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PubMed2002

The effect of phenylephrine and norepinephrine in patients with chronic pulmonary hypertension*.

In this study the effect of phenylephrine and norepinephrine for the treatment of systemic hypotension were evaluated in patients with chronic pulmonary hypertension. When systemic hypotension (systolic arterial pressure < 100 mmHg) occurred following induction of anaesthesia, either phenylephrine or norepinephrine were infused in a random manner to raise the systolic blood pressure by 30% and 50% above baseline values. Norepinephrine decreased the ratio of pulmonary arterial pressure to systemic blood pressure without a change in cardiac index. However, phenylephrine did not increase arterial blood pressure by more than 30% from baseline in one-third of patients and decreased cardiac index without a significant decrease in ratio of pulmonary arterial pressure to systemic blood pressure. These vasoconstrictors showed different systemic and pulmonary haemodynamic effects in patients with chronic pulmonary hypertension as compared to acute pulmonary hypertension. Norepinephrine was considered to be preferable to phenylephrine for the treatment of hypotension in patients with chronic pulmonary hypertension.

Adult↗

PubMed2002

Prior iontophoresis of saline enhances vasoconstriction to phenylephrine and clonidine in the skin of the human forearm.

AIMS: To determine whether postjunctional alpha1- and alpha2-adrenoceptors mediate vasoconstrictor responses in the cutaneous vasculature of the human forearm. METHODS: Drugs were administered transdermally by iontophoresis in the forearm of 20 healthy participants. Phenylephrine and clonidine were administered at sites pretreated with the relevant antagonist (terazosin and rauwolscine), and at additional untreated sites and sites pretreated with saline. To enhance the contrast between sites, the forearm was heated to 42 degrees C before flow was measured with the laser Doppler technique. RESULTS: After the iontophoresis of phenylephrine, blood flow at the site pretreated with terazosin was 24+/-37% (+/-95% confidence interval) greater than flow at the reference site, whereas flow was 53+/-24% lower than reference flow at the previously untreated site and 77+/-10% lower than reference flow at the site pretreated with saline (P<0.001). After the iontophoresis of clonidine, blood flow at the site pretreated with rauwolscine was 25+/-21% greater than flow at the reference site, whereas flow was 56+/-15% lower than reference flow at the previously untreated site and 72+/-8% lower than reference flow at the site pretreated with saline (P<0.001). The saline pretreatment enhanced vasoconstriction to phenylephrine (P<0.05) and clonidine (P=0.05). CONCLUSIONS: Pre-treatment with the appropriate antagonist blocked vasoconstrictor responses to phenylephrine and clonidine, consistent with the presence of both alpha-adrenoceptor subtypes in cutaneous vessels of the human forearm. In addition, iontophoretic pretreatment with saline facilitated vasoconstrictor responses, suggesting that a nonspecific effect of iontophoresis may enhance drug penetration through the stratum corneum.

Administration, Cutaneous↗

PubMed1998

Time course-dependent evolution of nitric oxide-mediated arterial hyporeactivity to phenylephrine in rats with ligated bile duct.

BACKGROUND: Nitric oxide (NO) may be heavily involved the phenomenon of arterial vasodilation in cirrhosis. However, the subject is still controversial. AIM: This study therefore characterizes the dynamic role of the NO system during development of experimental cirrhosis. METHODS: The contractile response to phenylephrine of thoracic rat aortic rings was studied in vitro before and after nitric oxide blockade. Experiments were performed 1, 2, 3, and 4 weeks after induction of cirrhosis via bile duct ligation with an appropriate control group. RESULTS: In bile duct-ligated rats reduction of the maximum contractile response to phenylephrine was 4.4 +/- 7.3% after 1 week, 22.7 +/- 8.7% after 2 weeks, 48.4 +/- 8.3% after 3 weeks, and 64.6 +/- 8.9% after 4 weeks, in comparison with the control group. This reduction in contractility to phenylephrine was completely reversed by blocking NO synthesis. CONCLUSION: The data presented indicate a dynamic decrease in contractile response to phenylephrine even at an early stage of secondary cirrhosis. Reversibility of the effect after NO synthesis blockade suggests that increased NO synthesis is a major factor in vascular hyporeactivity to vasoconstrictors in cirrhosis.

