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PubMed1981

Enhancement of phentolamine by nitrates in patients with congestive heart failure.

Phentolamine dilates the resistance bed and to a lesser degree the capacitance bed, while the nitrates have the opposite action. Therefore, in 7 patients with congestive heart failure due to congestive cardiomyopathy, hemodynamic measurements were made using a Swan Ganz thermodilution catheter and cardiac output computer. The patients received 5 mg of an IV infusion of phentolamine administered at 0.3 mg/minute. At the end of the infusion, the pressures and cardiac output were obtained. Then, 2 1/2 inches of nitroglycerin ointment was applied to the chest, and the hemodynamic parameters were obtained 30 minutes later. Phentolamine produced a significant reduction in the right and left ventricular filling pressures and a significant increase in the cardiac output. The hemodynamic effects of phentolamine are known to persist for an hour or longer. The addition of nitroglycerin ointment led to a further reduction in the right and left ventricular filling pressures. Thus, the combination of phentolamine and nitrates can be effectively used in the treatment of congestive heart failure.

Blood Pressure↗
PubMed1984

Hypotension and arteriovenous shunting: effects of intravenous infusion of nitroprusside, nitroglycerin and phentolamine.

The effects of nitroprusside, nitroglycerin and phentolamine on cardiac dynamics and on the fraction of cardiac output shunted through systemic arteriovenous communications, which may explain disparate responses elicited by these systemic vasodilators upon venous return, have been studied in 15 nonanesthetized dogs. Cardiac dynamic parameters were measured by electromagnetic flow probe placed at the root of the aorta. Quantitative measurements of total systemic arteriovenous shunting were determined from the fraction of 9 mu radioactively labeled microspheres, injected into the left atrium, recovered in the pulmonary artery. To provide a common basis for comparison, the mean arterial pressure was lowered by 15-20% either with an intravenous infusion of nitroprusside, nitroglycerin or phentolamine. At the fifteenth minute of infusion, nitroprusside produced significant decrease in stroke volume index (23%) and left ventricular power and work (28% and 40%). Nitroglycerin decreased significantly stroke volume index (12%), cardiac index (9%) and left ventricular work (22%). Phentolamine significantly increased heart rate (72%) and left ventricular maximum acceleration (30%) while it decreased stroke volume index (41%), left ventricular power and work (19% and 55%). Total peripheral resistance was significantly affected only by infusion of phentolamine (-18%). Left ventricular maximum velocity, mean systolic ejection rate and maximum systolic flow did not change significantly under infusion of these systemic vasodilators. Under control conditions, total systemic shunting of cardiac output averaged 8.9-10% and was not modified by any of the vasodilators used. Arteriovenous O2 difference and oxygen consumption, corroborated these findings since they remained within normal limits before and after infusion of nitroprusside, nitroglycerin or phentolamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Relief of acute pain in chronic idiopathic gastroparesis with intravenous phentolamine.

OBJECTIVE: To report a case in which complete relief of pain associated with gastroparesis, with promotion of gastric emptying, was achieved with administration of phentolamine. CASE SUMMARY: A 37-year-old opiate-tolerant female with a history of recurrent abdominal pain, gastroparesis, cyclic vomiting syndrome, and migraine headaches was admitted to the emergency department (ED) with severe acute abdominal pain, nausea, and vomiting. The patient had been previously implanted with a permanent gastric electrical stimulator and she was adherent to her prokinetic, antiemetic, analgesic, and migraine prophylactic medications. Pain relief was achieved rapidly and completely in the ED with sympatholysis by administration of intravenous phentolamine 0.5 mg/kg over 60 minutes, with continuous cardiac monitoring. At a 2 month follow-up visit, the patient reported chronic pain relief, and a decrease in opiate doses was maintained by oral administration of clonidine 0.1 mg twice daily. DISCUSSION: Gastroparesis represents a difficult treatment challenge because management of gastric dysmotility and the accompanying severe abdominal pain is often mutually exacerbating and ineffective. Sympatholysis by intravenous phentolamine provided profound and immediate relief of acute gastroparesis-related abdominal pain in our patient. The mechanism of phentolamine is believed to be receptor blockade at alpha-adrenergic receptors and, therefore, inhibition of the peripheral sensitizing effects of circulating norepinephrine. Although action at a peripheral nerve level is presumed, modulation of alpha-adrenoreceptors receptors is also possible at the dorsal root ganglion or at other central nervous system sites. CONCLUSIONS: The dramatic relief of acute pain in gastroparesis by phentolamine observed in this case would warrant investigation of a larger, controlled case series. Patients who respond to intravenous sympatholysis may likewise be candidates for longer term sympathetic modulation with oral sympatholytics.

