The effect of topically applied vasoactive agents and testosterone versus testosterone in the treatment of erectile dysfunction in aged men with low sexual interest. (1/11)

The objective was to evaluate the efficacy and safety of topically applied cream containing testosterone, isosorbide dinitrate and co-dergocrine mesylate compared to testosterone cream in the treatment of erectile dysfunction in aged men with low sexual interest. A randomised double-blind crossover trial was performed over two months. The subjects were 42 men with erectile dysfunction and low normal or slightly depressed testosterone level randomly allocated to two equal groups. Polypharmacy cream containing testosterone 0.8%, isosorbide dinitrate 0.5% and co-dergocrine mesylate 0.06% was applied for one month, and testosterone 0.8% cream for another month. The serum level of total testosterone was measured before and after each phase of treatment. Response to each therapy was assessed by a sexual questionnaire, measurement of tumescence and repeat penile duplex ultrasonography. Twenty-eight patients reported full erection and satisfactory intercourse with the polypharmacy cream. Thirteen men reported full erection and satisfactory intercourse with either cream. Polypharmacy cream increased penile arterial flow (P<0.001) and induced tumescence in 34 patients in lab. No patient in either phase of the study has tumescence or a significant increase in cavernous arterial peak systolic velocities after the application of testosterone cream. Serum level of total testosterone increased in all patients (P<0.05). Sexual desire was improved in 85% and 62% of patients during the treatment with polypharmacy cream and testosterone cream, respectively. No marked side effects were reported after either of them. Topical treatment with cream containing testosterone and vasoactive agents may represent a new effective treatment for erectile dysfunction associating with aging.  (+info)

Ginkgo biloba for cerebral insufficiency. (2/11)

1. By means of a critical review we tried to establish whether there is evidence from controlled trials in humans on the efficacy of Ginkgo biloba extracts in cerebral insufficiency. 2. The methodological quality of 40 trials on Ginkgo and cerebral insufficiency was assessed using a list of predefined criteria of good methodology, and the outcome of the trials was interpreted in relation to their quality. A comparison of the quality was made with trials of co-dergocrine, which is registered for the same indication. 3. There were eight well performed trials out of a total of 40. Shortcomings were limited numbers of patients included, and incomplete description of randomization procedures, patient characteristics, effect measurement and data presentation. In no trial was double-blindness checked. Virtually all trials reported positive results, in most trials the dosage was 120 mg Ginkgo extract a day, given for at least 4-6 weeks. For the best trials, there were no marked differences in the quality of the evidence of the efficacy of Ginkgo in cerebral insufficiency compared with co-dergocrine. The results of the review may be complicated by a combination of publication bias and other biases, because there were no negative results reported in many trials of low methodological quality. 4. Positive results have been reported for Ginkgo biloba extracts in the treatment of cerebral insufficiency. The clinical evidence is similar to that of a registered product which is prescribed for the same indication. However, further studies should be conducted for a more detailed assessment of the efficacy.  (+info)

Complementary medicines in psychiatry: review of effectiveness and safety. (3/11)

BACKGROUND: The use of complementary medicines in those with mental health problems is well documented. However, their effectiveness is often not established and they may be less harmless than commonly assumed. AIMS: To review the complementary medicines routinely encountered in psychiatric practice, their effectiveness, potential adverse effects and interactions. METHOD: Electronic and manual literature search on the effectiveness and safety of psychotropic complementary medicines. RESULTS: Potentially useful substances include ginkgo and hydergine as cognitive enhancers, passion flower and valerian as sedatives, St John's wort and s-adenosylmethionine as antidepressants, and selenium and folate to complement antidepressants. The evidence is less conclusive for the use of omega-3 fatty acids as augmentation treatment in schizophrenia, melatonin for tardive dyskinesia and 18-methoxycoronaridine, an ibogaine derivative, for the treatment of cocaine and heroin addiction. CONCLUSIONS: Systematic clinical trials are needed to test promising substances. Meanwhile, those wishing to take psychotropic complementary medicines require appropriate advice.  (+info)

On the pharmacology and biochemistry of the amine-uptake mechanism in human blood platelets. (4/11)

