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Biomedical subjects

W J Lang

Publications and source records attributed to W J Lang.

At least 19 recordsLinked to original sources

[Clinical application of cluster analysis in repairing prosthesis ears]

Along with developments and progresses of microsurgery,plastic surgery became very often used method to reconstruct orofacial defects,but for missing ears the prosthesis methods are still a better way comparing surgery The main merits are :no wound,short treatment time,100% success rate,easily figure established.For simplified steps and saving time in the procedure of making prosthesis ears.300 different types ears from recording cases models are analysed and special different type wax-up ears and special models are made to provide different patients as needing for selection.

Journal Article↗

Comparison of the vasodilator action of dopamine and dopamine agonists in the renal and coronary beds of the dog.

1 The effects of dopamine and the dopamine receptor agonists, SK&F 38393 and bromocriptine, on renal and coronary blood flow in the anaesthetized dog were examined. Dopamine was found to dilate both vascular beds, whereas SK&F 38393 increased renal blood flow but did not have any dilator activity in the coronary vasculature. Bromocriptine did not cause vasodilatation in either vascular bed. 2 The vasodilator responses to dopamine and SK&F 38393 were significantly reduced by the dopamine receptor antagonists, ergometrine or metoclopramide. 3 It is proposed that the selective action of SK&F 38393 on the renal vasculature suggests that the dopamine receptors of the renal and coronary vascular beds may be of different types.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Antihistamine-sensitive vasodilatation in the canine hindlimb evoked by electrical stimulation rostral to the hypothalamus.

Electrical stimulation was carried out at various sites in the brain of anaesthetized dogs pretreated with guanethidine. Stimulation at some sites elicited cholinergic vasodilator responses in the femoral vascular bed while stimulation at other sites produced non-cholinergic vasodilator responses which were prevented by histamine antagonists administered into the hindlimb. The central sites mediating the two types of responses were anatomically distinct.

Animals↗

Agonistic actions of DPI (2-(3,4-dihydroxyphenylimino)-imidazolidine) on alpha-adrenoceptors and dopamine receptors.

Some of the pharmacological actions of 2-(3,4-dihydroxyphenylimino)-imidazolidine (DPI) were studied in vivo and vitro. DPI (1 nM-100 micro M) had a similar affinity but a lower intrinsic activity on alpha-adrenoceptors in rabbit aortic strips to noradrenaline (1 nM-10 micro M). DPI did not affect the uptake of [3H]noradrenaline in guinea-pig isolated atria. The effects of DPI on dopamine receptors were examined in the dog coronary and renal vasculature and in the rat isolated, perfused kidney. In the dog coronary vasculature DPI (0.005-10 micrograms, i.a.), like dopamine (5-50 micrograms, i.a.), caused an increase in coronary blood flow which was antagonized by the dopamine receptor antagonist, ergometrine. In the renal vasculature of both the rat and the dog, dopamine (5-50 micrograms, i.a.) caused vasodilatation but there was no evidence of an effect of DPI on dopamine receptors. It appears that DPI is a selective agonist for dopamine receptors in the coronary vasculature.

Adrenergic alpha-Agonists↗

Hypertensive responses induced by phenylpropanolamine in anorectic and decongestant preparations.

The acute effects of a single capsule of each of two phenylpropanolamine-containing preparations were determined in a group of healthy young adults, by means of a double-blind comparison with matching placebo preparations. Supine diastolic blood-pressure rose to 100 mm Hg or more in 12 out of 37 subjects taking an anorectic preparation ('Trimolets'; 85 mg phenylpropanolamine per capsule) and in 4 out of 34 subjects taking a decongestant preparation ('Contac 500'; 50 mg phenylpropanolamine per capsule). 20 of the subjects taking trimolets reported adverse side effects. The frequency and extent of the hypertensive response to high-dose phenylpropranolamine-containing preparations suggest that clinical use of such preparations should be reviewed and that their availability without prescription may not be appropriate.

Adult↗

Changes occurring in self administration of nicotine by rats over a 28-day period.