Abdominal Pain↗
PubMed1998

Blocking effects of phentolamine on L-type calcium current and ATP-sensitive potassium current in guinea pig ventricular myocytes.

AIM: To study the effect of phentolamine on L-type calcium currents (ICa) and ATP-sensitive K+ currents (IK,ATP) in ventricular myocytes. METHODS: ICa and IK,ATP were observed using patch clamp techniques in whole-cell recording configuration. RESULTS: Phentolamine reduced ICa of ventricular myocytes in concentration-dependent and voltage-independent manners. Phentolamine 5, 25, and 100 mumol.L-1 decreased ICa from 370 +/- 99 nA to 310 +/- 95 nA (17% block, n = 6, P < 0.01), from 230 +/- 98 nA to 180 +/- 73 nA (23% block, n = 5, P < 0.05), and from 293 +/- 66 nA to 206 +/- 44 nA (30% block, n = 5, P < 0.01), respectively, without affecting the current-voltage relationship. Prazosin 100 mumol.L-1 and yohimbine 100 mumol.L-1, which were specific blockers of alpha 1 and alpha 2 adrenoceptors respectively, did not show the inhibitory effect on ICa. Phentolamine 100 mumol.L-1 also inhibited the IK,ATP induced by 2, 4-dinitrophenol (DNP) at 0 mV from 3.2 +/- 0.6 nA to 0.8 +/- 0.5 nA (75% block, n = 4, P < 0.01). CONCLUSION: Phentolamine directly inhibits ICa and IK,ATP in guinea pig ventricular myocytes.

Adrenergic alpha-1 Receptor Antagonists↗
PubMedDate not supplied

Phenothiazine compounds enhance phentolamine effects on platelet aggregation and thromboxane B2 production.

In the present study we investigated the influence of phentolamine and the phenothiazine compounds chlorpromazine and trifluoperazine on human platelet aggregation as well as the effect of the association of phentolamine and the phenothiazines on responses to adenosine diphosphate, collagen, thrombin, ionophore A23187 and phorbol-myristate acetate, release reaction, thromboxane B2 synthesis and intraplatelet cyclic adenosine monophosphate levels. Phentolamine and phenothiazines exerted a dose-dependent inhibitory effect on aggregation induced by different concentrations of adenosine diphosphate and decreased the response to other agonists; furthermore, the phenothiazines enhanced the inhibitory effects of phentolamine on aggregation and thromboxane B2 synthesis, without influencing intraplatelet cyclic adenosine monophosphate levels. Phorbol ester-induced platelet activation was also inhibited in a dose-dependent way by each compound and by an association of phentolamine and phenothiazines, suggesting that the antiplatelet properties of these compounds might also be ascribed to intracellular events.

Adenosine Diphosphate↗
PubMed1990

The effect of phentolamine on the pressor response to centrally administered clonidine in rats.

In the present study we investigate the effect of the previous injection of phentolamine (a nonspecific alpha-adrenergic antagonist) into the lateral hypothalamus (LH) and lateral ventricle (LV) on the pressor and bradycardic responses produced by the injection of clonidine (an alpha 2-adrenergic agonist) into these same areas of conscious rats. The injection of clonidine into the LV and LH produced pressor (39 +/- 5 and 38 +/- 3 mmHg, respectively) and bradycardic responses (-65 +/- 16 and -94 +/- 13 bpm, respectively). Previous injection of phentolamine into the LH or LV reduced the pressor response to clonidine injected into the same areas (delta MAP = 13 +/- 6 mmHg for LH and 1 +/- 3 mmHg for LV). No reduction was observed when clonidine was injected into the LV after the injection of phentolamine into the LH. No changes in bradycardic responses were observed after treatment with phentolamine. The present results show the participation of alpha-adrenergic receptors in the pressor response to centrally administered clonidine but not in the bradycardic response. The data also suggest that the pressor effect produced by the injection of clonidine into the LH is due to the activation of alpha-adrenergic receptors located specifically in this area. The pressor response after injection of clonidine into the LV and of phentolamine into the LH is due to the action of clonidine on other cerebral areas.

