase and decrease, respectively, GABAergic inhibition of mitral cells. The differential affinities of α1 and α2 noradrenergic receptor subtypes may allow for differential modulation of GABA release and olfactory processing as a function of the level of NE release, which in turn, is regulated by behavioral state.

Catecholamine-induced heart injury in mice: differential effects of isoproterenol and phenylephrine

The involvement of catecholamines in stress-induced heart injury is well documented. However, the contribution of adrenergic receptor types is less understood. Both the profile of plasma marker enzyme activities (lactate dehydrogenase-1 and aspartate transaminase) and the distribution and morphology of the lesions observed in tissue sections of adrenaline-injected mice resembled those of stressed (restraint and cold exposed) mice. Next, we compared the effect of isoproterenol (beta-adrenergic agonist) and phenylephrine (alpha1-adrenergic agonist) on both heart function and tissue injury. In Langendorff-perfused rat hearts, alpha1-adrenergic receptors made a minor contribution to the tonic effect of adrenaline, as indicated by the lack of effect on the heart rate and the delayed negative inotropic effect of phenylephrine. However, in whole mice, phenylephrine but not isoproterenol, induced an increase of both lactate dehydrogenase-1 and aspartate transaminase activities. Hearts of phenylephrine-injected mice showed necrotic lesions in subendocardial areas of the left ventricle. In addition a scattered focal leukocyte infiltration around single apoptotic-like myocytes was observed in the ventricle wall. Hearts of isoproterenol-injected mice showed a similar number of apoptotic-like myocytes, but a much lower number of necrotic areas, than phenylephrine-injected animals. Our results suggest that the cardiotonic effect of catecholamines involves mainly the beta-adrenergic receptors. However, the acute catecholamine-induced heart injury involves mainly alpha1-adrenergic receptors.

Ephedrine and Phenylephrine Use during Cesarean Delivery

Ephedrine and Phenylephrine Use during Cesarean Delivery

Hypocapnia Enhances the Pressor Effect of Phenylephrine During Isoflurane Anesthesia in Monkeys

Phenylephrine was administered to increase arterial blood pressure in 6 monkeys anesthetized with isoflurane during both normocapnia (arterial partial pressure of CO2 35 to 44 mm Hg) and hypocapnia (arterial partial pressure of CO2 23 to 29 mm Hg). The doses of phenylephrine required to increase mean blood pressure to 33% and 66% above control pressure during hypocapnia [1.7+/-0.9 and 3.1+/-1.7 microg/kg/min (mean+/-SD), respectively] were significantly less than the doses required to achieve the same changes in blood pressure during normocapnia (2.4+/-0.9 and 4.9+/-2.4 microg/kg/min, respectively, P<0.05). In patients with intracranial pathology, for whom hypocapnia is frequently induced, phenylephrine dosage may need to be appropriately reduced.

Use of paravascular admittance waveforms to monitor relative change in arterial blood pressure

Non-invasive methods to monitor ambulatory blood pressure often have limitations that can affect measurement accuracy and patient adherence [1]. Minimally invasive measurement of a relative blood pressure surrogate with an implantable device may provide a useful chronic diagnostic and monitoring tool. We assessed a technique that uses electrocardiogram and paravascular admittance waveform morphology analysis to one, measure a time duration (vascular tone index, VTI in milliseconds) change from the electrocardiogram R-wave to admittance waveform peak and two, measure the admittance waveform minimum, maximum and magnitude as indicators of change in arterial compliance/distensibility or pulse pressure secondary to change in afterload. Methods: Five anesthetized domestic pigs (32 ± 4.2 kg) were used to study the effects of phenylephrine (1-5 ug/kg/min) on femoral artery pressure and admittance waveform morphology measured with a quadrapolar electrode array catheter placed next to the femoral artery to assess the relative change in arterial compliance due to change in peripheral vascular tone. Results: Statistical difference was observed (p < 0.05) comparing baseline VTI to phenylephrine VTI (246 ± .05 ms to 320 ± .07 ms) and baseline admittance waveform maximum to phenylephrine admittance waveform maximum (0.0148 ± .002 siemens to 0.0151 ± .002 siemens). Conclusion: Chronic minimally invasive admittance measurement techniques that monitor relative change in blood pressure may be suitable for implantable devices to detect progression of cardiovascular disease such as hypertension.

