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 415 records · Page 23Linked to original sources
PubMed1990

[Plasma noradrenaline response to phentolamine in "latent" left-sided heart failure].

To estimate the pumping function of the left-sided heart in patients with "latent" left-sided heart failure due to heart disease which primarily affected the left-side of the heart (former NYHA class I and II), we measured (i) the increase of peripheral venous pressure in response to supine mild leg exercise (delta VP), and (ii) the increase of plasma noradrenaline (NA) concentration due to phentolamine (PH) injection (delta NAPH). We divided the patients into well-functioning left-sided heart group (delta CI/delta PAW greater than 0.180 L.min-1.M-2.mmHg-1) and poorly-functioning left-sided heart group (delta CI/delta PAW less than or equal to 0.180 L.min-1.M-2.mmHg-1) on the basis of a ratio (delta CI/delta PAW), relating the increase in cardiac index (delta CI) in response to exercise to the concomitant increase in mean pulmonary artery wedge pressure (delta PAW). This diving line (delta CI/delta PAW = 0.180 L.min-1.M-2.mmHg-1) correlated with delta VP (diving line: delta VP = 35 mmH2O) and with delta NAPH (diving line: delta NAPH = 0.353 ng/ml). Our results suggest that delta VP and delta NAPH reflected the pumping function of the left-sided heart with considerable accuracy.

Cardiac Output, Low↗
PubMed1989

Effects of phentolamine and propranolol on the changes of pain threshold and contents of MEK and LEK in rat brain after EA.

The contents of Met-enkephalin (MEK) and Leu-enkephalin (LEK) in striatum and MEK in hypothalamus of rat increased markedly after electroacupuncture analgesia (EAA). Intraperitoneal injection of phentolamine, a blocker of alpha receptor, potentiated the EAA and abolished the effects of EA increasing MEK and LEK contents; while injection of propranolol, a blocker of beta receptor, partially inhibited the EAA, as well as abolished the effects of EA increasing MEK and LEK concentrations in the striatum and the hypothalamus, and also elevated the MEK and LEK contents in hippocampus and MEK level in cortex. The results indicate that EA regulates metabolism of MEK and LEK, as well as EAA partially via alpha and beta receptors.

Animals↗
PubMed1978

Effects of phentolamine and clonidine on pituitary-adrenocortical axis during stress in conscious rats.

For evaluation of the effect of several drugs on the hypothalamo-pituitary-adrenocortical axis during stress, after testing various tress stimuli (swimming, restrain) the 15 min exposure of rats to novel environment was chosen. Subcutaneous administration of clonidine hydrochloride (BOEHRINGER; Ingelheim, 60 micorgram kg-1), a drug stimulating alpha-adrenergic receptors, did not result in any any changes in plasma corticosterone level either during basal or under stress conditions. In contrast, the administration of alpha-adrenergic blocking agent--phentolamine (RegitineR CIBA; 4 mg kg-1)--produced a significant elevation of resting corticosterone level, but failed to influence the stress-induced corticosterone increase.

Animals↗
PubMed1985

Impaired insulin secretion in human diabetes mellitus. Interactions between naloxone, phentolamine and lysine acetylsalicylate upon glucose induced insulin release.

Non insulin-dependent diabetes mellitus (Type II) is characterized by the loss of the acute insulin response to glucose. Met-enkephalin, catecholamines and prostaglandin E (PGE) have all been reported to inhibit the acute insulin response to glucose in normal humans. To evaluate the hypothesis that an increased sensitivity to these endogenous substances may play a role in defective insulin secretion in diabetes, we evaluated the effects of three blocking drugs upon the impaired insulin response to glucose in Type II diabetic subjects, as well as glucose-induced insulin secretion in normal humans. In diabetics, acute insulin responses to glucose were significantly increased by all the agents tested (naloxone, phentolamine and lysine acetylsalicylate), but only the cyclooxygenase inhibitor significantly augmented second phase insulin secretion and glucose disappearance rates. The combined infusion of the three agents caused a striking increase of the acute insulin response to glucose (response before: 3 +/- 2 uU/ml; after: 22 +/- 6 uU/ml, p less than 0.01). This was accompanied by a ninefold augmentation of the second phase of insulin secretion which was the result of a synergistic interaction between the three drugs (response significantly higher than the sum of single effects). In normals, insulin responses to glucose were also significantly increased by the combined infusions of the drugs, but to a significantly lesser extent than that of diabetics. This different degree of insulin potentiation between normals and diabetics under the infusion of the three agents persisted even when the prestimulus glucose level of normals was matched to that of diabetics by a glucose infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

[Vasodilator treatment of the acute phase of myocardial infarct with phentolamine. Analysis of hemodynamic results and therapeutic indications].

