Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PHENTOLAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMedDate not supplied

Influence of phentolamine on platelet aggregation, thromboxane B2 production and release reaction.

In this study the in vitro influence of phentolamine on platelet aggregating responses, thromboxane B2 (TxB2) production and intraplatelet cyclic AMP (cAMP) content has been investigated. The drug exerts a dose-dependent inhibitory effect on aggregating response to ADP, PAF, collagen, thrombin, sodium arachidonate and ionophore A 23187. Inhibiting phentolamine concentrations prevent also platelet release reaction and TxB2 synthesis. No significant influence on intraplatelet cAMP levels has been observed. The pre-incubation with low concentrations of ionophore A 23187 overcomes phentolamine inhibition of collagen-induced platelet aggregation. Our results provide evidence that phentolamine modulates the human platelet function and that its effects could also be related to a decrease of Ca++ availability.

Adenosine Diphosphate↗
PubMed1985

Hepatic microvascular regulatory mechanisms. VI. Effects of lodoxamide tromethamine or phentolamine-HCl on early hemodynamic and glucoregulatory alterations evoked by endotoxin.

Initial changes in hepatic microvasculature and systemic arterial blood pressure were measured in non-fasted and anesthetized Sprague-Dawley rats receiving an i.v. infusion, or a topical application to the surface of the liver, of endotoxin (S. typhimurium) and/or phentolamine or lodoxamide. Circulating blood glucose and hepatic glycogen content were determined in infused rats. Injection of 10 mg per kg b.w. endotoxin, or topical administration of 10 micrograms endotoxin and/or antagonists, elicited no change in carotid (arterial) blood pressure. Infusion was accompanied by an elevation in blood glucose within 15 min and a decrease in hepatic glycogen content by 35 min. Injection of 1.0 mg per kg b.w. phentolamine blocked the endotoxin-induced hyperglycemia without affecting hepatic glycogenolysis. However, the alpha-adrenergic antagonist by itself provoked systemic hypotension, mild hypoglycemia, and hepatic glycogen depletion within 35 min. In vivo microscopy revealed that 10 micrograms endotoxin evoked immediate constriction of portal venules and periportal sinusoids. Vasoconstriction was accompanied by an increase in the percentage of microvascular segments containing decreased cellular blood flow velocity. These responses were blocked by 0.1 microgram lodoxamide but not by 100 micrograms phentolamine. The lodoxamide-induced inhibition was reversed by reapplication of 10 micrograms endotoxin 15 min following blockade. Given these results, it is suggested that (a) microvascular responses elicited by endotoxin were mediated by released constituents from intrahepatic mast cells and not by activation of alpha-adrenergic receptors, and (b) phentolamine blocked endotoxin-induced initial hyperglycemia by virtue of its hypoglycemic, glycogenolytic and/or hypotensive effects.

Amino Acids↗
PubMed1985

Comparison of phentolamine and urapidil in controlling acute intra-operative hypertension in patients subjected to coronary artery bypass surgery.

Intra-operative hypertensive episodes are a frequent problem in patients undergoing coronary artery bypass grafting. The haemodynamic effects of the alpha-adrenergic blocking drugs phentolamine and urapidil, two alpha-adrenergic blocking drugs with a different alpha-receptor subtype specificity, when used to control intra-operative hypertension were evaluated. Ten patients received phentolamine (about 25 micrograms kg-1 min-1) and ten patients received urapidil (about 100 micrograms kg-1 min-1) to return arterial blood pressure to control levels. Both drugs decreased arterial pressure to baseline values within 2-3 minutes by reducing the elevated systemic vascular resistance. Treatment with phentolamine was accompanied by a marked increase in heart rate with a concomitant increase in cardiac index and the rate-pressure product. Urapidil caused no change in heart rate, but the cardiac index increased. Urapidil lowered the rate-pressure product significantly. Both drugs reduced mean pulmonary artery and pulmonary capillary wedge pressures. The different selectivity of phentolamine and urapidil to alpha 1-and alpha 2-adrenergic receptors induces the diverse haemodynamic effects. We conclude that the use of urapidil is the superior regimen when an alpha-adrenergic blocking agent is favoured as a vasodilator.

Acute Disease↗
PubMed1985

[Hemodynamic and respiratory effects of phentolamine in pulmonary hypertension secondary to chronic obstructive syndrome].