Animals↗

PubMed1988

Atypical alpha-adrenoceptor mediates phenylephrine-induced mydriasis in anesthetized cats.

Pupillary dilation and nictitating membrane (NM) contraction were elicited by pharmacological activation of alpha-adrenoceptors in vivo in anesthetized cats. A constant intravenous infusion of the alpha 1-adrenoceptor selective agonist phenylephrine (150 micrograms/min) was administered to produce a near maximal activation of both organs. Steady-state responses were attained about 15 minutes after starting the phenylephrine infusion. Administration of the alpha 1-adrenoceptor selective antagonist prazosin produced a dose-dependent blockade of NM contractions without altering phenylephrine-induced mydriasis when given as pretreatment (1.0 mg/kg i.v.) or post-treatment (0.01-1.0 mg/kg i.v.). In contrast, post-treatment with the alpha 1-adrenoceptor selective antagonist WB-4101 (0.1-1.0 mg/kg i.v.) or pretreatment with phenoxybenzamine (3.0 mg/kg i.v.) blocked both the NM and pupillary responses. These results suggest that the in vivo pupillary response to phenylephrine is mediated by an atypical alpha-adrenoceptor that cannot be readily classified as an alpha 1- or alpha 2-adrenoceptor. In contrast, the alpha-adrenoceptors of the NM appear to be of the classical alpha 1 subtype.

Adrenergic alpha-Antagonists↗

PubMed2005

Ephedrine and phenylephrine for the treatment of maternal hypotension in a chronic sheep model of increased placental vascular resistance.

BACKGROUND: We hypothesized that ephedrine and phenylephrine are equal with respect to uterine and placental haemodynamics and fetal acid-base status after exposure to maternal hypoxaemia and hypotension in a chronic sheep model of increased placental vascular resistance (R(UA)). METHODS: At 114-135 days gestation, chronically instrumented fetal sheep underwent placental embolization leading to increased R(UA). Twenty-four hours after embolization, the ewes were anaesthetized and randomized to receive boluses of ephedrine (n=7) or phenylephrine (n=6) for epidural-induced hypotension after maternal hypoxaemia. Uterine (Q(UtA)) and placental (Q(UA)) volume blood flows and uterine vascular resistance (R(UtA)) and R(UA) were recorded. Uterine (PI(UtA)) and umbilical artery (PI(UA)) pulsatility indices were obtained by Doppler ultrasonography. Fetal arterial blood samples were analysed for acid-base values and lactate concentrations. RESULTS: During hypotension, Q(UtA), fetal pH, BE, and Po(2) decreased whereas R(UtA), PI(UtA), R(UA), and fetal lactate concentration increased. With ephedrine, Q(UtA), R(UtA), PI(UtA), R(UA), and fetal Po(2) returned to baseline. Fetal pH, BE, and lactate concentration did not change from hypotensive values. With phenylephrine, Q(UtA) remained lower (P=0.007) and R(UtA) (P=0.007), PI(UtA) (P=0.013), and R(UA) (P=0.050) higher than at baseline. Fetal Po(2) returned to baseline and fetal pH and BE did not change from hypotensive values. However, fetal lactate concentration increased further (mean difference 1.49, 95% confidence interval 0.72-2.26 mmol litre(-1); P=0.004). CONCLUSIONS: In a chronic sheep model of increased placental vascular resistance, compared with ephedrine administration, phenylephrine administration was associated with impaired uterine and placental haemodynamics and increased fetal lactate concentrations.

Anesthesia, Epidural↗

PubMed1999

Epidural phenylephrine attenuates hypotension induced by alkalinized lidocaine epidural anesthesia.