1. The uptake of 5-hydroxytryptamine (5-HT) by human blood platelets in vitro has been studied with the object of identifying the biochemical mechanisms involved.2. Drugs active in adrenergic systems are only moderate inhibitors of uptake, although prenylamine is as active as the less potent tricyclic anti-depressive drugs; phenoxybenzamine is almost inactive as a competitive inhibitor but is effective if pre-incubated with the platelets beforehand. This parallels its pharmacological pattern of action.3. Inhibitors of oxidative phosphorylation do not inhibit 5-HT uptake, but iodoacetate inhibits, if pre-incubated with the platelets; p-chloromercuribenzoate does also, when the platelets are suspended in synthetic medium, but not in plasma.4. Ouabain causes significant inhibition at 10(-7)M; by 10(-6)M it achieves its maximal effect, namely 40% inhibition; in K(+)-deficient medium, uptake falls to 30% of normal; the K(+)-dependent fraction of the uptake includes the ouabain-sensitive component. Mg(++) has no effect.5. A drug not possessing the imipramine structure, which has been tried in the treatment of depressive illness, 4-phenyl bicyclo (2,2,2) octan-1-amine, is a highly potent inhibitor of 5-HT uptake.  (+info)

Renal actions of dihydroergocristine and of phentolamine in anaesthetized cats. (5/11)

1. Comparison has been made of the effects of dihydroergocristine (DCS) and phentolamine mesylate (phentolamine) on cardiac and respiratory rates, systemic arterial pressure, renal clearances of creatinine (C(Cr)) and of p-amino-hippuric acid (C(PAH)) and on the secretion of Na and K, in cats under chloralose anaesthesia.2. Phentolamine antagonized vasomotor tone and the pressor effect of circulating noradrenaline to comparable extent. The extent of reduction in urine flow, C(Cr), C(PAH) and Na excretion correlated with the fall in mean arterial pressure. Innervated and denervated kidneys responded similarly. Cardiac and respiratory rates rose slightly as arterial pressure fell.3. DCS, 10 to 20 mug/kg per min, did not reduce vasomotor tone, markedly reduced the pressor effect of exogenous noradrenaline, caused bradycardia and respiratory slowing but had little or no effect on renal function.4. DCS, 30 to 40 mug/kg per min, lowered mean arterial pressure by 15-25 mm Hg, decreased C(PAH) but not C(Cr), so raising the filtration fraction and caused a small reduction in urine flow and in Na excretion. Innervated and acutely denervated kidneys responded similarly.5. DCS, 30 to 40 mug/kg per min, raised mean arterial pressure, decreased C(PAH), urine flow and Na excretion but did not alter C(Cr) in animals pretreated with full alpha-adrenergic blocking doses of phentolamine.6. DCS, 30 to 40 mug/kg per min, increased the rate of secretion of sympathetic amines from the adrenal medulla and increased the concentration of renin in renal venous blood.7. Isolated kidneys perfused at constant pressure from pump-oxygenator circuits and in saline diuresis responded to DCS (15-17 mug/120 ml. blood) by diuresis and natriuresis and by a rise in the rate of secretion of renin. Higher concentrations of DCS (125-250 mug/120 ml.) were without effect on renal function and did not influence renin secretion.8. The renal effects of full alpha-adrenergic blocking doses of DCS and of phentolamine were comparable, in the whole animal.9. The evidence indicates that the release of noradrenaline by DCS 30-40 mug/kg per min from nerve terminals supplying the juxtaglomerular apparatus may have caused the enhancement of renin secretion.  (+info)

Vascular responses and noradrenaline overflows in the isolated blood-perfused cat spleen: some effects of cocaine, normetanephrine and -blocking agents. (6/11)

1. Vascular responses and noradrenaline overflows have been studied in the isolated blood-perfused cat spleen in response to electrical stimulation of the splenic nerve with trains of 200 supramaximal pulses at a frequency of 10 Hz given at 10 min intervals.2. In the absence of blocking agents the spleen gave well-defined responses and a mean maximum overflow of 436 +/- 96 pg noradrenaline per stimulus (n = 4) at the third train of stimuli.3. Cocaine (2 x 10(-5)M) increased the response nearly threefold and raised the overflow to 840 +/- 131 pg/stim (n = 4). At later stimulations the responses remained stable, but the overflows rose progressively to 1076 +/- 51 pg/stim after five trains of stimuli.4. Normetanephrine (10(-4)M) had no significant effect on response, but elevated the overflow to a mean maximum of 868 +/- 169 pg/stim (n = 4).5. Cocaine (2 x 10(-5)M) and normetanephrine (10(-4)M) given together increased the response by a factor of 6.5 and raised the overflow to 1258 +/- 247 pg/stim (n = 4).6. Hydergine (approx. 10(-5)M) almost completely abolished the response and raised the overflow to 859 +/- 173 pg/stim (n = 4).7. Cocaine (2 x 10(-5)M), normetanephrine (10(-4)M) and hydergine (approx. 10(-5)M) given in combination abolished the response and raised the overflow to 4089 +/- 1148 pg/stim (n = 4).8. Phenoxybenzamine (10(-4)M) abolished the response and elevated the overflow to 4215 +/- 738 pg/stim (n = 4).9. These results are interpreted in terms of selective and combined block of ;uptake I', ;uptake II' and alpha-adrenergic receptors. Facilitation of transmitter release by alpha-blocking drugs, and the possible existence of an uptake process associated with the alpha-receptors are discussed.  (+info)

