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PubMed1998

Phenylephrine increases T wave shock energy required to induce ventricular fibrillation.

INTRODUCTION: Previous reports in experimental models have suggested that ventricular fibrillation threshold (VFT) can be changed by manipulating cardiac neural tone using agents such as phenylephrine. The purpose of this study was to determine whether phenylephrine increased the energy required to induce VF in humans undergoing such induction using DC energy applied to the T wave. METHODS AND RESULTS: In this prospective investigation, 18 consecutive patients with previously implanted cardioverter defibrillators had induction of VF by placing DC monophasic shocks into the T wave coupled 310 msec after the eighth paced ventricular complex at 400 msec. The T wave shock energy was titrated from 0.2 to 12 J until sustained VF or ventricular tachycardia was induced. Phenylephrine was infused either before the first or second VF induction in a randomized fashion to increase systolic blood pressure by more than 20 mmHg. The mean energy required to induce VF was 1.1 J at baseline and increased to 1.7 J during phenylephrine infusion (P = 0.036). The mean arterial pressure increased from 88 to 114 mmHg (P < 0.001), and the mean sinus cycle length increased from 850 to 1070 msec (P < 0.001). Ten of 13 (77%) patients with sinus cycle length prolongation had increased energy requirements to induce VF compared with only 1 of 5 patients (20%) without sinus cycle length prolongation (P < 0.05). CONCLUSION: Phenylephrine increases VFT in humans presumably by reflex activation of the baroreceptors decreasing sympathetic and/or increasing parasympathetic cardiac efferent effects.

Adolescent↗

PubMed1984

The effect of phenylephrine on the accommodative process in man.

Accommodation was measured in a double-blind study on 10 healthy volunteers (22-29 years) before and after the instillation of 0.1%, 1.0% and 10% phenylephrine eye drops. Accommodation decreased exponentially with increasing concentration, reaching an average of 3 dioptres after one drop of 10% phenylephrine. The effect of adding phenylephrine to an atropinized eye was studied in 20 children (3-6 years). The children were randomized to placebo or phenylephrine treatment. The cycloplegic effect of atropine was unchanged in 8 out of 9 placebo-treated children, whereas 5 out of 11 phenylephrine-treated children showed a slight, but not significant, increase in hypermetropia.

Accommodation, Ocular↗

PubMed1987

The effects of thymoxamine, phenylephrine and cyclopentolate on the accommodative process in man.

Accommodation of the eye was measured in a cross-over study in 11 healthy volunteers (20-35 years). In 5 subjects the near point was determined before and after topical instillation of 5 microliter of 0.1% and 0.5%, and 5 x 5 microliter 0.5% thymoxamine, 5 microliter of 2% and 10%, and 5 x 5 microliter 10% phenylephrine and 5 microliter of 0.04%, 0.2%, and 1% cyclopentolate. All concentrations of thymoxamine increased the accommodative amplitude by about 1.5 dioptres. Accommodation decreased by about 0.5 dioptre after instillation of 5 x 5 microliter 10% phenylephrine. The cycloplegic effects of 0.2% and 1% cyclopentolate were similar. Accommodation was also determined after application of 5 microliter 1% cyclopentolate followed by either 5 x 5 microliter 0.5% thymoxamine or 10% phenylephrine. Addition of thymoxamine did not alter the cycloplegic response of cyclopentolate alone. Addition of phenylephrine caused a more prolonged but similar maximum response compared to that of cyclopentolate alone. In the 6 other test subjects, the accommodation was compared before and after topical instillation of 5 microliter of 0.2% and 1% and 40 microliter (one standard eye-drop) of 1% cyclopentolate and followed during 6 h. There was no difference between the maximum value of 5 microliter and 40 microliter 1% cyclopentolate. We conclude from these data that alpha-stimulation by phenylephrine decreases and alpha-inhibition by thymoxamine increases the accommodative amplitude in man.(ABSTRACT TRUNCATED AT 250 WORDS)

Accommodation, Ocular↗

PubMed1992

Contractions induced by phenylephrine and noradrenaline are differently affected by endothelium-dependent relaxation in rat aorta.

