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At least 343 records · Page 19Linked to original sources
PubMed1983

[Comparative evaluation of the effect of nitroglycerin, sodium nitroprusside and phentolamine on hemodynamics and myocardial contraction during coronary occlusion in the dog].

Acute experiments on 27 dogs were conducted to examine the effect of intravenous nitroglycerin, sodium nitroprusside and phentolamine on the hemodynamics and regional contractility of the left ventricle under conditions of experimental coronary occlusion. Nitroglycerin was the most effective agent versus the other drugs in decreasing the elevated diastolic pressure in the left ventricle whereas sodium nitroprusside showed the most pronounced hypotensive effect in relation to systemic arterial pressure. All these drugs produced indirect favourable chrono- and inotropic effects especially marked with phentolamine. The effect of nitroglycerin and sodium nitroprusside on the cardiac output may vary to a great extent: a decrease in the stroke volume occurred in the presence of the remaining high degree of peripheral vascular resistance and a fall in the elevated and diastolic pressure in the left ventricle, an increase in the stroke volume was observed in the case of a considerable drop in the overall peripheral vascular resistance and the persisting endodiastolic overburden of the left ventricle.

Animals↗
PubMed1981

[Effect of phentolamine on carotid reflexes induced by acetylcholine].

Acetylcholine was injected into the common carotid artery of 15 mongrel dogs. In the animals with tied internal carotid artery, hyperpnoea, bradycardia and hypotension was observed, and in the animals with free internal carotid artery the hyperphoea was followed by apnoea. The administration of phentolamine provokes a temporary decrease or abolition of the reflexes produced by acetylcholine. This action of the alpha-blocker is due to a local effect because when phentolamine is injected intravenously it does not happen and the reflexes produced by acetylcholine with starting place at the carotid sinus of the opposite side are not affected.

Acetylcholine↗
PubMed1978

[Role of vascular thermoreceptors in the mechanism of cold tremor inhibition by oxotremorine, seduxen and phentolamine].

Intravenous infusion of oxotremorine, seduxene, and phentolamine to cats not only decreased the cold-induced tremor, but also reduced the subcutaneous vein receptor impulses. Diminished activity of the vascular thermoreceptors served as an additional component in the mechanisms of the inhibitory effect of oxotremorine and seduxene on cold tremor. Reduction of the thermoreceptors activity after phentolamine administration is primary, and may be considered as the leading factor in the cold tremor inhibition.

Animals↗
PubMed1982

Blockade by phentolamine of induced inotropic responses in the canine heart in vivo.

Positive inotropic responses, measured as increases in the maximum derivative of left ventricular pressure (dP/dt), were induced by carotid artery occlusion (CAR), intravenous norepinephrine (NOR), or intravenous isoproterenol (ISO) in the canine heart in vivo. NOR and ISO also increased peak ascending flow velocity (V max). ISO increased heart rat (HR), while NOR and CAR produced comparatively little chronotropic response. Phentolamine (1 mg/kg) considerably reduced induced increases in dP/dt, Vmax and HR, while the same dose of propranolol almost completely abolished such increases. The results indicate that phentolamine, and alpha-adrenergic blocking drug, does have and ability to partially block induced positive inotropic responses in the canine heart, and perhaps chronotropic responses as well, although propranolol, a beta-blocker, is more effective. the results are in accord with the view that the principal cardiac adrenergic receptors are not adequately described either as classical beta- or alpha-adrenergic receptors.

Animals↗
PubMedDate not supplied

Peak pain relief is delayed and duration of relief is extended following intravenous phentolamine infusion. Preliminary report.

BACKGROUND AND OBJECTIVES: Intravenous phentolamine infusion (i.v.P) has been shown to produce pain relief in some patients with sympathetically maintained pain. Animal models of neuropathic pain have reported decreases in pain behavior lasting 5 days following phentolamine injection. However, no clinical study has prospectively assessed pain relief for longer than 24 hours. The aim of this preliminary report was to assess prospectively daily pain relief scores for 1 week following i.v.P METHODS: Thirty-seven consecutive patients with neuropathic pain were asked to complete a pain relief scale for 7 days following i.v.P All patients were first administered 35 mg i.v.P At least 1 week later, 16 patients were administered i.v.P at a higher dose, 50 mg or 75 mg. Data from a total of 45 infusions were collected. RESULTS: Sixteen patients experienced pain relief from i.v.P Twenty-seven infusions resulted in pain relief. Peak pain relief was delayed in 25 of 27 (93%) positive i.v.P: 7 patients experienced the onset of peak response the night immediately following an infusion, 13 the next day, 3 2 days later, and 1 each 4 and 5 days after infusion. All 16 patients who reported pain relief following i.v.P experienced at least 2 days of relief with each infusion. Eight patients experienced at least 1 week of pain relief. No differences in pain relief scores were seen with higher-dosage i.v.P. CONCLUSIONS: A delay in peak pain relief was reported following 25/27 i.v.Ps. Peak pain relief occurred most often at least 24 hours after infusion completion. In these patients, duration of pain relief was at least 2 days. Placebo controlled studies are needed to verify these observations.