Electrical and mechanical response of arteries to stimulation of sympathetic nerves. (7/11)

1. When common carotid arteries of sheep were studied in vitro by the sucrose-gap method, application of acetylcholine or nicotine caused small irregular spikes of depolarization. The discharge was prevented by hexamethonium, Hydergine, phentolamine, or chronic denervation, indicating that it represented electrical activity of groups of smooth muscle cells induced by the stimulation of sympathetic nerve fibres.2. The size of spikes produced by acetylcholine or nicotine, together with counts of the total number of smooth muscle cells in cross-sections of the arterial strips, indicated that the larger groups of smooth muscle cells activated by one sympathetic nerve fibre contained approximately 1300 cells.3. Sections of arteries treated with hot formaldehyde vapour contained numerous fluorescent fibres which were intensified by previous injection of noradrenaline into the animal and were scanty or absent after chronic sympathetic denervation. They are therefore believed to be post-ganglionic sympathetic nerve fibres.4. Most of these fibres ran circularly in the outer (1/2)-(3/4) of the media. A few ran longitudinally in the adventitia. There were none in the inner (1/4)-(1/2) of the media.5. Electrical stimulation of the cervical sympathetic nerve of anaesthetized sheep caused large contractions of the common carotid artery of the same side, reducing its external diameter by 30-39%.  (+info)

Studies on renal vasomotion. (8/11)

1. The present investigation was made on the left kidney of the dog. The animals were anaesthetized intravenously with pentobarbitone (30 mg/kg) and the kidneys were perfused with saline at room temperature (20 degrees -22 degrees C). The renal innervation was untouched.2. Stimulation of the left splanchnic major nerve at T10-T12, and of the renal nerves, consistently caused renal vasoconstriction.3. Repeated stimulation of both supradiaphragmatic vagi failed to induce any vasomotion in the kidney.4. The vasoconstrictor effect was not blocked by either nicotine or hexamethonium even in enormous doses (30,000 mug). This may indicate that renal ganglia do not exist, for these ganglion blockers would prevent transmission across the ganglia.5. Kidney perfusate, re-injected into the kidney after vasoconstriction induced by stimulation of the renal nerves, brought about a notable reduction in outflow. This effect was not observed when perfusate from a non-stimulated kidney was used. This points to the release of a vasoconstrictor substance after nervous stimulation.6. Acetylcholine (ACh) in concentrations ranging from 0.001 mug/ml. caused a reduction in renal outflow. Thresholds were extremely variable. Higher concentrations of ACh (100-1,000 mug/ml.) often induced vasodilatation. The vasoconstrictor effect of ACh was not blocked by atropine.7. Nicotine and hexamethonium (10,000-30,000 mug) induced blockade which elevated the threshold for ACh to values of 1,000 mug/ml.8. Noradrenaline (0.0001 mug/ml.) induced a strong renal vasoconstriction.9. Hydergine (5-10 ml. solutions in concentrations ranging from 15 to 30 mug/ml.) blocked the renal response to nerve stimulation. This suggests that the nature of the renal innervation is adrenergic.10. In diseased kidneys which show reduction of the lumen of the arterioles, the thresholds for ACh, nicotine and noradrenaline are greatly increased, which might explain why we failed to show any effect of these drugs on renal vasomotion in several kidneys, many of which were not examined histologically.11. The collision technique was applied in an attempt to discover the nature of the fibres activated by ACh. It was found that ACh greatly reduced the size of the action potentials generated by splanchnic stimulation. This would seem to indicate that these impulses are conducted antidromically by sympathetic postganglionic fibres.12. These findings are discussed in relation to the hypothesis that the renal innervation is chiefly adrenergic and that ACh acts as a sympathetic transmitter, liberating noradrenaline, and that this effect is blocked at postganglionic endings, or at some structure intervening between adrenergic nerve endings and the effector cells, or at sensory nerve endings.  (+info)

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