In rings of rat aorta precontracted with phenylephrine (10 microM) or noradrenaline (10 microM), addition of carbachol (10 microM) produced an endothelium-dependent relaxation. However, regardless of the concentration of agonist tested, both the intensity and duration of the relaxation were significantly less when noradrenaline, rather than phenylephrine, was used as the precontracting agent. The different responses observed do not appear to be related to destruction of endothelium-derived relaxing factor by autoxidation of noradrenaline since neither EDTA (30 microM) nor superoxide dismutase (30 units mL-1) improved the relaxation to carbachol. In addition, in endothelium-free rings, the noradrenaline (1 microM)-induced contraction was less sensitive than the phenylephrine (1 microM)-induced contraction to sodium nitroprusside (0.1 microM) or to 8-Br-cGMP (300 microM). With phenylephrine-, but not noradrenaline-, induced contraction, the relaxation triggered by carbachol was significantly reduced by pretreatment of the aortic rings with chloroethylclonidine (50 microM), which inactivates a subpopulation of alpha 1-adrenoceptors. Thus, the results confirm that both alkylation sensitive and resistant alpha 1-adrenoceptors exist in rat aorta and indicate that EDRF may discriminate between these two alpha 1-adrenoceptor subtypes which are differently affected by phenylephrine and noradrenaline.

Animals↗

PubMed1990

Vasoactive peptides and phenylephrine actions in isolated teleost hepatocytes.

The metabolic actions of the vasoactive peptides vasotocin and isotocin and the alpha-agonist phenylephrine are examined in hepatocytes isolated from three teleost species: brown bullhead, rainbow trout, and American eel. These three compounds influenced hepatic gluconeogenesis and glycogenolysis with significant species differences. Vasotocin and isotocin affected only eel hepatocytes activating gluconeogenesis by 1.7-fold and glycogenolysis by 3-fold. Phenylephrine increased glycogenolysis by 7-fold in bullhead hepatocytes and gluconeogenesis by 1.4-fold in trout cells. Vasotocin and phenylephrine actions were correlated with increases in adenosine 3',5'-cyclic monophosphate (cAMP). The vasotocin effects were unaffected by beta- and alpha-antagonists supporting a V2-type receptor on eel hepatocytes. Phenylephrine effects were abolished by propranolol and reduced by prazosin and yohimbine (alpha 1- and alpha 2-antagonists, respectively). Phenylephrine, therefore, affected fish hepatocyte metabolism either by a mixed alpha/beta-receptor mechanism emphasizing beta-adrenoceptors or the classic alpha/beta agonist/antagonist scheme defined for mammals is not appropriate for these fish preparations.

1-Methyl-3-isobutylxanthine↗

PubMed1995

Phenylephrine contracts rat tail artery by one electromechanical and three pharmacomechanical mechanisms.

There are at least four mechanisms hypothesized to account for excitation-contraction coupling in arterial smooth muscle. 1) Contractile agonists and changes in extracellular [K+] ([K+]o) induce contraction by depolarization, which increases Ca2+ influx; this is the only mechanism involving a change in membrane potential (Em). 2) Contractile agonists release Ca2+ from the intracellular Ca2+ store. 3) Contractile agonists increase Ca2+ influx without changing Em either by activating voltage-dependent L-type Ca2+ channels or by opening other Ca(2+)-permeable channels. 4) Contractile agonists increase intracellular Ca2+ ([Ca2+]i) sensitivity of force; this is the only mechanism that does not involve changes in [Ca2+]i. Each of these mechanisms has been demonstrated in intact, skinned, or dissociated smooth muscle preparations. However, these four mechanisms have not been compared in the same preparation. The goal of this study was to determine which of these four contractile mechanisms are physiologically relevant in the intact rat tail artery. We stimulated deendothelialized rat tail artery with phenylephrine and high [K+]o. We then measured Em with microelectrodes, [Ca2+]i with fura 2, and isometric force with a strain gauge transducer. We find that all four mechanisms contributed to phenylephrine-induced rat tail artery contraction. The majority of phenylephrine-induced contraction was caused by depolarization and by increases in the [Ca2+]i sensitivity of force. Low concentrations of phenylephrine also increased [Ca2+] independent of changes in Em, potentially by increases in Ca2+ influx. Release of Ca2+ from intracellular stores was only observed with high concentrations of phenylephrine. Smooth muscle appears to invoke multiple mechanisms for excitation-contraction coupling.