Adrenergic alpha-Antagonists↗
PubMed1997

[The effects of thoracic epidural anesthesia combined with phentolamine infusion in a patient with low left ventricular ejection fraction undergoing resection of aortic abdominal aneurysm].

The subject was a 73 year old man scheduled for resection of abdominal aortic aneurysm. The patient had a past history of myocardial infarction and his left ventricular ejection fraction was 21%. Anesthesia was maintained with thoracic epidural anesthesia combined with light general anesthesia using NLA technique. Phentolamine was infused for after-load reduction. We maintained the intravascular volume with infusion therapy and mild hemodilution was performed. As the result of these procedures, systemic vascular resistance decreased and cardiac index increased after the induction of anesthesia. Forrester classification was subset I at any point during the surgery. Hemodynamic changes were not significant after clamping and unclamping of the aorta. We conclude that successful anesthetic management of this patient was due to the epidural anesthesia and combined use of phentolamine as a vasodilator.

Aged↗
PubMed1997

Effects of Phentolamine on Responses to PAMP in the Hindquarters Vascular Bed of the Rat.

BACKGROUND: Responses to proadrenomedullin NH(2)-terminal 20 peptide (PAMP), a novel hypotensive peptide formed from preproadrenomedullin, and the effects of inhibition of adrenergic vasomotor tone with the alpha-receptor antagonist, phenolamine, on responses to PAMP were investigated in the systemic and hindquarters vascular bed of the rat. METHODS AND RESULTS: Intravenous injections of PAMP decreased systemic arterial pressure and in the hindquarters vascular bed of the rat under conditions of controlled hindquarters blood flow, intra-arterial injections of PAMP decreased perfusion pressure in a dose-related manner. Following administration of the alpha receptor blocking agent, phenotlamine, systemic depressor and hindquarters vasodilator responses to PAMP were not significantly decreased, whereas phentolamine significantly decreased systemic and hindquarters pressor responses to norepinephrine. Phentolamine had no significant effect on vasodilator responses to bradykinin, albuterol, or to nitroglycerin. CONCLUSIONS: The present data show that PAMP has significant systemic vasodepressor and vasodilator activity in the hindquarters vascular bed of the rat and suggest that vasodepressor and hindquarters vasodilator responses to PAMP are not dependent upon the presence of adrenergic vasomotor tone.

Journal Article↗
PubMed1979

The effect of propranolol phentolamine and pimozide on drug-induced anorexia in the mouse.

Pimozide was a potent antagonist of (+)amphetamine, diethylpropion, mazindol and phentermine anorexia in the mouse. Phentolamine and propranolol produced no such antagonism, but either potentiated or had no effect on the drug-induced anorexia. Although the mechanism of action of the four anorectic agents appears to involve dopamine receptor agonist activity, an antagonist or partial agonist effect at noradrenergic receptors may also be involved.

Animals↗
PubMed1975

Effect of phentolamine and preperfusion with glucose on insulin release from the isolated perfused pancreas from fasted and fed rats.

Starvation of rats for 24 hrs resulted in decreased insulin release from the isolated rat pancreas. The effect of fasting could not be counteracted by elevation of the glucose level in the equilibration medium from 0.8 to 1.5 mg/ml. The alpha-adrenergic blocking agent phentolamine (10 mug/ml) stimulated glucose induced insulin release to approximately the same extent in fasted as in fed rats. These findings illustrate the importance of endogenous catecholamines in the regulation of insulin secretion from the isolated pancreas. Our experiments suggest that the impairment of insulin secretion on fasting is due neither to the inhibitory effect of catecholamines nor to the lack of substrate in the pancreas at the initiation of the stimulation.