Animals↗
PubMed1988

Endothelial potentiation of relaxation response to phentolamine in rat thoracic aorta.

In this study the role of the endothelium was evaluated in the relaxation of rat aortic rings induced by a number of alpha adrenergic antagonists. Phentolamine, a nonselective alpha adrenergic antagonist, relaxed rat aortic rings that were previously contracted with an EC80 dose of phenylephrine, in a concentration-dependent manner. Removal of the endothelium significantly reduced the sensitivity but not the amplitude of the response. The presence of endothelium also enhanced the vascular relaxation induced by yohimbine, a specific alpha-2 adrenergic antagonist (10(-8)-10(-6) M), and by prazosin, a specific alpha-1 adrenergic antagonist (10(-11)-10(-9) M). Both methylene blue (10(-5) M), an inhibitor of soluble guanylate cyclase, and eicosatetraynoic acid (3.2 X 10(-5) M) blocked the endothelial augmentation of vascular relaxation to phentolamine. Vessels precontracted with potassium chloride were slightly relaxed by phentolamine (10(-8)-10(-6) M) only with the endothelium was intact. Both methylene blue and eicosatetraynoic acid also inhibited the response to phentolamine in the intact vessels precontracted with potassium chloride. Prazosin (10(-9)-10(-7) M) and yohimbine (10(-8)-10(-6) M), unlike phentolamine, failed to induce relaxation in potassium chloride-precontracted vessels. When the vessels were precontracted with the thromboxane analog U46619 none of the three alpha antagonists induced vascular relaxation. These results indicate that the endothelium has a significant role in promoting relaxation induced by the three alpha adrenergic antagonists tested.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1985

Functional involvement of vasopressin in the maintenance of systemic arterial blood pressures after phenoxybenzamine or phentolamine administration: studies in Long-Evans and Brattleboro rats.

The alpha adrenoceptor antagonists phenoxybenzamine and phentolamine are reported to have opposite effects on vasopressin release, the former inhibiting and the latter enhancing it. In this study we have assessed the functional involvement of vasopressin in the maintenance of blood pressure in conscious rats after administration of either phenoxybenzamine or phentolamine. In normal (Long-Evans) rats, phenoxybenzamine caused a small fall in arterial blood pressure, whereas phentolamine initially caused a profound hypotension which was followed by a fluctuating recovery back to normotensive levels. Similar effects were seen in rats deficient in hypothalamic vasopressin (Brattleboro strain). Administration of an antagonist of the cardiovascular actions of vasopressin [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-8-D-arginine vasopressin] in the presence of either alpha adrenoceptor antagonist alone was without effect in Long-Evans or Brattleboro rats, but, under these conditions, subsequent administration of captopril caused a profound and sustained hypotension in both strains. Administration of captopril in the presence of either alpha adrenoceptor antagonist alone caused a prompt fall in blood pressure which was sustained for the duration of the experiment in the Brattleboro rats. However, under these conditions, the blood pressure of the Long-Evans rats showed some recovery over the subsequent 45 min; this recovery was antagonized by [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-8-D-argine vasopressin]. It is concluded that after alpha adrenoceptor antagonism with either phenoxybenzamine or phentolamine, the renin-angiotensin system exerts a major pressor influence. However, after captopril administration in the presence of phenoxybenzamine or phentolamine, vasopressin contributes to the maintenance of arterial blood pressure in Long-Evans rats; the magnitude of this contribution is similar irrespective of the alpha adrenoceptor antagonist used.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Intravenous infusion of phentolamine: effects on cardiovascular dynamics and regional blood flow distribution in conscious dogs.