The hemodynamic and respiratory effects of phentolamine i.v. (15-30 mg/h) on pulmonary hypertension following chronic obstructive pulmonary disease (COPD) have been studied in 13 patients under stable conditions. Phentolamine produced a significant reduction in mean pulmonary arterial pressure, right and left ventricular filling pressures and right ventricular stroke work index. Cardiac index and oxygen delivery increased significantly. Individual analysis showed that in 7 patients the driving pressure decreased across the pulmonary circulation with concomitant increase in cardiac output, suggesting a direct vasodilating effect of phentolamine on the pulmonary circulation. Pulmonary gas exchange did not change significantly. In conclusion, in patients with pulmonary hypertension following COPD phentolamine given i.v. may have beneficial effects on right ventricular function and peripheral oxygen delivery without detrimental effect on gas exchange.

Aged↗
PubMed1982

Depression of reflex vagal bradycardia by a central action of phentolamine in the spinal cat.

Cats were anaesthetized with a mixture of alpha-chloralose and urethane and artificially ventilated. The spinal cord was transected at the C-1 level and the fourth cerebral ventricle cannulated. Phentolamine (500 microgram) administered into the fourth cerebral ventricle depressed the reflex vagal bradycardic responses elicited by intravenous pressor doses of noradrenaline. Enhancement of reflex bradycardia occurred following intracerebroventricular administration of L-DOPA (3.0 mg) which was reversed by subsequent administration of phentolamine into the fourth cerebral ventricle of spinal cats. These results suggest that central noradrenergic stimulation enhances and noradrenergic blockade suppresses the reflex vagal activation. In midcollicular decerebrate cats, intracerebroventricular administration of phentolamine reduced the reflex bradycardic responses elicited by intravenous noradrenaline. It is suggested that the action of phentolamine to depress baroreceptor mediated reflex vagal activation is on sites within the pontomedullary areas of the cat.

Animals↗
PubMed1977

[Effect of phentolamine on cerebral circulation].

The influence of phentolamine hydrochloride on the volumentric circulation rate of the cerebral blood flow, the tone of the cerebral vessels and oxygen tension in the cerebral tissue was studied in acute experiments on anesthetized and nonanesthetized cats. Injected intravenously, phentolamine hydrochloride was found to lower the intra- and extracranial vessels for a long time, the latter to a greater extent. The circulation rate of the cerebral blood flow decreased under conditions of a significant hypotension caused by phentolamine hydrochloride and increased with a stable perfused pressure; pO2 changes in the cerebral tissue corresponded mostly to the blood flow. Preliminary atropinization of the animals and denervation of the carotid regions failed to influence the effect of phentolamine hydrochloride. The latter decreased or prevented the vasoconstrictor action of norepinephrine and phenylephrine hydrochloride (mesatone) on the cerebral vessels.

Animals↗
PubMed1997

Comparative study of papaverine plus phentolamine versus prostaglandin E1 in erectile dysfunction.

PURPOSE: We compared the efficacy and short-term adverse effects of 1 ml. 30 mg./ml. papaverine plus 0.5 mg./ml. phentolamine versus 1 ml. 30 micrograms./ml. prostaglandin E1 in patients undergoing pharmacological erection testing. MATERIALS AND METHODS: A total of 60 patients (mean age 58 years) with a history of sexual erectile dysfunction longer than 6 months was randomly classified into 6 groups to be tested 1 week apart with the 2 solutions and with placebo to evaluate erection response and short-term adverse effects. RESULTS: Of the patients tested with papaverine plus phentolamine 54% responded with erections adequate for penetration, compared to 50% of those tested with prostaglandin E1 (p > 0.05). Prolonged erection occurred in 18% of patients tested with papaverine plus phentolamine and 15% of those tested with prostaglandin E1 (p > 0.05). Pain was reported by 15 and 35% of patients, respectively (p < 0.05). CONCLUSIONS: One ml. 30 mg./ml. papaverine plus 0.5 mg./ml. phentolamine has the same efficacy and equal prolonged erection rate as 1 ml. 30 micrograms./ml. prostaglandin E1 but the latter agent induces significantly more pain.

Adult↗
PubMed1994

Phentolamine reversal of epinephrine-induced digital vasospasm. How to save an ischemic finger.