Treatment by phentolamine was carried out in 30 patients presenting with an acute myocardial infarction complicated by left ventricular failure, 8 of which had cardiogenic shock. The response to treatment was closely related to the level of overload of the left ventricle. Significant improvement in the haemodynamic state was only observed in the most severe cases of cardiac failure, and in these cases was accompanied by only a minimal and insignificant change in mean arterial pressure and heart rate.

Acute Disease↗
PubMedDate not supplied

[Effect of the adrenaline, euphyllin, phentolamine and obzidan on serotonin bronchospasm in guinea pigs].

It has been shown in experiments on 81 guinea-pigs that variation of the functional status of alpha- and beta-adrenoreceptors produces a substantial effect on marked serotonin bronchospasm. The blockade of beta-adrenoreceptors with obsidan (1--2 mg/kg) increases the spasm of bronchial smooth muscles in response to serotonin (10 micrograms/kg). The alpha-adrenolytic phentolamine (2 mg/kg) and the myotropic spasmolytic euphylline (8 mg/kg) remove the hypersensitivity of the bronchi to serotonin 20 min after adrenaline administration and potentiate its protective effect in serotonin bronchospasm after administering the beta-adrenoblocker obsidan.

Adrenergic beta-Antagonists↗
PubMed1980

Bladder neck dysfunction: the effect of the alpha-adrenergic blocking agent phentolamine on bladder neck dysfunction and a fluorescent histochemical study of bladder neck smooth muscle.

Urodynamic examinations and fluorescent histochemical studies suggest that patients with bladder neck obstruction can be divided into two main groups (responders and nonresponders) based on the response of their urinary flow rate to phentolamine and that the adrenergic nervous system of the bladder neck has an important effect on the response in responders.

Adrenergic Fibers↗
PubMed1978

[1st experiences with the alpha-receptor blockader phentolamine in achalasia].

Through direct research on isolated human esophagus muscle systems in achalasia patients we found a deviation in the distribution pattern of the contractory alpha-receptors and dilatory beta-receptors in the region of the lower esophagus sphincter in favour of the alpha-receptors. Consequently, the motility of the lower esophagus sphincter was extremely impaired. On the basis of these results, we treated achalasia patients with the alpha receptor blocking drug phentolamine. All patients were soon symptom-free subjectively and improved objectively. Surgical intervention was avoidable in all cases.

Acetylcholine↗
PubMed1984

[Effect of bulbar microinjections of noradrenaline, isoproterenol and phentolamine on the spino-bulbo-spinal reflex in the cat].

In chloralose-anesthetized cats a long lasting depression of spino-bulbo-spinal (SBS) reflex discharges following microinjections of noradrenaline and its agonist (isoproterenol) in the medial bulbar reticular formation was revealed. Microinjections of phentolamine (alpha-adrenoceptor antagonist) were followed by prominent enhancement of SBS-reflexes. Depressive action of the locus coeruleus stimulation on SBS-responses essentially decreased after these microinjections. The data evidence for a specific noradrenergic nature of inhibitory locus coeruleus influences on reticular centre of SBS-reflexes.

Animals↗
PubMed1981

Influence of phentolamine and other drugs on proliferation of hemopoietic stem cells and on postirradiation survival of Swiss mice.

The effect of combination of drugs composed of phentolamine (PHE), 5-hydroxytryptophan (5-HTP), dopamine (DA), and haloperidol (HAL), which is known to inhibit differentiation of lymphocytes [15, 16, 17] on the hemopoietic stem cells forming colonies in the spleen (CFU-S) of mice was investigated. the mixture of drugs administered for 3 consecutive days produced more then twofold increase in transplantable CFU-S content in bone marrow of donor Swiss mice. Similar effect was observed after 5-HTP or PHE administered as single drugs. The other components of the mixture appeared to be ineffective. PHE injected into the recipients of bone marrow 1 h after its transplantation reduced the percentage of CFU-S in the phase of DNA synthesis (S-phase of the cell cycle) from approx. 61 to 40%. the above result in view of the simultaneous increase in CFU-S content in bone marrow of donor mice suggests that the inhibitory effect of PHE on differentiation of CFU-S exceeds its effect on their proliferation. The increase in the mean survival time of animals irradiated with 700 and 750 R 1 h after the last injection of PHE, administered alone or in combination with drugs for 3 consecutive days, was also observed. This effect was less pronounced than might be expected from the obtained increase in CFU-S content.