We have studied hemodynamic changes induced by infusion of phentolamine (100 micrograms/kg/min) over 15 min in conscious dogs in order to clarify its mechanism of action. Dogs were prepared with an electromagnetic flow probe, and microspheres (9 microns) were used to measure regional blood flow distribution before and after 15 min of infusion of phentolamine. Controlled hypotension (15-20%) was maintained throughout the infusion, and this hypotensive state was associated with the following significant changes: heart rate increased by 50-70%, stroke volume decreased by 35-42%, left ventricular power and work fell by 15-19% and by 49-56%, respectively, maximum acceleration increased by 26-34%, and total peripheral resistance decreased by 20% while cardiac index was unaffected. Regional blood flow studies showed that phentolamine at the 15th min of infusion induced a significant increase in blood perfusion to all components of the myocardium (range 30-51%) while their vascular resistances showed a significant decrease (35-41%). Blood flow to liver (hepatic artery), spleen, and intestine was also modified (-14, -14, and -15%, p less than 0.05) while their vascular resistances were only slightly decreased. At the time measurements were made, blood flow to cerebral and renal tissues was not affected while their local vascular resistances decreased significantly (15-20%). For each organ studied blood perfusion was uniform. These results indicate that phentolamine elicits both central and peripheral hemodynamic changes and that in most vascular beds studied the vasodilator effect of phentolamine can still be observed at the 15th minute of infusion.

Animals↗
PubMed1983

[Therapy of primary pulmonary hypertension with phentolamine].

The effect of phentolamine was studied in 5 patients with pulmonary hypertension, of whom 3 had primary pulmonary hypertension and 2 had secondary pulmonary hypertension after pulmonary embolism. They received intravenous phentolamine in doses of 0.5 mg/min to 2 mg/min (i.e. up to a total dose of 27.5 mg in 25 minutes) during diagnostic cardiac catheterization. Under phentolamine infusion only 2 of the 3 patients with primary pulmonary hypertension showed a significant rise in cardiac index, from 1.4 to 2.0 and from 1.8 to 2.2 l/min/m2 respectively, a fall in pulmonary artery mean pressure from 100 to 93 and from 42 to 33 mm Hg respectively, and a decrease in pulmonary vascular resistance from 2950 to 1900 and from 1160 to 725 dyn X sec X cm-5 respectively. In 1 patient with primary, and 2 patients with secondary pulmonary hypertension, infusion of phentolamine had no effect. Interestingly, in the two patients with primary pulmonary hypertension who responded well to phentolamine the condition was very severe. It appears that even in cases with very advanced primary pulmonary hypertension there is a vasospastic component which can be influenced by vasodilators.

Adult↗
PubMed1978

Effects of prazosin and phentolamine on responses to field stimulation and to noradrenaline in vas deferens and anococcygeus muscle of the rat.

The effects of phentolamine (10(-6)M) and prazosin (10(-7)M) on contractile responses, in the presence of cocaine or nortriptyline, were investigated in vas deferens and anococcygeus muscle of rat. Cocaine (10(-5)M) and nortriptyline (10(-6)M) had no effect on maximum responses to field stimulation, (--)-noradrenaline, methoxamine, and acetylcholine in anococcygeus muscle. However, both cocaine (3.3 x 10(-5)M) and nortripthline (10(-6)M) potentiated maximum responses to (--)-noradrenaline without altering the maximum response to field stimulation in vas deferens. In vas deferens, phentolamine potentiated or inhibited the responses to field stimulation depending on the frequency whereas prazosin inhibited all responses to field stimulation. In anococcygeus muscle, both phentolamine and prazosin inhibited all responses to field stimulation. In vas deferens and anococcygeus muscle, prazosin was a more potent antagonist of responses to (--)-noradrenaline than phentolamine. These results show that prazosin is a more potent postsynaptic alpha-adrenoceptor antagonist than phentolamine and suggest that prazosin has little or no affinity for presynaptic alpha-adrenoceptors.

Animals↗
PubMed1976

Phentolamine and isoproterenol: comparison of effects on vascular resistance and oxygen uptake in skeletal muscle during hypotension.