A 17-year-old girl accidently injected her thumb with an adult autoinjector epinephrine syringe, resulting in rapid digital ischemia. Local infiltration of 0.5% phentolamine mesylate injected at the puncture site immediately resolved the ischemia and resulted in no long-term sequelae. Similar cases of epinephrine-induced digital ischemia are reviewed herein, revealing phentolamine to be the drug of choice for reversal of this type of ischemia. Alternative attempts to restore blood flow included warm water immersion, amyl nitrite inhalations, metacarpal nerve block, and application of topical nitroglycerin paste; each was found to be ineffective. We conclude that digital ischemia secondary to accidental injection of epinephrine can be quickly and safely reversed with the use of 0.5% phentolamine locally infiltrated in the region of accidental injection.

Accidents↗
PubMed2000

Phentolamine prevents the adverse effects of adenosine on glycolysis and mechanical function in isolated working rat hearts subjected to antecedent ischemia.

Adenosine inhibits glycolysis from exogenous glucose, reduces proton production and enhances post-ischemic left ventricular minute work (LV work) following ischemia in isolated working rat hearts perfused with glucose and fatty acids. In hearts partially depleted of glycogen by antecedent ischemic stress (AIS)--two cycles of ischemia (10 min) and reperfusion (5 min)--adenosine stimulates rather than inhibits glycolysis, increases proton production and worsens recovery of post-ischemic LV work. We determined if the switch in adenosine effect on glycolysis and recovery of LV work following ischemia in hearts subject to AIS was due to the reduction in glycogen content per se or because of alpha-adrenoceptor stimulation. One series of hearts underwent a 35-min period of substrate-free Langendorff perfusion (substrate-free glycogen depletion; SFGD) and a second series of hearts was subjected to AIS. Both series of hearts had a similar glycogen content (approximately 70 micromol/g dry wt) prior to drug treatment. In SFGD hearts perfused aerobically, adenosine (500 microM) inhibited glycolysis from exogenous glucose and reduced proton production. In SFGD hearts reperfused after prolonged ischemia, adenosine exerted similar effects on glucose metabolism and enhanced recovery of post-ischemic LV work (87.2 +/- 2.2% of preischemic values) relative to untreated hearts (25.9 +/- 13.3% of preischemic values). In AIS hearts perfused aerobically or subject to ischemia and reperfusion, phentolamine (1 microM) given in combination with adenosine, prevented adenosine-induced stimulation of glycolysis from exogenous glucose and reduced calculated proton production from glucose. Recoveries of post-ischemic LV work in AIS hearts for untreated, adenosine, phentolamine and adenosine/phentolamine groups were 34.4 +/- 11.4%, 8.6 +/- 3.9%, 16.3 +/- 13.5% and 73.2 +/- 13.1% respectively, of preischemic values. Glycogen depletion in the absence of ischemia does not switch the effect of adenosine from inhibition to stimulation of glycolysis or alter the cardioprotective properties of adenosine in hearts subject to ischemia and reperfusion. The detrimental switch in the metabolic and cardioprotective effects of adenosine, in hearts subject to AIS, can be prevented by phentolamine, an alpha-adrenoceptor antagonist. These data support the concept that modulation of glucose metabolism is an important factor in the mechanical functional recovery of the post-ischemic heart.

Adenosine↗
PubMed1975

Effects of phentolamine, dihydroergocristine and isoxsuprine on the blood pressure and heart rate in normotensive, hypotensive and hypertensive rats.

Phentolamine, dihydroergocristine and isoxsuprine were compared for their effects on the blood pressure in anaesthetized normotensive rats, in rats made hypotensive by ganglionic blockade or by pithing and in rats with noradrenaline-induced hypertension. Their ability to inhibit pressor responses elicited by electrical stimulation of the posterior hypothalamus and of the sympathetic outflow from the spinal cord was also investigated. All three drugs appeared very potent in inhibiting noradrenaline-induced hypertension and caused a dose-dependent fall in blood pressure in normotensive rats, which however was less pronounced with dihydroergocristine than with phentolamine and isoxsuprine. In hypotensive rats, dihydroergocristine caused a rise in blood pressure. At higher doses than those required to block noradrenaline-induced hypertension, the three drugs inhibited pressor responses elicited by electrical stimulation and were equally active on peripherally- and centrally-evoked responses. Simultaneous recording of heart rate and blood pressure, both in anaesthetized and in pithed rats, indicated a reflex origin for phentolamine-induced tachycardia and a direct cardiac stimulation for isoxsuprine. Reflex changes of heart rate were not observed with dihydroergocristine.

