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J Sharkey

Publications and source records attributed to J Sharkey.

68 records · Page 4Linked to original sources
PubMed1985

Vasomotor responses of cerebral arterioles in situ to putative dopamine receptor agonists.

The vasomotor responses of individual cerebral pial arterioles on the convexity of the cerebral cortex to subarachnoid perivascular micro-injections of dopamine and the putative dopamine receptor agonists, apomorphine, SKF 38393 and LY 141865, have been examined in 38 anaesthetized cats. The perivascular microapplication of dopamine (10(-9)-10(-3)M) effected dose-dependent reductions in pial arteriolar calibre, with the maximum reductions in calibre (22 +/- 2% from preinjection levels: mean +/- s.e.) being observed at 10(-3)M. The cerebrovascular constriction produced by dopamine (10(-5)M) could be significantly attenuated by the concomitant perivascular administration of phentolamine (10(-6)M) or methysergide (10(-6)M). The perivascular microapplication of apomorphine (10(-8)-10(-4)M) effected dose-dependent increases in arteriolar calibre, with the maximum increase (31 +/- 6%) being observed with apomorphine (10(-5)M). The perivascular administration of the putative dopamine D1-receptor agonist, SKF 38393 (10(-9)-10(-4)M) increased arteriolar calibre, with the maximum response (24 +/- 3%) being observed with injection of 10(-7)M. The putative dopamine D2-receptor agonist, LY 141865, also increased cerebral arteriolar calibre, but only at high concentrations (maximum calibre increase 25 +/- 6.1 with 10(-4)M). The cerebrovascular dilatations elicited by apomorphine and by SKF 38393 were markedly attenuated by the concomitant perivascular microapplication of the putative dopamine D1-receptor antagonist, SCH 23390 (10(-8)M). The perivascular administration of SCH 23390 (10(-9)-10(-5)M) per se did not alter arteriolar calibre nor the arteriolar dilatation provoked by microinjections of acidic cerebrospinal fluid. These results point to the presence on cat cerebral arterioles of dopamine receptors (probably of D1 subtype) mediating dilation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1979

Prosthetic valve endocarditis resulting from Nocardia asteroides.

Nocardia asteroides was isolated from the prosthetic valve of a 64-year-old woman who had died of endocarditis after aortic valve replacement. Multiple blood cultures had all been negative. This organism is increasingly being recognised as a pathogen and is usually sensitive to sulphonamides. These should be tried in culture negative endocarditis unresponsive to standard therapy.

Aortic Valve↗
PubMed1978

Treatment of demyelinating and degenerative diseases by electro stimulation of the spinal cord.

Electrical stimulation was applied to the spinal cord of 75 patients who had demyelinating and degenerative diseases of the central nervous system, and 3 patients who had sustained spinal cord injuries. The electrical energy was delivered to the central nervous system by the percutaneous technique. The amount of electrical energy required to produce the perception of paresthesias was measured in 11 patients. The minimum power necessary was 76.89 muW, the maximum was 868 muW, and the average was 448.8 muW. The patients were evaluated by 4 examiners by means of routine neurologic examination, videotape movies, and measurement of urinary bladder function. Continued improvement in neurological status, which allowed the patient to live a better lifestyle, occurred in 30 of the 61 patients with multiple sclerosis, and 6 of the 10 patients with ataxia. The patient with transverse Myelitis, the patient with primary lateral sclerosis, and 1 patient with olivopontocerebellar atrophy; also noted similar enhancement of neurological function. The patients with amyotrophic lateral sclerosis and spinal cord injuries had no changes of significance. Thirty-two out of 44 patients who were ambulatory had significant improvement, whereas 10 of the 19 patients who were not ambulatory had improvement. There was no evidence that electrical stimulation of the spinal cord, when applied via dorsally placed percutaneous electrodes and when carried only to the perception of a paresthesias, has any adverse effect on neurological function. It is hypothecated that the electrical current alters neurotransmitters to enhance the transmission along nervous and neurochemical pathways. The exact mechanisms are unknown at the present time.

Amyotrophic Lateral Sclerosis↗
PubMedDate not supplied

Electrostimulation of the nervous system for patients with demyelinating and degenerative diseases of the nervous system and vascular diseases of the extremities.

The results of electrostimulation of the spinal cord for symptoms other than that of pain are recorded in this publication. 50% of patients with multiple sclerosis, primary lateral sclerosis and hereditary spino-cerebellar disorders were observed to have enduring favourable changes in neurological function during the 15 to 27 months they have been followed. The patients who were the least severely disabled had the greatest amount of increased function and were benefitted the most by the stimulation. Those who had the fewest neurological pathways affected make the most rapid progress. For example, the patient with only an ataxic or spastic gait was observed to improve faster than the patient with an ataxic and a spastic gait. The long-term effect of electrostimulation of the spinal cord on patients with these diseases is unknown at the present time. The purpose of the stimulation is to increase neurological function so that the patient can live a better life style. It is not thought that the electrical current is responsible for a 'cure' of the basic disease process. Electrostimulation of the posterior spinal roots and spinal cord, while not new, has not been used extensively for the treatment of patients with arterial disease. The patients who have responded the most dramatically to electrostimulation are those with vasospastic disorders. A larger percentage of patients showed a greater response to implanted stimulation than to transcutaneous stimulation. Electrostimulation of the nervous system is not designed to replace standard therapeutic measures of treatment of patients with vascular disease but to supplement them.

Ataxia↗