5-Hydroxytryptophan↗
PubMed1982

Effects of Dl- and l-propranolol, labetalol, and phentolamine on rabbit iris blood flow determined by hydrogen clearance method.

In rabbits anesthetized with urethane, blood flow in the iris and the eye lid was 104.0 to 120.0 and 96.6 to 112.4 ml/min/100 g tissue (determined by the hydrogen clearance method), respectively. Dl-propranolol (1.0 mg/kg, i. v.) or phentolamine (0. 5 mg/kg, i. v.) decreased blood flow in both iris and eye lid to a similar degree, and also decreased blood pressure. Neither saline solution (0.5 ml/kg, i. v.) nor d-propranolol (1.0 mg/kg, i. v.) changed blood flow in both iris and eye lid and blood pressure. Labetalol (1.0 mg/kg, i. v.) decreased blood flow in the iris markedly and that in the eye lid moderately with a moderate decrease in blood pressure ; blood pressure/iris blood flow ratio increased significantly without changes in blood pressure/eye lid blood flow ratio. None of the drugs tested changed pupil size of the anesthetized rabbits. It is suggested that labetalol decreases iris blood flow because of blood pressure decrease plus other mechanisms that might be different from alpha- and beta-adrenergic blockade.

Animals↗
PubMed1981

[Effect of atropine, propranolol, phentolamine, and orciprenaline on minute-rhythmic fluctuations of heart rate in urethane-anesthetized mice].

The effects of atropine, propranolol, phentolamine, and orciprenaline on the minute-rhythmic fluctuations of the heart rate were investigated in urethane-anaesthetized mice. These drugs influenced the parameters of the minute rhythm (amplitude, length of period). However, the rhythm was not suppressed over any length of time. After blocking the vagus with atropine, the rhythm was maintained unchanged. In the other cases, the rhythm was not demonstrable only during the transition to a new level of heart rate. Immediately after the injection of each drug, the amplitude of the minute rhythm was very low for the most part but gradually increased in size again. After the injection of each drug, there existed the same correlations between the length of period of the fluctuations of heart rate and the respective mean rate (i.e., the arithmetic mean of both extreme values of a period) as after the injection of urethane alone. The same rhythms as are characteristic for the respective ranges of heart rate after the injection of urethane alone were also observed. The possible central and peripheral mechanism of origin of this minute rhythm are discussed. Since neither the blockade of the vagus nor the blockade of the sympathetic innervation could suppress the occurrence of periodic fluctuations of the heart rate for a long time, a peripheral origin of this minute rhythm may be assumed. Moreover, because there are no indications for a direct influence of urethane on the cardiac pacemaker, urethane might be supposed to produce the conditions for a pronounced appearance of the latently existing autogenic rhythm of the heart by acting on the central nervous system. Therefore, the visceral nervous system would be responsible only for the modification of the parameters (amplitude, length of period) of this rhythm.

Anesthesia↗
PubMed1981

[Effect of phentolamine, diphenhydramine and cyproheptadine on arginine-induced growth hormone secretion (author's transl)].

Arginine stimulation test was performed on 36 healthy volunteers from both sexes, in order to determine whether alpha-adrenergic histaminergic or serotoninergic mechanisms was involved in growth hormone (GH) secretion. Arginine alone (30 gr/30 min) induced a clearcut GH response significantly different versus basal values in two different control groups. This response was accompanied by a slight, statistically non-significant, decrease in glucose and FFA levels. The concomitant administration of the alpha-adrenergic blocker phentolamine (0.5 mg/min x 90 min) did not alter the GH secretory pattern elicited by arginine. The addition of the H-1 histaminergic blocker diphenhydramine (50 mg i.v. as bolus 15 min before and 50 mg infused with arginine) completely suppressed the arginine induced GH secretion. Diphenhydramine, was also able to reduce GH basal values. Almost identical results were obtained with cyproheptadine, a serotoninergic, histaminergic and cholinergic blocker agent (2 mg q.i.d.; per os x 2 days and 4 mg per os 120 min before arginine). This drug suppressed arginine induced GH secretion without altering basal GH values. Blood glucose or FFA levels were not altered by any pharmacological manipulation vs. the control arginine group. It is concluded that either histaminergic H-1 or both histaminergic and serotoninergic blockade inhibit GH secretion elicited by arginine. On the other hand an alpha-adrenergic pathway in the arginine action is ruled out.