Animals↗

PubMed1996

Phenylephrine suppresses outward K+ currents in rat atrial myocytes.

The modulation of whole cell K+ currents by the alpha 1-adrenergic agonist, phenylephrine, was studied in isolated rat atrial myocytes by use of perforated-patch whole cell recording techniques. The out ward K+ current in these myocytes consists of two inactivating components (iK,f and iK,s), which differ in the kinetics of inactivation and recovery from inactivation, and a noninactivating component, (iK,ss). Superfusion of these myocytes with 10 microM phenylephrine caused a rapid suppression of iK,ss, with little effect on the other current components. This effect of phenylephrine could be mimicked by exogenous application of 1,2-dioctanoyl-sn-glycerol (20 microM), a membrane-permeant diacylglycerol analogue; however, it was clearly distinct from the effect of 5 nM alpha-dendrotoxin, which selectively suppressed the slowly inactivating current component, iK,s, while having no effect on iK,ss. At a dose of 50 microM, phenylephrine also suppressed iK,s. There was no significant effect of phenylephrine (10 or 50 microM) or alpha-dendrotoxin (5 nM) on the rapidly inactivating current component, iK,f. The kinetic and pharmacological differences between these current components suggest that they represent the activity of distinct K+ channels.

Animals↗

PubMed1998

R-R variability detects increases in vagal modulation with phenylephrine infusion.

High-frequency power, measured from power spectral analysis of R-R variability, reflects vagal modulation of the sinus node. Unexpectedly, a recent study reported a decrease in high-frequency power during the infusion of phenylephrine despite a prolongation of R-R intervals, indicating an increase in vagal activity. To better define the limitations of high-frequency power to quantify vagal modulation, we measured high-frequency power during the infusion of phenylephrine (0.4, 0.8, and 1.2 micrograms.kg-1.min-1) into 10 normal subjects. We found increasing doses of phenylephrine produced progressive increases in systolic blood pressure from 118 +/- 4 to 129 +/- 5 mmHg (P < 0.005), R-R intervals from 881 +/- 44 to 1,274 +/- 69 ms (P < 0.0001), and the logarithm of high-frequency power from 5.83 +/- 0.22 to 7.73 +/- 0.24 ln(ms2) (P < 0.0001). The conclusion was high-frequency power increases with increasing doses of phenylephrine. These data strongly support the ability of high-frequency power to detect an increase in vagal modulation during baroreceptor activation from an increase in systolic blood pressure with the infusion of phenylephrine.

Adult↗

PubMedDate not supplied

Hyperosmolarity enhances smooth muscle contractile responses to phenylephrine and partially impairs nitric oxide production in the rat tail artery.

The respective effects of hyperosmolarity caused by impermeant solutes, such as mannitol and sucrose, on the endothelium and smooth muscles cell responses were investigated in the rat tail artery. The vessels, with or without endothelium, were infused and superfused with an isosmolar saline solution, and were repeatedly stimulated with phenylephrine. Superfusing with hyperosmolar fluid (390-420 mosm/l) produced a transient increase in the arterial basal perfusion pressure which peaked after approximately 5 min and then declined within 15 min to a stable nonsignificant value above control values in subsequent experiments. In arteries with functional endothelium, the effect of phenylephrine was about 1.9-fold larger in hyperosmotic medium compared to that in isosmotic medium. In hyperosmotic media the response was still more than twofold enhanced in endothelium-denuded vessels compared to those with endothelium. In the latter, indomethacin (10 microM) had no effect, but N omega-nitro-L-arginine methylester (L-NAME; 30 mumol/l), an inhibitor of NO production, enhanced the response to phenylephrine to reach the same magnitude of response as seen in endothelium-denuded arteries. This effect of L-NAME was antagonized by L-arginine. Relaxation induced by the NO donor SIN-1 was unchanged by hyperosmolarity, indicating that the effect of NO was not impaired. It is concluded that, in the rat tail artery, the enhancement in phenylephrine-induced contractions produced in a hyperosmolar solution is due to both an endothelium-independent increase in smooth muscle responses and a moderate decrease in the production of NO, or an NO-like factor, by the endothelium. In spite of this reduction, endothelium-derived NO still plays a major role in attenuating phenylephrine-induced contractions in hyperosmolar medium.