Effects of drugs on precapillary vessels and oxygen uptake may differ from effects on resistance vessels and total flow in skeletal muscle. This study was performed to compare effects of phentolamine and isoproterenol, two drugs which are used to treat shock, on oxygen uptake in skeletal muscle. Oxygen uptake of gracilis muscle (GVO2) was measured in muscles perfused at constant flow or constant pressure in normotensive dogs. We compared effects of the drugs on oxygen uptake at doses chosen so that both drugs produced comparable effects on vascular resistance. With flow constant, phentolamine increased but isoproterenol decreased or did not alter GVO2. With constant pressure, phentolamine produced significantly greater increases in GVO2. For example, increases in GVO2 occurred with all three doses of phentolamine, but only with the high dose of isoproterenol. Neither drug altered oxygen-hemoglobin affinity of red blood cells or oxygen consumption of skeletal muscle in vitro. The results suggest that phentolamine produces more favorable effects than isoproterenol on oxygen uptake in skeletal muscle, presumably because of greater dilator action on precapillary sphincters.

Animals↗
PubMed1981

Therapeutic effects of intraarterial phentolamine in "Raynaud's syndrome".

Five patients suffering from "Raynaud's syndrome" were studied as regards the effects of increasing doses of intraarterially administered phentolamine on the blood flow to the digital arteries. Upon angiography they had shown multiple occlusions of their digital arteries. Venous occlusive plethysmography of the forearm, volume pulse amplitude of a finger tip of treated and untreated extremity, respectively, intraarterial pressure in the brachial artery and ECG lead II have been monitored continuously. The blockade of the alpha-adrenoceptors by phentolamine resulted in a favourable effect upon the accompanying functional component: The volume pulse amplitude of and the blood flow to the treated extremity increased considerably, without significant changes in the other hemodynamic parameters upon administration of doses up to 0.5 mg of phentolamine. A dose of 0.5 to 1.0 mg of phentolamine seems to be the optimum, higher doses yielding no better results. The effective blockade of the alpha-adrenoceptors could be demonstrated by the influence on the arterial blood pressure during a Valsalva maneuver, on the venous reflex response, and the diminished effectiveness of noradrenaline in the treated extremity.

Adult↗
PubMed1984

[Continuous phentolamine perfusion in the treatment of severe arterial hypertension associated with neuroblastoma].

Treatment of severe arterial hypertension associated with neuroblastoma is not well discussed in the literature. A six-month-old boy was referred for evaluation of an abdominal mass which proved to be neuroblastoma stage IV. Arterial hypertension of 26/16 kPa (190/110 mmHg) was also found. Because of the degree of malignancy and the risk of intra-tumoral haemorrhage, urgent management of the hypertension was required before proceeding to surgery. Phentolamine, a short-acting alpha-blocking agent, was administered as a continuous infusion of a 0.01 per cent solution, at a rate of 1 to 4 microgram X kg-1 X min-1 titrated according to the arterial blood pressure (BP), central venous pressure and urinary output. BP was rapidly controlled and the child went to surgery within 48 hours. The operation was uneventful but only 80 per cent of the tumour could be resected. Phentolamine was discontinued intraoperatively but was reinstituted postoperatively when hypertension recurred. With the return of normal intestinal function five days after surgery, phenoxybenzamine was begun p.o. and phentolamine was tapered over 24 hours and discontinued. A continuous infusion of phentolamine provided satisfactory control pre- and post-operatively with no significant hypotension. We consider this technique to be potentially very useful in the management of severe arterial hypertension associated with neuroblastoma, as it permits early surgical intervention under optimal conditions.

Abdominal Neoplasms↗
PubMed2000

Heparin and phentolamine combined, rather than heparin alone, improves hepatic microvascular procurement in a non-heart-beating donor rat-model.

Improvement of organ procurement from non-heart-beating donors (NHBDs) could increase the donor organ pool for liver transplantation. Whether anti-coagulative and anti-vasospastic substances can improve hepatic microvascular preservation from NHBDs is unknown. In donor rats which were pretreated with either heparin (n = 6) or heparin combined with phentolamine (n = 7) 10 min prior to cardiac arrest, the extent and homogeneity of hepatic microvascular reperfusion was assessed at the end of a 60-min period of cardiac arrest using in situ fluorescence microscopy. Non-pretreated animals with cardiac arrest for 60 min served as controls (n = 6). In the non-treated NHBDs, arterial gravity perfusion of 100 cm H2O with HTK-solution led to a hepatic acinar reperfusion of only approximately 22 % with a remarkably diminished sinusoidal density. Application of heparin prior to cardiac arrest resulted in a two-fold, but insignificant increase of acinar perfusion and sinusoidal density with a still considerable heterogeneity of both parameters. Livers of NHBDs that additionally received phentolamine exhibited significantly increased values of both acinar perfusion and sinusoidal density. Phentolamine was found to reduce heterogeneity of organ microperfusion. Thus, our results indicate that the combined application of heparin and phentolamine is a useful additive for optimizing the quality of organs harvested from NHBDs.