Animals↗
PubMed1987

Induction of penile erection by intracavernosal injection: a double-blind comparison of phenoxybenzamine versus papaverine-phentolamine versus saline.

Recent data suggest that intracavernous injections of phenoxybenzamine in saline, and/or papaverine with phentolamine mesylate in saline, result in erection in otherwise impotent men. A double-blind study using normal saline and normal saline mixed with phenoxybenzamine or papaverine-phenotolamine mesylate showed that none of 11 subjects with organic erection dysfunction responded with appreciable penile swelling to saline injection, but all responded with some degree of penile swelling to the other solutions. The mechanism of penile erection in response to intracavernous injections is still unclear, but it is thought to be related to the alpha-adrenergic blocking and/or smooth muscle relaxant actions of these drugs; the volume of the injection or the normal saline content of the solution are not factors in causing penile tumescence.

Adult↗
PubMed1977

Importance of cardiac and vascular beta-receptors in the action of phentolamine.

To determine to what extent the effects of phentolamine (PHE) are mediated by the cardiac and vascular beta-receptors, the action of the drug was studied in anaesthetized cats pretreated with beta-blockers. Blockade of the cardiac beta-receptors with either propranolol or metoprolol entirely prevented the increases in heart rate, dP/dt and cardiac output caused by PHE. In animals pretreated with propranolol (in a dose blocking the vascular beta-receptors) or metoprolol (in a purely cardio-selective dose) PHE significantly lowered blood pressure to the same extent as in untreated controls. The effects of PHE on the heart are thus conditional on the integrity of cardiac beta-receptors, whereas it seems improbable that vascular beta-receptors have any part in its vasodilative action. Evidence presented in the literature rather suggests a predominantly central mode of action.

Animals↗
PubMed1981

Effects of haloperidol, methylergometrine and phentolamine on the frog ERG.

The effects of 3 x 10(--5) solutions of haloperidol (HAL), methylergometrine (ME) and phentolamine (PHA) in a dose of 27 microliters on the ERG of isolated frog eye cup preparations were examined. HAL induced a decrease in the amplitude of both the b- and d-waves which began about 20 min after the application. The dominating ME effect was a fast increase of the b-wave amplitude, while PHA did not induce any significant influences on the ERG.

Animals↗
PubMedDate not supplied

Comparison of the cardiovascular effects of phentolamine, sodium nitroprusside and nitroglycerin in anaesthetized cats (comparison of vasodilators).

The effects of phentolamine (PH), sodium nitroprusside (NP) and nitroglycerin (GTN) were compared in experiments on anaesthetized cats. All three agents diminished vascular resistance and lowered blood pressure, although they differed in the intensity of their effects (NP greater than PH = GTN) and in the steepness of their dose-response curves (NP greater than PH greater than GTN). NP and GTN did not cause consistent changes in heart rate and dP/dt, whereas PH produced marked, dose-dependent increases in these two variables and in cardiac output, which was augmented to a lesser extent by NP and not affected by GTN. It is concluded that whereas the beneficial therapeutic effects of NP and GTN are presumably due exclusively to the reduction of preload and afterload, PH has an additional cardiostimulant action.

Animals↗
PubMedDate not supplied

Phentolamine as a treatment for poor mixing in transposition of the great arteries with adequate intraatrial communication.

Patients with transposition of the great arteries often show poor mixing for different reasons, even after adequate balloon atrial septostomy. We present a patient with such a lesion whose clinical status improved dramatically after phentolamine was applied. We believe this improvement is due to reduction in afterload caused by the alpha(2) blocker and also possibly as a response to a presumptive effect of the drug on the diastolic function of the right ventricle, allowing more left-to-right shunt across the atrial septal defect. Both phenomena can improve cardiac output in such a situation.

Abnormalities, Multiple↗
PubMed1987

Decreases in REM sleep after phentolamine depend on the ambient temperature.

According to monoaminergic theories of rapid-eye-movement (REM) sleep, phentolamine (PHEN), an alpha-adrenoceptor antagonist that diminishes noradrenergic activity, should decrease REM sleep. However, PHEN also causes a fall in body temperature (Tb) that depends on the ambient temperature (Ta). When REM sleep and Tb were recorded in the same rats at 4 Ta's, after intraperitoneal injections of either PHEN or saline, the two measures were highly correlated. When PHEN lowered Tb, at Ta 20 degrees C, latency to REM sleep increased and total REM time decreased compared to controls. At Ta 32 degrees C, where PHEN had no effect on Tb, drug-treated rats had as much REM sleep as did controls.