Effects of Topical Phenylephrine and Tafluprost on Optic Nerve Head Circulation in Monkeys with Unilateral Experimental Glaucoma

To compare the effects of a topical alpha agonist (vasoconstrictor) and a prostaglandin receptor (FP) agonist (vasodilator) on circulation in the optic nerve head (ONH) in experimental glaucomatous and normal eyes of monkeys. Tissue blood velocity in the ONH (NB(ONH)) was determined using the laser speckle method in both eyes of eight normal cynomolgus monkeys under systemic anesthesia for 180 minutes after bilateral instillation of 5% phenylephrine. The effect of 0.0015% tafluprost, a potent FP agonist, was also studied after single and once-daily 7-day instillations. Measurements were repeated in both eyes of the eight monkeys after establishment of unilateral laser-induced glaucoma. NB(ONH) decreased significantly in both eyes of normal monkeys 30 to 120 minutes after phenylephrine instillation by a maximum of 9% to 11% (P < 0.05) without significant change in intraocular pressure (IOP). A similar decrease in NB(ONH) was found in non-laser-treated eyes in glaucomatous monkeys despite the absence of significant changes in contralateral experimental glaucomatous eyes. NB(ONH) increased by 16% (P < 0.05) 60 minutes after a single instillation and also after 7-day repeated instillations of tafluprost in both eyes of normal monkeys. A similar increase in NB(ONH) occurred in both eyes after the establishment of unilateral glaucoma but was completely abolished by 5 mg/kg indomethacin injected intravenously 15 minutes after tafluprost instillation. Tafluprost significantly reduced IOP only in experimental glaucomatous eyes by 34%. The ONH vasculature in glaucomatous and normal eyes reacts differently to an exogenous alpha agonist, whereas it reacts similarly to an FP agonist.

Phenylephrine decreases frontal lobe oxygenation at rest but not during moderately intense exercise

Whether sympathetic activity influences cerebral blood flow (CBF) and oxygenation remains controversial. The influence of sympathetic activity on CBF and oxygenation was evaluated by the effect of phenylephrine on middle cerebral artery (MCA) mean flow velocity (Vmean) and the near-infrared spectroscopy-derived frontal lobe oxygenation (ScO2) at rest and during exercise. At rest, nine healthy male subjects received bolus injections of phenylephrine (0.1, 0.25, and 0.4 mg), and changes in mean arterial pressure (MAP), MCA Vmean, internal jugular venous O2 saturation (SjvO2), ScO2), and arterial PCO2 (PaCO2) were measured and the cerebral metabolic rate for O2 (CMRO2) was calculated. In randomized order, a bolus of saline or 0.3 mg of phenylephrine was then injected during semisupine cycling, eliciting a low (approximately 110 beats/min) or a high (approximately 150 beats/min) heart rate. At rest, MAP and MCA Vmean increased approximately 20% (P<0.001) and approximately 10% (P<0.001 for 0.25 mg of phenylephrine and P<0.05 for 0.4 mg of phenylephrine), respectively. ScO2 then decreased approximately 7% (P<0.001). Phenylephrine had no effect on SjvO2, PaCO2, or CMRO2. MAP increased after the administration of phenylephrine during low-intensity exercise (approximately 15%), but this was attenuated (approximately 10%) during high-intensity exercise (P<0.001). The reduction in ScO2 after administration of phenylephrine was attenuated during low-intensity exercise (-5%, P<0.001) and abolished during high-intensity exercise (-3%, P=not significant), where PaCO2 decreased 7% (P<0.05) and CMRO2 increased 17% (P<0.05). These results suggest that the administration of phenylephrine reduced ScO2 but that the increased cerebral metabolism needed for moderately intense exercise eliminated that effect.

L-Arginine and Antioxidant Diet Supplementation Partially Restores Nitric Oxide-Dependent Regulation of Phenylephrine Renal Vasoconstriction in Diabetics Rats