Animals↗

PubMed1989

Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine.

Pure alpha-adrenergic agonists, such as phenylephrine, and mixed alpha- and beta-adrenergic agonists, such as epinephrine, raise perfusion pressure for heart and brain during cardiopulmonary resuscitation (CPR). However, with the high doses used during CPR, these drugs may directly affect vascular smooth muscle and metabolism in brain and heart. We determined whether at equivalent perfusion pressure, continuous infusion of phenylephrine (20 micrograms/kg/min) or epinephrine (4 micrograms/kg/min) leads to equal organ blood flow, cerebral O2 uptake, and cerebral electrophysiologic function. During 20 minutes of CPR initiated immediately upon ventricular fibrillation in anesthetized dogs, left ventricular blood flow was similar with epinephrine (45 +/- 9 ml/min/100 g) or phenylephrine (47 +/- 8 ml/min/100 g) infusion. The ratio of subendocardial to subepicardial blood flow fell equivalently during CPR with either epinephrine (1.23 +/- 0.06 to 0.70 +/- 0.05) or phenylephrine (1.32 +/- 0.07 to 0.77 +/- 0.05) administration. At similar levels of cerebral perfusion pressure (44 +/- 3 mm Hg), similar levels of cerebral blood flow were measured in both groups (27 +/- 3 ml/min/100 g). Cerebral O2 uptake was maintained at prearrest levels in both groups. Somatosensory-evoked potential amplitude was modestly reduced during CPR, but it promptly recovered after defibrillation. During CPR and at 2 hours after resuscitation, there were no differences between drug groups in the level of regional cerebral or coronary blood flow, cerebral O2 uptake, or evoked potentials. Therefore, with minimal delay in the onset of CPR and with equipotent pressor doses of phenylephrine and epinephrine, we found no evidence that one agent provides superior coronary or cerebral blood flow or that epinephrine by virtue of its beta-adrenergic properties adversely stimulates cerebral metabolism at a critical time that would impair brain electrophysiologic function. Moreover, epinephrine did not preferentially impair subendocardial blood flow as might be expected if it enhanced the strength of fibrillatory contractions.

Animals↗

PubMed1994

Endogenous angiotensin II enhances phenylephrine-induced tone in hypertensive rats.

Subthreshold concentrations of angiotensin II (Ang II) potentiate agonist-induced tone in a variety of blood vessels. We measured in vivo the mesenteric artery diameter and blood flow in 12-week-old normotensive Wistar-Kyoto (WKY) rats (n = 20) and spontaneously hypertensive rats (SHR, n = 20); systemic blood pressure was monitored continuously. Phenylephrine (10 mumol/L) superfused on the exteriorized mesentery reduced arterial diameter from 480 +/- 40 to 256 +/- 18 microns (P < .05) in WKY rats and from 562 +/- 26 to 273 +/- 7 microns (P < .05) in SHR, whereas blood flow was lowered by 77% in WKY rats and 76% in SHR (P < .05 in both strains). Topical superfusion of an angiotensin-converting enzyme inhibitor (perindoprilat, 10 and 100 mumol/L) attenuated the phenylephrine-induced decrease in diameter and blood flow in both strains (P < .05). The Ang II type 1 receptor blocker losartan (10 mumol/L) attenuated the phenylephrine-induced decrease in diameter and blood flow in both strains (P < .05). The relaxing effect of losartan was significantly accentuated by the addition of perindoprilat (10 mumol/L) to the superfusate (P < .05 in both strains). Systemic blood pressure was unaffected by the topical application of phenylephrine (10 mumol/L), perindoprilat (10 or 100 mumol/L), or losartan (10 mumol/L). We conclude that phenylephrine-induced tone impairment by angiotensin-converting enzyme inhibition and Ang II type 1 receptor blockade in vivo probably reflects the role of endogenous Ang II in the potentiation of the adrenergic response during the control of vascular tone. This role is identical in both normotensive and hypertensive rats.