After rats at reduced body weight had established responding by lever pressing for nicotine injections under a food delivery schedule (FT60 sec) for 1 hr daily sessions for 14 days, the rate of responding was maintained over a second 14-day period even after removal of the schedule. However, the rate was not maintained by rats lever pressing for normal saline without the schedule over the second 14-day period after self administration had been established for nicotine under the schedule. Other rats maintained at reduced body weight were allowed to lever press for nicotine over a 28-day period without the food delivery schedule. Their rate of self administration increased from initially low levels until at the end of the 28-day period the rate had reached that of rats self administering nicotine adjunctive to the food delivery schedule throughout the same period. Without the schedule, rats at reduced body weight self administering normal saline or rats at normal body weight self administering nicotine, continued to lever press only at very low rates throughout the 280-day period. It is suggested that rats maintain self administration of nicotine if the behavior can be established for a critical intake of nicotine over a critical period of time. The food delivery schedule appears only to hasten the establishment of the behavior but is not essential for self administration of nicotine by rats.

Animals↗

Dopamine-induced vasodilatation in the isolated perfused rat kidney.

The administration of dopamine (5--100 microgram) in rat kidneys perfused with physiological solution containing vasopressin and pretreated with an alpha-adrenoreceptor antagonist produced dose-dependent vasodilatation. The dopamine receptor antagonist haloperidol produced marked dilatation in the preparation at high doses (10--50 microgram), while a low dose of haloperidol (5 microgram) had no significant effect on the response to dopamine. The response to dopamine, however, was significantly reduced by the dopamine receptor antagonist, ergometrine (50 microgram). This dose of ergometrine had no significant effect on the vasodilator response to acetylcholine (0.01--0.2 microgram) or glyceryl trinitrate (GTN, 0.05--1 microgram). Administration of the beta-adrenoreceptor antagonist propranolol (0.5 mg) had no significant effect on the response to dopamine.

Adrenergic alpha-Antagonists↗

A comparison of the responses to some dopamine-receptor agonists and antagonists in the isolated perfused rat kidney.

Bromocriptine (5-100 microgram; 6.7 X 10(-9) - 1.3 X 10(-7) mol.), SK&F 38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine, 0.5-5 mg; 1.7 X 10(-6)-1.7 X 10(-5) mol.) and apomorphine (20-200 microgram; 6.4 X 19(-8)-6.4 X 10(-7) mol.) administered into rat kidneys perfused with physiological solution containing vasopressin and pretreated with an alpha-adrenoreceptor antagonist produced vasodilator responses similar to dopamine (50-100 microgram; 2.6 X 10(-8)-5.3 X 10(-7) mol.). THe responses to bromocriptine, SK&F 38393 and apomorphine were found to be significantly reduced by the dopamine receptor antagonist ergometrine (50 microgram; 1.1 X 10(-7) mol.). Metoclopramide (250 microgram; 7.4 X 10(-7) mol.) was found to be an effective antagonist of dopamine, bromocriptine, SK&F 38393 and apomorphine. Apomorphine (20, 50 microgram; 6.4 X 10(-8), 1.6 X 10(-7) mo.) was found to act as a partial agonist on dopamine receptors in this preparation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Evidence for dopaminergic vasodilator innervation of the canine paw pad.

1 In chloralose-anaesthetized dogs pretreated with guanethidine and pancuronium, electrical stimulation (0.2 to 5 Hz) of the peripheral end of the cut tibial nerve caused a frequency-dependent increase in femoral blood flow which was restricted to the paw pads. 2 This neurogenic vasodilatation was not attenuated by atropine, mepyramine plus burimamide, indomethacin or propranolol. It was, however, attenuated in a dose-dependent manner by intra-arterial administration of the dopamine receptor antagonist, ergometrine (0.05 to 0.5 mg). 3 The effect of ergometrine could not be explained by non-specific effects on axonal conduction or transmission or by vasospasm of the blood vessels of the paw-pads. 4 In dogs with intact tibial nerves, a pharmacologically similar dilator response localized to the paw-pads could be elicited by electrical stimulation of loci in the ipsilateral diencephalon and midbrain. This response was not due to inhibition of adrenergic vasomotor tone and was abolished by systemic ganglion blockade or by tibial nerve section as well as by femoral arterial administration of ergometrine. 5 It is suggested that the vasculature of the canine paw pads is innervated by a population of autonomic axons which utilize dopamine or a related substance as a transmitter substance and activation of which causes vasodilation.

Animals↗

Cardiovascular responses produced by the injection of dopamine into the cerebral ventricles of the unanaesthetized dog.