Animals↗
PubMed1982

Evidence that phentolamine is not an inhibitor of extraneuronal uptake.

1. Tracheal segments from guinea-pigs pretreated with 6-hydroxydopamine were incubated in isoprenaline at 37 degrees C for 5 min in the absence or presence of phentolamine. Catechol-O-methyl transferase was inhibited by 100 mumol l-1 U-0521. Tissues were prepared for fluorescence histochemistry and accumulated isoprenaline in trachealis smooth muscle cells (fluorescence) was measured by microphotometry. 2. Phentolamine, in concentrations up to 100 mumol l-1, had no effect on isoprenaline fluorescence. 3. It is concluded that phentolamine does not inhibit extraneuronal uptake in concentrations used to block alpha-adrenoceptors in isolated tissue experiments. Thus, is can be present in experiments designed to examine the effects of extraneuronal uptake inhibitor drugs on beta-adrenoceptor-mediated responses.

Animals↗
PubMed1977

Inhibition of adrenaline-induced platelet aggregation by the orally administered alpha-adrenergic receptor blocker phentolamine (Regitine).

In eight healthy volunteers pretreatment with phentolamine 40 mg p o inhibited platelet aggregation (1st and 2nd phases) induced by low concentrations of adrenaline (2, 1 and 0.5 muM) in plasma from blood sampled 30 min after administration of the compound. The lower the concentration of adrenaline use, the greater was the degree of inhibition elicited. These results are indicative of competitive inhibition of the action of adrenaline on the platelet membrane by phentolamine. Four to six hours after administration of the compound, the aggregation characteristics had reverted to normal. It is concluded that the increased tendency toward platelet aggregation associated with elevated blood levels of catecholamines can be prevented by therapeutic doses of phentolamine.

Administration, Oral↗
PubMed1978

Treatment of chronic heart failure with slow release phentolamine.

Oral medication with phentolamine SR produced subjective and objective improvement in all 45 patients with refractory chronic heart failure of various aetiologies, who were already receiving digitalis and diuretics. This was shown by an increase in pulse-pressure amplitude and urine volume, a decrease in bodyweight and marked reduction in cardiac size and pulmonary congestion, the latter changes being more pronounced in patients with arteriosclerotic heart disease (ASHD). Exercise tolerance tests in a further 34 patients with less severe chronic heart failure demonstrated that phentolamine SR markedly increased physical capacity. This effect was more pronounced in patients with slightly compromised cardiac status (functional Class 2, NYHA) than in those with moderately compromised cardiac status (Class 3). The improvement in clinical condition was attributed mainly to arterial and venous dilatation, as well as to the positive inotropic effect of the drug. The most important side-effects were diarrhoea and, in the patients with ASHD, increased attacks of angina pectoris; The side-effects were well controlled by the anticholinergic agent oxyphenonium bromide (Antrenyl) and a slight increase in the dose of nitrates. It is concluded that oral phentolamine SR may be a valuable therapeutic adjunct in the management of patients with refractory chronic heart failure.

Adult↗
PubMed1982

The effect of phentolamine on synaptosomal phosphatidylinositol in experimental galactose toxicity.

Abnormal myo-[2-3H]inositol incorporation into phosphatidylinositol has been found in phentolamine-treated synaptosomes that were isolated from the cerebral hemispheres of galactose toxic rats and incubated with [33P]Pi and myo-[2-3H] inositol. In galactose toxic rats phentolamine-stimulated myo-[2-3H]inositol labeling of phosphatidylinositol was 70% greater than in normal animals. This enhanced labeling of synaptosomal phosphatidylinositol in galactose toxic rats during stimulation with phentolamine is in marked contrast to the depressed myo-inositol labeling of phosphatidylinositol reported with acetylcholine stimulation.

Animals↗
PubMed1990

[Effect of pituitrin or phentolamine alone or in combination on WHVP and systemic hemodynamics in patients with liver cirrhosis].