UNLABELLED: In this double-blinded, randomized study, we examined the hemodynamic effects of lumbar epidural injection of alkalinized lidocaine with phenylephrine in 81 patients undergoing inguinal herniorrhaphy. Patients assigned to four equal groups received 20 mL of alkalinized lidocaine (17 mL of 2% lidocaine + 3 mL of 7% sodium bicarbonate) with one of four doses of phenylephrine: 0 (Group 1), 50 (Group 2), 100 (Group 3), or 200 microg (Group 4) injected via a lumbar epidural catheter. Blood pressure, heart rate, and skin temperature on the foot were recorded every 5 min for 1 h after injection and were compared among groups. Hypotension was defined as mean arterial pressure < 80% of baseline. The incidence of hypotension was 45%, 55%, 35%, and 15% in Groups 1-4, respectively. Patients in Group 4 showed the smallest reduction in blood pressure compared with Groups 1 and 2 (one-sided Fisher's exact test, P < 0.05). We conclude that the 200-microg dose of epidural phenylephrine (1:100,000 concentration) reduced the incidence of hypotension after epidural anesthesia with alkalinized lidocaine. IMPLICATIONS: Hypotension after epidural anesthesia is common in general clinical practice. Phenylephrine administered epidurally in combination with alkalinized lidocaine may reduce the incidence of hypotension.

Aged↗

PubMed1984

The effects of subarachnoid lidocaine and phenylephrine on spinal cord and cerebral blood flow in dogs.

To investigate the central nervous system circulation during spinal anesthesia, local spinal cord blood flow (SCBF) and cerebral blood flow (CBF) were measured simultaneously by the hydrogen clearance technique following subarachnoid lidocaine, phenylephrine, or a combination of both. The mean control values of SCBF and CBF were 22.4 +/- 7.9 ml X 100 g-1 X min-1 and 53.1 +/- 12.0 ml X 100 g-1 X min-1, respectively, in dogs lightly anesthetized with halothane. The subarachnoid administration of lidocaine solutions (1, 2, 3, and 5%), 1 ml, failed to produce statistically significant changes in SCBF (P greater than 0.05). Whereas, when phenylephrine (0.1, 0.2, 0.3, and 0.5%), 1 ml, was injected into the spinal subarachnoid space, SCBF decreased significantly with concentrations greater than 0.2% (P less than 0.05). When a mixture of lidocaine (24 mg) and phenylephrine (1 mg) was administered into the subarachnoid space, SCBF decreased significantly and returned to control within 60-90 min. CBF did not change significantly with any of the injections, remaining within less than +/- 12% of control. Dextrose solutions in water (5 and 7.5%), which were used for dilution of the drugs, did not affect either SCBF or CBF. These results indicate that local spinal cord blood flow can be affected significantly during spinal anesthesia when phenylephrine is added to the local anesthetic solution. However, the circulatory effects of drugs injected into the spinal subarachnoid space appear to be restricted to the local spinal cord per se and do not involve other parts of the CNS.

Anesthesia, Spinal↗

PubMed1988

Response of cerebral blood flow to phenylephrine infusion during hypothermic cardiopulmonary bypass: influence of PaCO2 management.

Twenty-eight adult patients anesthetized with fentanyl, then subjected to hypothermic cardiopulmonary bypass (CPB), were studied to determine the effect of phenylephrine-induced changes in mean arterial pressure (MAP) on cerebral blood flow (CBF). During CPB patients managed at 28 degrees C with either alpha-stat (temperature-uncorrected PaCO2 = 41 +/- 4 mmHg) or pH-stat (temperature-uncorrected PaCO2 = 54 +/- 8 mmHg) PaCO2 for blood gas maintenance received phenylephrine to increase MAP greater than or equal to 25% (group A, n = 10; group B, n = 6). To correct for a spontaneous, time-related decline in CBF observed during CPB, two additional groups of patients undergoing CPB were either managed with the alpha-stat or pH-stat approach, but neither group received phenylephrine and MAP remained unchanged in both groups (group C, n = 6; group D, n = 6). For all patients controlled variables (nasopharyngeal temperature, PaCO2, pump flow, and hematocrit) remained unchanged between measurements. Phenylephrine data were corrected based on the data from groups C and D for the effect of diminishing CBF over time during CPB. In patients in group A CBF was unchanged as MAP rose from 56 +/- 7 to 84 +/- 8 mmHg. In patients in group B CBF increased 41% as MAP rose from 53 +/- 8 to 77 +/- 9 mmHg (P less than 0.001). During hypothermic CPB normocarbia maintained via the alpha-stat approach at a temperature-uncorrected PaCO2 of approximately equal to 40 mmHg preserves cerebral autoregulation; pH-stat management (PaCO2 approximately equal to 57 mmHg uncorrected for temperature, or 40 mmHg when corrected to 28 degrees C) causes cerebrovascular changes (i.e., impaired autoregulation) similar to those changes produced by hypercarbia in awake, normothermic patients.