Animals↗
PubMed1992

Analgesia from the periaqueductal gray in the developing rat: focal injections of morphine or glutamate and effects of intrathecal injection of methysergide or phentolamine.

The aim of these experiments was to examine the changes in antinociception elicited by morphine or glutamate stimulation of the periaqueductal gray of the midbrain (PAG) during the postnatal development of the rat. Pups, aged 3, 10, and 14 days, were implanted with cannulas aimed at either the dorsal or the ventral aspect of the PAG, and glutamate (vehicle, 60 mM or 180 mM) or morphine (vehicle, 2 micrograms or 6 micrograms) was microinjected into one of those two sites. Pups were tested for analgesia against noxious thermal and mechanical stimuli. Morphine produced analgesia at 3 and 10 days of age only when administered to the ventral part of the PAG and the thermal noxious stimulus was tested. Conversely, analgesia induced by glutamate was seen at 3 and 10 days of age only when glutamate was given to the dorsal aspect of the PAG and the mechanical stimulus was used. In 14-day-old pups, both drugs produced analgesia against both types of noxious stimuli regardless of their site of administration within the PAG. Systemically administered naloxone attenuated the analgesic effects of both drugs when they were administered to the ventral PAG, but did not consistently attenuate the analgesic effect of either compound given to the dorsal aspect of the PAG. When either morphine or glutamate was injected into the ventral PAG, intrathecal injections of methysergide attenuated analgesia against the thermal stimulus to a significantly greater degree than the mechanical stimulus and intraspinal injection of phentolamine attenuated analgesia against the mechanical stimulus more potently. When glutamate was given to the dorsal PAG, analgesia against both stimulus types was significantly attenuated. These results indicate that the morphine- and glutamate-induced analgesia mediated by the PAG are developmentally differentiated. These ontogenetic differences most likely reflect differences in the mechanism of action by which these drugs produce analgesia when administered to the PAG, as well as neuroanatomical differences within the dorsal and the ventral regions of the PAG.

Aging↗
PubMed1977

Effects of phentolamine, phenoxybenzamine and desipramine on clonidine-induced blockade of cardiac acceleration in the dog.

Clonidine reduced cardiac acceleration induced by low frequency electrical stimulation of cardiac sympathetic nerve fibers in anesthetized and vagotomized dogs. This effect of clonidine was abolished by short periods of high frequency electrical stimulation. The inhibitory effect of clonidine was observed with 10- as well as with 90-sec periods of electrical stimulation of sympathetic nerve fibers; it was antagonized by phentolamine, phenoxybenzamine and desipramine. This suggests the presence of alpha-adrenoceptors at the peripheral sympathetic nerve ending in the dog.

Animals↗
PubMed1980

Inhibition by local anesthetics, phentolamine and propranolol of [3H]quinuclydinyl benzylate binding to central muscarinic receptors.

[3H]Quinuclydinyl benzylate ([3H]QNB) binding was carried out on crude synaptosomal membranes isolated from cat cerebral cortex. The specific binding showed a single type of site with KD 0.25 nM, Hill number 0.89 and Bmax 114 pmol/g protein. The local anesthetics procaine, tetracaine and dibucaine, and the adrenergic antagonists phentolamine and propranolol, in concentrations between 1 nM and 500 microM, inhibited [3H]QNB binding with Ki varying between 9 microM for procaine and 80 microM for propranolol. The Hill coefficients obtained from logit/log plots suggested that there was no cooperativity between the binding sites for local anesthetics. At various concentrations the inhibition by procaine and propranolol may appear as competitive or non-competitive. The Hill numbers obtained from the saturation curves suggest that there was no cooperativity between anesthetics and [3H]QNB binding sites. Neither 1 mM Ca2+ nor Mg2+ affected [3H]QNB binding or the action of the drugs. The effect of local anesthetics and adrenergic antagonists was reversible and these drugs did not protect the muscarinic receptor from the deleterious effect of Triton X-100 as was the case with muscarinic agents. Our findings suggest that local anesthetics inhibit [3H]QNB binding to the muscarinic receptor by acting at some accessory site but not on the true receptor site. The possible mechanism of action and local anesthetics on synaptic transmission is discussed.

Anesthetics, Local↗