Angiotensin II↗

PubMed1989

Responsiveness of superficial hand veins to phenylephrine in essential hypertension. Alpha adrenergic blockade during prazosin therapy.

Patients with essential hypertension show an increase in vascular resistance. It is unclear whether this is caused by structural changes in the arterial wall or by hyperresponsiveness of vascular smooth muscle to endogenous alpha adrenergic agonists. Using the dorsal hand vein compliance technique we compared the changes in diameter of superficial veins in response to phenylephrine, an alpha 1 adrenergic receptor agonist, and to nitroglycerin, a venorelaxant, in patients with essential hypertension and in normotensive subjects. The dose of phenylephrine that produced 50% of maximal venoconstriction (ED50) in the hypertensive subjects was 257 ng/min (geometric mean; log mean +/- SD was 2.41 +/- 0.54). In the control subjects the ED50 was 269 ng/min (geometric mean; log mean was 2.43 +/- 0.43). Maximal response (Emax) for phenylephrine was 84 +/- 13% in the hypertensive subjects and 90 +/- 6% in the control subjects. Differences in the group means of the ED50 (P = 0.92) or the Emax (P = 0.27) were not significant. There were no significant differences in the ED50 (P = 0.54) or the Emax (P = 0.08) for nitroglycerin between the two groups. These results show no evidence for a generalized change in alpha adrenergic responsiveness in hypertension and support the concept that increased blood pressure responses to alpha adrenergic stimulation in hypertensives are due to structural and geometric changes in the arterial wall rather than to an increased responsiveness of postsynaptic alpha adrenergic receptors. The phenylephrine studies were repeated in seven hypertensive patients during treatment with prazosin, an alpha 1 adrenergic antagonist. The mean dose ratio of the shift in phenylephrine ED50 (ED50 during prazosin therapy/ED50 before prazosin therapy) was 6.1. This indicates that small doses of prazosin (1-2 mg) cause significant in vivo shifts in the dose-response relationship of alpha adrenergic agonists. The dorsal hand vein compliance technique is useful in detecting systemic effects of alpha adrenergic antagonists.

Adrenergic alpha-Antagonists↗

PubMed1994

Comparisons of tetracaine spinal anesthesia with clonidine or phenylephrine in normotensive and hypertensive humans.

To compare the hemodynamics and anesthetic effects of spinal tetracaine containing either clonidine or phenylephrine administered to normotensive or hypertensive patients, we studied 75 patients allocated to one of three groups, each of which included nine hypertensive patients: clonidine group (n = 25) received 2 mL of 0.5% tetracaine (10 mg) containing clonidine (0.15 mg); phenylephrine group (n = 25) received 2 mL of 0.5% tetracaine (10 mg) containing phenylephrine (3 mg); and control group (n = 25) received 2 mL of 0.5% tetracaine (10 mg) alone. Analgesic levels and the intensity of motor block obtained did not differ significantly among the three groups. However, the regression of sensory block (skin dermatome) was significantly slower in patients given clonidine (T9 +/- 3) or phenylephrine (T9 +/- 3) at 300 min after the injection than in those (L1 +/- 3) in the control group (P < 0.01). Between normotensive and hypertensive patients, there was no significant difference in sensory and motor block in the three groups. Mean blood pressure (MBP) in both hypertensive and normotensive patients given tetracaine-clonidine remained approximately 20% lower than that in the control group for as long as 7 h after the injection (P < 0.05). We conclude that the inclusion of clonidine can provide similar effects to that of phenylephrine with respect to prolongation of hyperbaric tetracaine spinal anesthesia, but could cause more hypotension, without bradycardia, in both normotensive and hypertensive patients for a prolonged time (i.e., 420 min).

Adult↗

PubMed1994

Phenylephrine does not reduce cerebral perfusion during canine cardiopulmonary bypass.