Aged↗

PubMed1989

Phenylephrine increases regional cerebral blood flow following hemorrhage during isoflurane-oxygen anesthesia.

Using the radioactive microsphere technique regional cerebral blood flow (rCBF) and total CBF (tCBF) were examined in rats at three time periods: baseline (CBF1) during 1.5 MAC inspired isoflurane-oxygen anesthesia, CBF2; during 1.5 MAC inspired isoflurane anesthesia combined with hypotension induced by hemorrhage and CBF3; during isoflurane and hemorrhage plus phenylephrine infused to restore mean arterial pressure (MAP) to baseline. For CBF1 MAP was 89 +/- 3 mmHg (mean +/- SEM, n = 9) with PaCO2 44 +/- 1 mmHg. For CBF2 following graded hemorrhage MAP was 48 +/- 2 mmHg and PaCO2 43 +/- 1 mmHg. For CBF3 MAP was 93 +/- 2 and PaCO2 45 +/- 1 mmHg, following infusion of phenylephrine (PE) at 13.9 +/- 4.0 micrograms.kg-1.min-1. Total CBF1 was 1.84 +/- 0.18 ml.g-1.min-1, tCBF2 1.32 +/- 0.09 ml.g-1.min-1 (P less than 0.05 vs. tCBF1) and tCBF3 2.60 +/- 0.18 (P less than 0.05 vs. tCBF1 and 2). For tCBF3 hemoglobin concentration had decreased 23% from 14.2 +/- 0.2 g.100 ml-1 to 11.0 +/- 0.5 g.100 ml-1 (P less than 0.05). Regional CBF decreased significantly in seven of 12 regions examined from CBF1 to CBF2 and was significantly higher in all regions for CBF3. For CBF1-3 infratentorial blood flows (cerebellar and brain stem) were significantly higher than flows to the supratentorial structures (cerebral cortical and basal ganglia). During isoflurane anesthesia, phenylephrine infused to support MAP following hemorrhagic hypotension effectively maintains rCBF and tCBF. There is no indication that phenylephrine infused to increase MAP following hemorrhage results in cerebral vasoconstriction in rats anesthetized with isoflurane.

Anesthesia, Inhalation↗

PubMed1996

Phenylephrine increases cerebral blood flow during low-flow hypothermic cardiopulmonary bypass in baboons.

BACKGROUND: Although low-flow cardiopulmonary bypass (CPB) has become a preferred technique for the surgical repair of complex cardiac lesions in children, the relative hypotension and decrease in cerebral blood flow (CBF) associated with low flow may contribute to the occurrence of postoperative neurologic injury. Therefore, it was determined whether phenylephrine administered to increase arterial blood pressure during low-flow CPB increases CBF. METHODS: Cardiopulmonary bypass was initiated in seven baboons during fentanyl, midazolam, and isoflurane anesthesia. Animals were cooled at a pump flow rate of 2.5 l.min-1.m-2 until esophageal temperature decreased to 20 degrees C. Cardiopulmonary bypass flow was then reduced to 0.5 l.min-1.m-2 (low flow). During low-flow CPB, arterial partial pressure of carbon dioxide (Pco2) and blood pressure were varied in random sequence to three conditions: (1) Pco2 30-39 mmHg (uncorrected for temperature), control blood pressure; (2) Pco2 50-60 mmHg, control blood pressure; and (3) Pco2 30-39 mmHg, blood pressure raised to twice control by phenylephrine infusion. Thereafter, CPB flow was increased to 2.5 l.min-1.m-2, and baboons were rewarmed to normal temperature. Cerebral blood flow was measured by washout of intraarterial 133Xe before and during CPB. RESULTS: Phenylephrine administered to increase mean blood pressure from 23 +/- 3 to 46 +/- 3 mmHg during low-flow CPB increased CBF from 14 +/- 3 to 31 +/- 9 ml.min-1.100 g-1, P < 0.05. Changes in arterial Pco2 alone during low flow bypass produced no changes in CBF. CONCLUSIONS: Although low-flow CPB resulted in a marked decrease in CBF compared with prebypass and full-flow bypass, phenylephrine administered to double arterial pressure during low-flow bypass produced a proportional increase in CBF.