Adult↗
PubMed1978

In vitro and in vivo effects of adrenaline and phentolamine on platelet function.

In vitro and in vivo effects of adrenaline (ADR) on platelet aggregation, on platelet factor 3 (PF3) availability and on platelet factor 4 (PF4) release were studied in man. Inhibitory action of an alpha-blocker, phentolamine (PHEN) was investigated in the same conditions. The threshold concentration (TC) of ADR inducing the typical two-phase response in aggregation tests when added to platelet-rich plasma (PRP) varied in different pools of plasma, but always induced an evident PF4 release and increased PF3 availability. A further increase in both parameters was obtained with higher concentrations but without any significant dose/response correlation. Adding PHEN alone to PRP did not induce platelet aggregation or modify PF4 release induced by stirring, but it reduced PF3 availability. On the other hand, PHEN prevented the effects of ADR in different platelet tests, at appropriate concentrations. Intravenous infusion of ADR lowered the TC, and increased PF3 availability and PF4 release. In vivo administration of PHEN, in contrast, increased TC and reduced PF3 availability, while PF4 remained unchanged.

Blood Platelets↗
PubMed1980

[Lack of action of phentolamine, fenfluramine and cyproheptadine on the growth hormone secretion induced by glucagon (author's transl)].

The role of alpha-adrenergic and serotoninergic systems in the glucagon induced growth hormone (GH) release, has been investigated in 25 normal volunteers of both sexes divided into four groups. Group I received only glucagon (Gn) 1 mg s.c.; Group II received after Gn an phentolamine infusion over 150 min at the rate of 0.5 mg/min; Group III 30 min after Gn received fenfluramine 20 mg as a bolus injection, followed by another 20 mg infused over 90 min period; and Group IV after two days of treatment with cyproheptadine (2 mg p.o., q i d) received the last dose of 4 mg, 120 min before Gn administration. Gn elicited a clear-cut GH release in the four groups irrespective of treatment. GH peaked at 150 min and this elevation was significantly different from the basal values. No significant differences were present among the groups regarding GH, glucose or free fatty acid levels. These results suggest that the alpha-adrenergic and serotoninergic systems are not involved in the Gn induced GH release.

Adolescent↗
PubMed1995

Microwave-induced lethal heat stress: effects of phentolamine, prazosin and metoprolol.

Previous studies have shown that adrenergic antagonists can alter physiological responses to microwave-induced heating. In the present experiments, 33 ketamine-anesthetized Sprague-Dawley rats were exposed to 2450-MHz microwaves at an average power density of 60 mW/sq cm (whole-body average specific absorption rate of approximately 14 W/kg) until death occurred. The effects of intraarterial injections of the nonselective alpha-adrenoceptor antagonist phentolamine (10 mg/kg body weight), the alpha 1-adrenoceptor antagonist prazosin (5 mg/kg), and the beta 1-adrenoceptor antagonist metoprolol (2 mg/kg) on physiological responses (including changes in body temperature, heart rate, blood pressure, and respiratory rate) were examined. A group of saline-injected animals was included for comparison. There were no significant differences in lethal temperatures, survival times, or rates of temperature change among the different groups. In all groups, heart rate increased continuously during exposure; mean arterial blood pressure increased until colonic temperature reached 41-41.5 degrees C, and then decreased. These heart rate and blood pressure changes were similar to those that occur during environmental heat stress. Despite differences in absolute values of heart rate and mean arterial blood pressure among groups, there were no significant differences in changes from baseline levels among groups. From these results, taken together with previous findings in our laboratory, it may be hypothesized that selective alpha 1 blockade (without concurrent alpha 2 blockade) and beta 2 blockade (with or without concurrent beta 1 blockade) are effective in altering physiological responses to microwave exposure.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1995

Accidental epinephrine auto-injector-induced digital ischemia reversed by phentolamine digital block.

The use of epinephrine-containing auto-injectors as a prescription medication for treating routine to severe anaphylactic reactions is now widely accepted. Associated with this trend is an increasing number of accidental injections of epinephrine into digits, causing severe vasoconstriction and the risk of ischemic necrosis. When epinephrine is accidentally discharged into a digit, ischemic skin necrosis resulting from the alpha-adrenergic blocking effects of this agent can lead to the need for multiple operations, wound infection, and even loss of the digit. The alpha-adrenergic blocking characteristics of phentolamine administered by a variety of methods have proved effective in reversing the effects of epinephrine in these cases. The authors urge that the described treatment protocol become more widely disseminated among primary care and emergency physicians.

Adult↗