Gaseous microemboli during cardiopulmonary bypass (CPB) could injure the blood-brain barrier so that cerebral vasoconstriction would result from infusing alpha-agonist drugs, such as phenylephrine. Cerebral blood flow (radioactive microspheres) and metabolism were measured in seven dogs after rewarming from 150 min hypothermic CPB with bubble oxygenators used to produce gaseous microemboli. Phenylephrine (40 micrograms/min) was infused directly into the brachiocephalic artery so that aortic pressure before (80 +/- 2 mm Hg) and during (79 +/- 3 mm Hg) the infusion did not change. Neither blood flow to the cerebral hemispheres (P = 0.960), cerebellum (P = 0.854), and brainstem (P = 0.694) nor the cerebral metabolic rate for oxygen (P = 0.862) differed when values obtained before and after 30 min of phenylephrine infusion were compared. Cerebral vascular resistance was also unchanged by phenylephrine, being 1.22 +/- 0.10 mm Hg.mL-1.min-1 x 100 g-1 before infusion and 1.25 +/- 0.17 mm Hg.mL-1.min-1 x 100 g-1 during infusion (P = 0.849). Phenylephrine does not cause cerebral vasoconstriction after rewarming from hypothermic CPB, a finding which suggests that the blood-brain barrier is preserved during bypass.

Animals↗

PubMed1990

The effects of phenylephrine on right ventricular performance in patients with pulmonary hypertension.

Pulmonary hypertension causes right ventricular ischemia and failure as a result of increased afterload combined with reduced coronary blood flow. Increasing coronary driving pressure by raising aortic pressure with phenylephrine has been shown to reverse right ventricular ischemia from pulmonary hypertension in animals. Since vasodilators often fail to reduce afterload, we tested whether raising the coronary driving pressure would improve right ventricular function in man. Ten patients with pulmonary hypertension had hemodynamics and right ventricular coronary driving pressure measured before and 10 minutes after a steady state was reached with a phenylephrine infusion titrated to raise aortic pressure by 25 percent. Phenylephrine caused a significant (p less than .01) increase in mean aortic pressure (84 to 108 mm Hg) and right ventricular coronary driving pressure (46 to 69 mm Hg). In response, there was a significant (p less than .01) rise in mean pulmonary artery pressure (58 to 67 mm Hg), right ventricular end-diastolic pressure (10 to 16 mm Hg) and wedge pressure (5 to 9 mm Hg), and an insignificant fall in cardiac output (3.26 to 3.09 L/min) and pulmonary artery O2 saturation (57 to 49 percent). Although phenylephrine increased right ventricular coronary driving pressure, it worsened right ventricular function as manifest by a rise in end-diastolic pressure and fall in cardiac output. Any benefit of raising right ventricular coronary driving pressure may have been offset by alpha vasoconstriction of right ventricular coronary blood flow and/or pulmonary arterial vasoconstriction. Phenylephrine does not appear to be a useful therapy of right ventricular failure from pulmonary hypertension in patients who fail vasodilators.

Adult↗

PubMed1986

Further evidence implicating diacylglycerol generation and protein kinase C activation in agonist-induced increases in glucose uptake. Insulin-like effects of phenylephrine in BC3H-1 myocytes.

We have previously suggested that insulin effects on 2-deoxyglucose (2-DOG) uptake in BC3H-1 myocytes are due to increases in de novo phospholipid synthesis, diacylglycerol generation, and protein kinase C activation. To test this hypothesis further, we examined the effects of phenylephrine, an agonist that increases diacylglycerol and protein kinase C activity through phospholipase C activation. As evidence for phospholipase activation in BC3H-1 myocytes, we found that phenylephrine increased acute 32PO4 incorporation into phosphatidic acid and phosphatidylinositol, generation of [3H]inositol phosphates from prelabeled [3H]inositol phospholipids, cytosolic Ca2+, and membrane-bound protein kinase C. Phenylephrine also provoked dose-related increases in [3H]2-DOG uptake that were similar in magnitude and time course to those induced by insulin. As with insulin, phenylephrine effects on 2-DOG uptake were not apparent in myocytes that were maximally stimulated with 12-O-tetradecanoylphorbol-13-acetate, a diacylglycerol analogue that activates protein kinase C. These findings support our hypothesis that diacylglycerol generation and protein kinase C activation may be important in the stimulation of glucose uptake by agents such as phenylephrine and insulin that activate the phosphoinositide cycle.