Adrenergic alpha-Agonists↗

PubMed1998

Benzodiazepines differentially inhibit phenylephrine-induced calcium oscillations in pulmonary artery smooth muscle cells.

BACKGROUND: Modulation of intracellular free calcium is a critical determinant of vasomotor tone. The authors investigated the effects of three benzodiazepines on alpha-adrenergic-induced oscillations in intracellular free calcium in individual pulmonary artery smooth muscle cells. METHODS: Pulmonary artery smooth muscle cells were cultured from explants of canine intrapulmonary artery. Fura-2-loaded pulmonary artery smooth muscle cells were continuously superfused with phenylephrine (10 microM) at 37 degrees C on the stage of an inverted fluorescence microscope. Intracellular free calcium was measured using a dual wavelength spectrofluorometer. After establishment of steady-state intracellular free calcium oscillations induced by phenylephrine, lorazepam, diazepam, or midazolam was added to the superfusate. The amplitude and frequency of the intracellular free calcium oscillations were compared before and after addition of each agent. RESULTS: Resting mean +/- SEM values of intracellular free calcium were 68 +/- 8 nM. Phenylephrine stimulated dose-dependent oscillations in intracellular free calcium, which reached a peak concentration of 676 +/- 35 nM and a frequency of 1.08 +/- 0.1 transients/min. Addition of lorazepam (1 microM) inhibited (P < 0.05) the amplitude (591 +/- 32 nM) but not the frequency (0.97 +/- 0.1 transients/min) of the oscillations. Conversely, diazepam (1 microM) decreased (P < 0.05) the frequency (0.79 +/- 0.1 transients/min) but not the amplitude (663 +/- 37 nM) of the oscillations. These effects were dose-dependent. In contrast, midazolam (1-30 microM) had no effect on the amplitude or frequency of intracellular free calcium oscillations. At concentrations higher than 100 microM, however, all three benzodiazepines inhibited both the amplitude and frequency of the intracellular free calcium oscillations. CONCLUSION: Lorazepam and diazepam but not midazolam exerted differential inhibitory effects on phenylephrine-induced intracellular free calcium oscillations. Benzodiazepines may alter the pulmonary vascular response to sympathetic alpha-adrenoreceptor activation by direct inhibition of intracellular free calcium signaling in pulmonary artery smooth muscle cells.

Adrenergic alpha-Agonists↗

PubMed2005

Prevention of hypotension during spinal anesthesia for cesarean delivery: an effective technique using combination phenylephrine infusion and crystalloid cohydration.

BACKGROUND: Many methods for preventing hypotension during spinal anesthesia for cesarean delivery have been investigated, but no single technique has proven to be effective and reliable. This randomized study studied the efficacy of combining simultaneous rapid crystalloid infusion (cohydration) with a high-dose phenylephrine infusion. METHODS: Nonlaboring patients scheduled to undergo elective cesarean delivery received an intravenous infusion of 100 mug/min phenylephrine that was started immediately after spinal injection and titrated to maintain systolic blood pressure near baseline values until uterine incision. In addition, patients received infusion of lactated Ringer's solution that was given either rapidly (group 1, n = 57) or at a minimal maintenance rate (group 0, n = 55). Maternal hemodynamic changes and neonatal condition were compared. RESULTS: Six patients were excluded from analysis. Only 1 of 53 patients (1.9% [95% confidence interval, 0.3-9.9%]) in group 1 experienced hypotension versus 15 of 53 patients (28.3% [95% confidence interval, 18.0-41.6%]) in group 0 (P = 0.0001). Compared with group 0, patients in group 1 had greater values for the following: serial measurements of systolic blood pressure (P = 0.02), minimum recorded systolic blood pressure (P = 0.0002), and minimum recorded heart rate (P = 0.013). Total phenylephrine consumption was smaller in group 1 compared with group 0 (P = 0.008). Neonatal outcome and maternal side effects were similar between groups. CONCLUSIONS: Combination of a high-dose phenylephrine infusion and rapid crystalloid cohydration is the first technique to be described that is effective for preventing hypotension during spinal anesthesia for cesarean delivery.