We observed the effect of pituitrin and phentolamine alone or in combination on wedged hepatic venous pressure (WHVP) and systemic hemodynamics in 28 patients with cirrhosis. The results showed that either of these drugs used separately could lead to reduction in WHVP, each of them could also cause by-effects on systemic hemodynamics. When pituitrin in combination with phentolamine was administered, no change could be found in inferior vena cava pressure, mean arterial pressure, pulse rate and cardiac index. This suggested that pituitrin in combination with phentolamine could not only efficaciously decrease WHVP, but also counteract side effects on systemic hemodynamics of each other and improve hepatic microcirculation. Our study provided evidence for the usefulness of the combination of the two drugs in controlling bleeding from esophagus varices.

Adult↗
PubMed1992

Different effects of prostacyclin and phentolamine on delivery-dependent O2 consumption and skin microcirculation after cardiac surgery.

Inadequate tissue oxygen uptake autoregulation has been reported during the first hours after extracorporeal circulation for cardiac surgery. In the present study, we examined whether a dependence of oxygen consumption (VO2) on oxygen delivery (DO2) can be detected 24 hr after cardiac surgery using two different vasodilating agents. Cardiac output in triplicate was measured by thermodilution. Oxygen saturation of arterial and mixed venous blood was measured using a CO-oximeter. Oxygen consumption was assessed from the reverse Fick equation. In addition skin blood flow was assessed continuously by laser Doppler flowmetry. To investigate the VO2/DO2 relationship in 15 patients an increase in cardiac output and DO2 of at least 15% was achieved by systemic vasodilatation with iv prostacyclin (5-10 ng.kg-1.min-1) or phentolamine (5-10 g.kg-1.min-1). Infusion of phentolamine produced a 29 +/- 2% (mean +/- SE) increase in DO2 which was associated with a 20 +/- 6% increase in VO2. In contrast, prostacyclin produced a 22 +/- 3% increase in DO2 without change in VO2. Phentolamine did not alter skin microvascular blood flow, whereas prostacyclin increased skin microvascular blood flow by 33 +/- 3%. The results of the present study demonstrate a supply-dependency of VO2 in clinically stable patients 24 hr after cardiac surgery, suggesting the presence of an inadequate tissue O2 uptake autoregulation. The type of the vasodilator used to increase DO2 seems to play an important role in detecting such a supply-dependency of VO2, as well as changes of skin blood flow.

Adult↗
PubMed2000

Glucose dilution can detect fluid redistribution following phentolamine infusion in dogs.

OBJECTIVE: We have recently reported that the initial distribution volume of glucose (IDVG) reliably measures the central extracellular fluid (ECF) volume in the presence of fluid gain or loss. However, it is not clear if IDVG consistently reflects central-ECF volume when redistribution of fluid occurs in the absence of fluid gain or loss. This study was designed to investigate changes in fluid volumes during phentolamine infusion in dogs. DESIGN: Prospective animal study. SETTING: Institutional animal research laboratory. SUBJECTS: Fourteen anesthetized and ventilated mongrel dogs. INTERVENTIONS: Anesthetized animals were mechanically ventilated and received infusions of normal saline (n = 7) or phentolamine (10 microg kg min) (n = 7). Plasma volume was estimated using the indocyanine green (ICG) dilution method (PV-ICG) and IDVG was calculated using a one-compartment model by simultaneous administration of ICG 0.5 mg/kg and glucose 100 mg/kg before, during, and after infusion of either drug. MEASUREMENTS AND RESULTS: PV-ICG during infusion was not different between groups. However, IDVG significantly decreased (P < 0.05) following phentolamine infusion when compared with normal saline infusion. CONCLUSION: Our results suggest that IDVG rather than PV-ICG consistently measures central extracellular fluid volume, even when redistribution of fluid occurs.

Adrenergic alpha-Antagonists↗
PubMed1977

Afterload reduction with phentolamine in patients with acute pulmonary edema.

Phentolamine in amounts of 10 to 40 microgram/kg/min was infused intravenously for the emergency treatment of acute pulmonary edema due to left ventricular failure. Fourteen patients with arteriosclerotic heart disease, ranging in age from 52 to 87 years, had clinical and roentgenographic signs of pulmonary edema. The pulmonary artery wedge pressure was increased to an average of 24 mm Hg and the cardiac index was decreased to 1.9 liters/min/m2 or less prior to the administration of phentolamine. A reduction in the pulmonary artery wedge pressure to 14 mm Hg and an increase in the cardiac index to 2.5 liters/min/m2 was observed in response to this alpha adrenergic blocking agent. Reduction in peripheral resistance with phentolamine was associated with reversal of pulmonary edema.

Acute Disease↗