Animals↗

PubMed2006

Effects of increasing infusion rates of dopamine, dobutamine, epinephrine, and phenylephrine in healthy anesthetized cats.

OBJECTIVE: To determine the cardiopulmonary effects of increasing doses of dopamine, dobutamine, epinephrine, and phenylephrine and measure plasma concentrations of norepinephrine, epinephrine, and dopamine in cats anesthetized with isoflurane. ANIMALS: 6 healthy adult cats. PROCEDURES: Each cat was anesthetized with isoflurane (1.5 X minimum alveolar concentration) on 4 occasions. Cardiopulmonary measurements were obtained after a 30-minute stabilization period; 20 minutes after the start of each infusion dose; and 30, 60, and 90 minutes after the infusion was discontinued. Cats received 5 progressively increasing infusions of epinephrine or phenylephrine (0.125, 0.25, 0.5, 1, and 2 microg/kg/min) or dobutamine or dopamine (2.5, 5, 10, 15, and 20 microg/kg/min). The order of treatment was randomly allocated. Results-All 4 treatments increased oxygen delivery. Heart rate (HR) increased during administration of all drugs except phenylephrine, and mean arterial pressure increased during administration of all drugs except dobutamine. A progressive metabolic acidosis was detected, but whole-blood lactate concentration only increased during administration of epinephrine and dobutamine. Systemic vascular resistance index increased during administration of phenylephrine, decreased during administration of dobutamine, and remained unchanged during administration of dopamine and epinephrine. A positive inotropic effect was detected with all treatments. CONCLUSIONS AND CLINICAL RELEVANCE: During anesthesia in cats, administration of dopamine, dobutamine, and epinephrine may be useful for increasing cardiac output, with dopamine having the most useful effects. Administration of phenylephrine increased cardiac and systemic vascular resistance indexes with minimal effect on HR and may be useful for increasing mean arterial pressure without increasing HR.

Adrenergic Agonists↗

PubMed1989

Effect of phenylephrine, ergonovine, oxytocin and norepinephrine as an extender ingredient on viability of bovine spermatozoa.

We evaluated effects of three concentrations of phenylephrine, ergonovine, oxytocin and norepinephrine (myometrial stimulants) on viability of spermatozoa when they were included in a seminal extender. Using a split ejaculate technique, ejaculates from each of 10 bulls were extended in egg-yolk citrate to a final concentration of 35 x 10(6) sperm/ml, including 20 mg/ml, 2 mg/ml and .2 mg/ml, of phenylephrine or ergonovine, 20 IU/ml, 2 IU/ml and .2 IU/ml oxytocin or 200 micrograms/ml, 20 micrograms/ml and 2 micrograms/ml norepinephrine prior to freezing. Extended semen without a myometrial stimulant served as the control. Percentage of intact acrosomes was determined prior to freezing for all treatments. Motility and percentage of intact acrosomes were determined immediately after thawing (0 h) and again after 4 h incubation at 37 degrees C. Percentage of intact acrosomes was reduced (P less than .05) prior to freezing by phenylephrine (20 mg/ml) and ergonovine (20 mg/ml) (phenylephrine = 56%; ergonovine = 63%; control = 74%). The same doses of phenylephrine and ergonovine reduced (P less than .05) post-thaw motility and percentage of intact acrosomes at both 0 and 4 h compared with controls. Sperm exposed even to the intermediate concentration (2 mg/ml) of ergonovine had lower (P less than .05) motility 4 h post-thaw. No other compound or concentration of compound or concentration of compound affected percentage of intact acrosome or motility. There were no two or three-way bull x compound and concentration interactions (P greater than .2).(ABSTRACT TRUNCATED AT 250 WORDS)

Acrosome↗