Adult↗

PubMed1989

Myocardial response to alpha-agonist (phenylephrine) in relation to age.

We studied the inotropic effect of the alpha-agonist phenylephrine on human and rat myocardium in relation to age. Strips of human atrial myocardium, discarded during cardiac surgery, were obtained from pediatric (2 to 18 months) and adult (40 to 60 yr) patients, and their electrically driven contractions were studied. The inotropic response of pediatric myocardium to phenylephrine was five times larger than that of the adult myocardium (p less than .05). The beta-agonist, isoproterenol, was also administered to the same myocardial specimens, and the average pediatric myocardial response was three times larger than that of the adult myocardium (p less than .05). Strips of right ventricular myocardium were obtained from four age groups of rats: 14 days, 3 months, 6 months, and 18 months, and exposed to phenylephrine. We demonstrated two age-related phenomena: a) a biphasic response with an early short negative inotropic effect preceding a sustained positive inotropic effect was registered in most of the rats aged 3 months and older, but in none of the youngest age group. b) A high mean positive inotropic response (211% of basal response) was generated in the youngest age group, whereas the oldest age group of rats showed only a slight response (8% of basal response, p less than .05). We conclude that loss of myocardial responsiveness to alpha and beta-agonist with increasing age is a prominent feature. The pattern of the ventricular responsiveness to phenylephrine also changes during aging as it turns from monophasic to biphasic.

Adult↗

PubMedDate not supplied

Renin release induced by a nonvasoconstrictor dose of phenylephrine is independent of the renal prostaglandin system in anesthetized dogs.

We examined the relationship between prostaglandin (PG) production and renin release induced by a nonvasoconstrictor dose of an alpha-agonist, phenylephrine, in anesthetized dogs. Intrarenal infusion of phenylephrine (1 microgram/min) did not affect systemic blood pressure or renal blood flow, but increased the renin secretion rate about twofold. The effect of phenylephrine on renin release was abolished by the intrarenal infusion of the alpha-antagonist phentolamine (50 micrograms/min), but was not affected by the intravenous administration of the PG synthetase inhibitor indomethacin (5 mg/kg). Urine flow and urinary sodium excretion rate were not altered by phenylephrine. These results suggest that a nonvascular and nontubular alpha-adrenoceptor mechanism, which is independent of the renal PG system, may be involved in renin release.

Anesthesia↗

PubMed2002

Thromboxane A2 in vasomotor effects of phenylephrine, acetylcholine, and bradykinin in rat mesenteric bed.

In vessels, pharmacological agents displace the balance between relaxing and contracting factors. A cross-talk between those factors has been shown in some vascular beds. To examine whether NO may regulate the vascular tone by modulating prostanoid synthesis or release, we analyzed the response of resistance rat mesenteric arterial bed to vasoactive agents. Phenylephrine, bradykinin (BK), and acetylcholine (ACH) were administered in the absence or in the presence of either NO synthesis inhibition (N(G)-nitro-L-arginine methyl ester [L-NAME]), cyclo-oxygenase inhibition (indomethacin), and/or a thromboxane A2 (TXA2) receptor antagonist (S18886), or a combination thereof. In the presence of L-NAME, the response to phenylephrine was markedly increased. Indomethacin limited these changes, which are attributed to TXA2 release since they were abolished by S18886 and a marked increase in TXB2 release (stable metabolite of TXA2) was found during phenylephrine infusion under NO blockade. Similarly, BK response under NO blockade was markedly attenuated with an improved response with indomethacin and a restoration of vasorelaxation with S18886. In contrast, indomethacin decreased further the response to ACH during L-NAME treatment, and TXA2 inhibition had no effect. Thus, in pathophysiological conditions where an endothelial dysfunction is present, TXA2 stimulation induced by NO release impairment may contribute to an altered response to phenylephrine or BK.

Acetylcholine↗

PubMed1982

Mydriatic effectiveness of dilute combinations of phenylephrine and tropicamide.