Alanine Transaminase↗
PubMed1988

Effects of phentolamine and atropine on angina pectoris induced by handgrip test in patients with variant angina.

In 19 patients with variant angina, handgrip test as an isometric exercise was performed in 3 conditions on different successive days in the early morning: in the control, after administration of phentolamine (0.3 mg/kg) and after administration of atropine sulfate (0.04 mg/kg). Angina associated with ST-segment elevation on the electrocardiogram was induced in 5 patients (26%) in the control condition, in 14 (74%) after phentolamine and in 5 of 16 (31%) after atropine. All anginal events but 1 occurred after the cessation of the exercise and were not associated with the significant increase of rate-pressure products. These attacks were considered to be due to coronary spasm. The frequency of the induction of angina was significantly higher after phentolamine than in the other 2 conditions (p less than 0.01). It is concluded that the attack can be induced by the handgrip exercise in a sizable number of patients with variant angina, and that the administration of phentolamine increases the incidence of angina induced by handgrip exercise. The mechanism or mechanisms by which coronary spasm is induced by handgrip exercise remains to be elucidated.

Adult↗
PubMed1982

Effects on sleep of phentolamine and epinephrine infused into the locus coeruleus of cats.

The sleep-wavefulness behavior of cats was studied after infusion of phentolamine (3 micrograms, bilateral) or epinephrine (60 micrograms, bilateral) into the locus coeruleus. The drugs exerted opposite effects: phentolamine increased rapid eye movement (REM) sleep and decreased light slow wave sleep; epinephrine decreased REM sleep, increased light slow wave sleep and augmented wakefulness. The REM-enhancing effect of phentolamine was due to more REM periods than in control experiments, with a shortening of the sleep cycle. Epinephrine, by contrast, resulted in fewer REM periods and a prolongation of the sleep cycle. The data support the hypothesis that pontine catecholamines inhibit REM sleep and facilitate wakefulness in cats, and implicate the rostral pons as an important site for the REM-increasing effect of systemically administered phentolamine.

Animals↗
PubMed1988

Analgesia induced by continuous versus intermittent cold water swim in the rat: differential effects of intrathecal administration of phentolamine and methysergide.

Continuous cold water swim produces analgesia that is partially mediated by a noradrenergic mechanism, but is independent of both serotonergic and opioid systems. On the other hand, intermittent cold water swim elicits analgesia which is partly mediated by an opioid mechanism; the contribution of the monoamines to the production of this analgesia is not known. Therefore, the present study was done to determine whether intermittent cold water swim is also mediated by noradrenergic and/or serotonergic substrates. Prior to either continuous (3.5 min) or intermittent (10 sec in, 10 sec out for 6 min) cold water (4 degrees C) swim, male Sprague-Dawley rats (225-250 g) were administered either the noradrenergic receptor blocker phentolamine (30 micrograms), the serotonergic blocker methysergide (30 micrograms) or artificial cerebrospinal fluid to the fifth lumbar vertebral spinal level via chronic intrathecal catheters. Phentolamine significantly attenuated the analgesia resulting from both continuous and intermittent cold water swim. Methysergide attenuated intermittent cold water swim analgesia, but was without effect on continuous cold water swim analgesia. Phentolamine, but not methysergide, also attenuated continuous footshock- (2.5 mA for 3 min) induced analgesia. The similarity between the effects of phentolamine and methysergide on continuous footshock and continuous cold water swim analgesia suggests that the effects of these drugs on cold water swim analgesia are not attributable to changes in thermoregulation. These results suggest that a spinal noradrenergic mechanism is involved in the mediation of both forms of cold water swim analgesia, whereas a spinal serotonergic mechanism is involved in only intermittent cold water swim analgesia.

Animals↗