The increase of reactive oxygen species (ROS) in diabetes potentiates the vascular effects of phenylephrine through nitric oxide (NO) impairment, facilitating the development of diabetic nephropathy. We propose that the combination of an antioxidant and L-arginine as diet supplements could prevent the increased vascular response to phenylephrine in diabetic animals. Changes in the adrenergic system play an important role in the development of vascular complications in the prediabetic condition. The vasoconstrictor effects of phenylephrine are regulated by NO, and the impairment of endothelium-dependent vasodilation in diabetes is associated with ROS. Diabetes was induced with a low dose (55 mg/kg body weight) of streptozotocin in 7-week-old rats. Diabetic rats were fed with a diet supplement containing a combination of vitamin E, vitamin C, eicosapentaenoic acid, docosahexaenoic acid, and L-arginine, and the effects on phenylephrine-induced renal vascular responses were evaluated. Phenylephrine increased the renal perfusion pressure of isolated perfused kidneys from diabetic rats compared with nondiabetic rats. This effect was associated with reduced nitrite release as well as reduced plasma tetrahydrobiopterin and increased superoxide anions in the renal tissue. Diet supplementation with a combination of L-arginine and vitamins in diabetic rats partially prevented the generation of superoxide associated with recovery of the renal release of NO and decreased phenylephrine-induced vasoconstrictor effects, compared with untreated diabetic rats. However, the administration of L-arginine or vitamins alone did not affect phenylephrine-induced vasoconstriction. Vitamin treatment alone did decrease superoxide generation. The protective mechanism of NO on the vasoconstrictor effects of phenylephrine in the kidney is lost during the development of diabetes, probably via the actions of ROS through a decrease in tetrahydrobiopterin, thus contributing to the pathogenesis of diabetic nephropathy. Restoration of this protective NO mechanism can be achieved by simultaneously stimulating NO synthesis and preventing the effects of ROS through the use of L-arginine and a combination of vitamins E and C as diet supplementation.

The effect of phenylephrine on the onset time of rocuronium

BackgroundSeveral studies have demonstrated that ephedrine shortens the onset time of muscle relaxants, and it does so probably by increasing the cardiac output. However, elevation of the systemic blood pressure through α adrenergic stimulation via ephedrine may affect the onset of muscle relaxants during the induction of anesthesia. We investigated the effect of phenylephrine, which is a selective α-1 agonist, on the onset time of rocuronium and the intubating conditions in adults after the administration of propofol.MethodsSixty-four patients were randomly assigned to two groups. Phenylephrine (0.9 µg/kg) (P group) or the same volume of saline (S group) was injected before rocuronium (0.6 mg/kg) administration. Anesthesia was induced with fentanyl 2 µg/kg and propofol 2 mg/kg. The onset time was defined as the time from the end of rocuronium injection to the time when a single twitch height gets to 0% or the minimum level. A well-trained anesthesiologist who was 'blinded' to the treatment groups evaluated the intubating conditions. The mean arterial pressure and heart rate were recorded before induction, before intubation, immediately after intubation and 1 minute and 2 minutes after intubation.ResultsThe onset time was 84 ± 18 sec in the P-group and 72 ± 14 sec in the S-group. There was no difference of the intubating conditions, the mean arterial pressure and the heart rate between the two groups.ConclusionsA small dose of phenylephrine, which has a limited effect on blood pressure, delayed the onset time of rocuronium after the administration of propofol, and the vasoconstriction effect of phenylephrine may affect the prolongation of the rocuronium onset time at the induction of anesthesia with using propofol.

The influence of constitutive cox-2 in smooth muscle tissue on the contractile effect of phenylephrine in the rat abdominal aorta

Prostanoids are involved in the phenylephrine-induced contraction of the aorta. Here, we examined whether or not constitutive cyclooxygenase-2 (phosholipases C and A2) is the source of prostanoids in the smooth muscle of the arterial wall of the thoracic and abdominal aorta. Both cyclooxygenase isoforms (COX-1 and COX-2) were expressed in the two aortic segments, but their expression was not altered by phenylephrine, the protein synthesis inhibitor cycloheximide, or the phospholipase A2 inhibitors arachidonyl trifluoromethyl ketone and methyl arachidonyl fluorophosponate. Indomethacin and NS398, which are a non-selective and selective COX-2 inhibitor, respectively, but not SC-560, which is a COX-1-selective inhibitor, inhibited the effect of phenylephrine on the abdominal, but not the thoracic, aorta. Similarly, U73122, which is a phospholipase C inhibitor, and RHC80267, which is a diacylglycerol lipase inhibitor, inhibited the effect of phenylephrine. These findings suggest that prostanoids, which are produced by constitutively active COX-2, influence the contractile response of the abdominal aorta and that the production of arachidonic acid relies on phospholipase C and diacylglycerol lipase.