The effects of two solutions, each consisting of a combination of tropicamide and phenylephrine at lower than conventional concentrations, were studied in 79 students at Pacific University College of Optometry. Clinically effective diameters (CED's), measured when the eye was illuminated for direct ophthalmoscopy, were followed for 90 min after mydriatic instillation. Intraocular pressure (IOP), systolic arterial blood pressure (sBP), and the systolic BP/IOP ratio were also monitored for 90 min. Both combination A (0.25% tropicamide + 1.25% phenylephrine) and combination B (0.125% tropicamide + 2.0% phenylephrine) produced CED's as large as produced by 0.5% tropicamide in the opposite eye. By combining a low concentration of a sympathomimetic with a parasympatholytic agent, it is possible to achieve mydriasis superior to that produced by 0.5% tropicamide or 2.5% phenylephrine while reducing the risk of systemic or ocular side effects.

Adult↗

PubMed1994

Sepsis decreases phenylephrine- and KCl-induced aortic ring contraction and decreases the frequency of oscillations in active wall tension.

Impaired vascular contractility is a hallmark of sepsis and endotoxemia. The purpose of the present investigation was to determine mechanisms responsible for the abnormal contractility in sepsis using the rat cecal ligation and perforation (CLP) model. 24 h after CLP or sham surgery, rats were anesthetized with halothane and a segment of the thoracic aorta removed. Aortic rings measuring 1.6-2.0 mm in length were mounted in a water bath and stretched to optimal diameter. Aortic rings from control rats demonstrated a 57% increase in maximum contraction to phenylephrine and a 68% increase to KCl compared to aortic rings from rats with sepsis (p < .01). There was no difference in the concentrations of phenylephrine or KCl which elicited a half-maximal contraction (EC50) in control versus septic aortic rings. Removal of the endothelium increased the sensitivity of aortas to both phenylephrine and KCl in septic and control aortic rings but did not reverse the defects in contraction in sepsis. Treatment of the aortic rings with N gamma-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, increased contraction in aortic rings from both septic and control rats but also failed to correct the contractile defect in sepsis. The frequency and amplitude of the oscillations in wall tension which occurred with phenylephrine were slower, i.e., .07 +/- .10 vs. .17 +/- .02 Hz, for septic and control rings, respectively (p < .05), and had a greater amplitude .65 +/- .01 vs. .41 +/- .09 mN/mm, for septic and control rings, respectively (p < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed2002

Differential involvement of guanylate cyclase and potassium channels in nitric oxide-induced hyporesponsiveness to phenylephrine in endotoxemic rats.

This study evaluated the involvement of nitric oxide (NO), guanylate cyclase, and potassium channels in the long-lasting vascular hyporesponsiveness to phenylephrine induced by Escherichia coli lipopolysaccharide (LPS) in vitro and in vivo. Experiments in rat aorta rings with endothelium incubated with LPS (10 microg/mL) for 12 h showed that the hyporesponsiveness depends on guanylate cyclase activity and tetraethylammonium-sensitive, but not voltage- or ATP-dependent, potassium channels. Pressor responses to phenylephrine were reduced by 50% in rats injected 8 and 24 h before with LPS (10 mg/kg, intraperitoneally). Pretreatment with NO synthase inhibitors (iNOS; Nomega-nitro-L-arginine methyl ester [L-NAME], 55 micromol/kg or aminoguanidine, 244 micromol/kg, intraperitoneally) fully prevented LPS-induced hyporesponsiveness. When administered just before phenylephrine, L-NAME (11 micromol/kg, intravenously) reversed the hyporesponsiveness in rats injected 8 h, but not in those injected 24 h before with LPS, whereas 1H-[1,2,4]-oxadiazolo-[4,3-a]-quinoxalin-1 (ODQ, 11 micromol/kg, intravenously) reversed the hyporesponsiveness in animals injected 24 h, but not in those injected 8 h before with LPS. Tetraethylammonium (360 micromol/kg, intravenously) reestablished normal responses to phenylephrine in rats injected 8 and 24 h before with LPS. Again, neither voltage- nor ATP-dependent potassium channels appears to be involved. Western blot showed that iNOS expression peaked at 8 h, decreasing to low levels 24 h after LPS injection. Therefore, NO is important in initiating LPS-induced hyporesponsiveness to vasoconstrictors, but not in maintaining it for long periods. Once NO has exerted its effects and even when iNOS expression is minimal, the long-lasting hyporesponsiveness appears to depend on a complex interplay between guanylate cyclase and potassium channel activation.

Animals↗