1 The injection of dopamine (100 to 500 microgram) into the cerebral ventricles (i.c.v.) of 10 unanaesthetized dogs produced a dose-dependent increase in arterial blood pressure and heart rate. The dogs licked, swallowed, sometimes vomited and became sedated. 2 Autonomic ganglion blockade with hexamethonium (10 mg/kg i.v.) abolished cardiovascular responses to i.c.v. dopamine, indicating that dopamine was exerting its effect within the central nervous system. 3 The dopamine receptor antagonists, haloperidol (500 microgram), chlorpromazine (200 micrograms) and ergometrine (500 micrograms), each given i.c.v., sugsequently abolished the cardiovascular responses to dopamine. 4 Pretreatment with either the beta-adrenoceptor antagonist, propranolol (600 microgram) or the alpha-adrenoceptor antagonist, phentolamine (1 mg) given i.c.v. had no significant effect on the response to dopamine. 5 It is suggested that dopamine injected into the cerebral ventricles of the unanesthetized dog causes hypertension and tachycardia by activating central dopamine receptors.

Animals↗

Pharmacological and biochemical properties of isomeric yohimbine alkaloids.

The stereochemical and pharmacological properties of yohimbine and some of its isomers are briefly reviewed. Several pharmacological and physical properties of a selection of the isomers have been determined with a view to elucidating which might be important in the elaboration of the known behavioral effects produced by them. Activity is not dependent upon lipid solubility or on the ease of access to the central nervous system. The isomers are weak inhibitors of rat-brain acetylcholinesterase and weak antagonists at muscarinic cholinergic receptors. In the rat brain in vitro they do not possess significant monoamine oxidase-inhibiting properties nor do they inhibit the uptake of serotonin. They are relatively potent antagonists of 5HT on the rat isolated fundus preparation and their potency in this preparation may be related to their ability to produce behavioral and cardiovascular effects in man and dogs.

Animals↗

Schedule induced self injections of nicotine with recovered body weight.

In a recent series of experiments we have shown that high rates of self injection of nicotine were acquired when rats are at 80% body weight on an FT-1 min food delivery schedule. This rate was significantly higher than that of rats at reduced or normal body weight without food delivery schedules or that of rats injecting saline under three parallel control conditions. In the present experiment naive rats were trained to acquire nicotine self injection at 80% body weight with an FT-1 min food delivery schedule. These rats maintained their self injection rates after they were allowed to regain free feeding body weight. The data indicate that once nicotine intake behavior is established it can be maintained with changing nutritional factors.

Animals↗

Effects of renal dopamine receptor and beta-adrenoreceptor blockade on rises in blood angiotensin after haemorrhage, renal ischaemia and frusemide diuresis in the dog.

1. In chloralose-anaesthetized dogs, central venous and arterial angiotensin (AII) levels were monitored by blood-bathed bioassay during venous haemorrhage of 20 ml/kg, acute renal ischaemia induced by suprarenal aortic stenosis and frusemide-induced diuresis. 2. Blockade of intrarenal dopamine receptors with ergometrine reduced markedly the increments in arterial AII associated with haemorrhage or suprarenal aortic stenosis, but did not consistently affect the corresponding increments in venous AII. 3. Ergometrine or renal denervation did not affect the increases of blood AII associated with frusemide diuresis. 4. Blockade of beta-adrenoreceptors with propranolol, by contrast, reduced blood AII increments associated with all three procedures. 5. It is suggested that renin release during moderate haemorrhage and acute suprarenal aortic stenosis is, in the dog, partly due to activation of intrarenal dopaminergic nerves. 6. The possibility is discussed that propranolol may depress renin release in the dog by an action other than that of blocking beta-adrenoreceptors.

Angiotensin II↗

Interaction between yohimbine alkaloids and amphetamine in mice.

The toxicity (LD50) of the isomers yohimbine, beta-yohimbine, and corynanthine was determined in mice. The LD50 of amphetamine in the presence of a constant dose of a yohimbine isomer and that of the isomer in the presence of a constant dose of amphetamine were determined in aggregated mice. Isobolograms were constructed from these data and used to evaluate the interaction of the yohimbine alkaloids and amphetamine. Beta-yohimbine was found to be approximately twice as toxic as yohimbine and corynanthine about one fifth as toxic. There was a mutual potentiation between the toxicities of yohimbine and amphetamine. Potentiation of the toxicity of amphetamine occurred with beta-yohimbine but the effect was not as marked as with yohimbine. In contrast, corynanthine antagonized the toxicity of amphetamine. The interaction between yohimbine and amphetamine is unlikely to be due to noradrenergic mechanisms but could conceivably involve serotonergic or dopaminergic mechanisms.

Animals↗