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Biomedical subjects

J Goldfarb

Publications and source records attributed to J Goldfarb.

At least 109 records · Page 6Linked to original sources
PubMed1982

The effect of echothiophate on the biphasic response of rabbit ocular pressure to dipivefrin.

A time-course study was performed on the intraocular pressure response of pigmented rabbit eyes. Dipivefrin administration produced in initial hypertensive phase lasting less than two hours followed by a prolonged hypotensive phase. Echothiophate iodide therapy produced a more pronounced and prolonged hypertensive response; there was no hypotensive phase. Administration of echothiophate plus dipivefrin resulted in a hypertensive phase similar to that from echothiophate alone; as previously reported, this combination was not followed by a hypotensive phase. The alpha-blocker phentolamine mesylate prevented the echothiophate-induced hypertension. When dipivefrin was administered with echothiophate plus phentolamine, there was an immediate hypotensive effect. It was concluded that the hypertensive effect of echothiophate in pigmented rabbit eyes may mask the hypotensive action of dipivefrin. This, rather than an echothiophate-induced inhibition of esterases, may explain why combination therapy with these drugs seemed ineffective.

Animals↗
PubMed1981

Effects of electrolytic and 6-hydroxydopamine lesions of the lateral hypothalamus on rotation evoked by electrical stimulation of the substantia nigra in rats.

Contralateral rotation evoked by electrical stimulation of the left substantia nigra was studied in rats before and after electrolytic or 6-hydroxydopamine (6-OHDA) lesions of the lateral hypothalamus. Electrolytic lesions (2 mA DC, 15 sec) which produced mean ipsilateral striatal dopamine depletion of 58% significantly reduced the rotation at 2 h to 14 days postlesion. 6-OHDA (8 microgram in 4 microliter) which produced mean ipsilateral striatal dopamine depletion of 93% significantly increased the rotation at 3 to 14 days postlesion. Haloperidol 0.1 and 0.5 mg/kg i.p. partially reduced rotation in both control and lesioned rats in a dose-related manner. Control and lesioned rats showed no significant differences in haloperidol sensitivity. If stimulus induced rotation were mediated by activation of dopaminergic neurons, one would have expected lesion effects in the present experiments to parallel those on rotation caused by pharmacologically evoked release of dopamine. The lesions effects we obtained on stimulus induced rotation, however, parallel those on rotation evoked by the predominantly directly acting dopamine agonist, apomorphine, rather than those on rotation evoked by the indirect (presynaptic) action of amphetamine. We suggest that contralateral rotation evoked by electrical stimulation of the substantia nigra may reflect direct activation of neurons postsynaptic to the dopaminergic nigrostriatal neurons.

Animals↗
PubMed1980

Footshock-induced rotation: lack of effect of haloperidol and AMPT.

Non-lesioned, drug naive rats were administered footshock to determine whether aversive stimuli would induce rotational behavior. Circling was produced at 1, 2 and 4 mA. The direction of circling was consistent upon retest. Circling was not blocked by either haloperidol or alpha-methyl-p-tyrosine (AMPT) and the direction of circling induced by shock was independent from that exhibited spontaneously during the 24 h prior to the test. These findings suggest that aversive-stimulus-induced circling is not mediated by the nigrostriatal dopamine system.

Amphetamine↗
PubMed1972

Reversible differential block of saphenous nerve by cold.

1. This report is concerned with the question of whether the alpha and delta groups of myelinated A fibres show conduction failure at different temperatures.2. The experiments were done on cat saphenous nerve in vitro. Stimuli were applied to both ends of the nerve and biphasic recordings were taken adjacent to an 11 mm segment of nerve, whose temperature was varied. Before cooling commenced, the stimuli were adjusted so that the action potential which passed through the cold zone and was recorded, collided with the action potential initiated at the opposite end of the nerve.3. Upon cooling the nerve, it was always observed that the delta peak of the action potential which had been previously occluded by collision reappeared at a temperature at which the alpha peak remained occluded.4. The reappearance of the delta peak was reversible upon warming the nerve and was not affected by increasing the interstimulus interval.5. The mean temperature for reappearance of the delta peak was 13.5 degrees C, for reappearance of the alpha peak, 5.3 degrees C.6. In any given nerve, the blocking temperature was replicable and was dependent on the temperature of the cooled segment rather than the gradient between that segment and the remainder of the nerve.7. We conclude that in cat saphenous nerve, the delta group of myelinated A fibres shows conduction failure at a higher temperature than does the alpha group.

Action Potentials↗
PubMedDate not supplied

Superficial venous thrombosis presenting as a painful popliteal fossa mass in a child.

We report an unusual case of superficial venous thrombosis in a cyanotic 12-year-old child who had undergone recent appendectomy. Although compression, color Doppler, and duplex ultrasound techniques remain the keys to the diagnosis of venous thrombosis, SieScape sonography was beneficial in demonstrating the extent of the thrombi and their location along a superficial thrombosed vein.

Acute Disease↗
PubMedDate not supplied

Modulation of coronary vascular resistance in female rabbits by estrogen and progesterone.

OBJECTIVE: To study the roles of estradiol and various progestins on the regulation of coronary flow in female rabbits. METHODS: Ovariectomized adult female rabbits were treated with estradiol, with progesterone (or one of the following synthetic progestins: megace, norethindrone, or medroxyprogesterone acetate), or with both an estradiol and a progestin. Hearts were isolated and perfused at constant pressure by a modified Langendorff technique. Changes in coronary flow were determined at baseline and in response to direct infusion into the coronary circulation of NG-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide (NO) synthase. RESULTS: Coronary flow rates were 40-50% greater in hearts of animals treated with estradiol than in control hearts of animals not treated with the hormone. Treatment of the animals with progestin alone had little effect on coronary flow. However, when administered with estradiol, it abrogated the estradiol-related increase in coronary flow. The increments in coronary flow evoked by estradiol were virtually abolished by L-NNA, an inhibitor of NO synthase. In hearts of animals treated with estradiol plus progesterone, L-NNA had no additional inhibitory effect on coronary flow to that of progesterone. CONCLUSION: Estradiol decreases coronary vascular resistance (CVR) and hence increases coronary flow. Progestins attenuate this effect of estradiol.

Animals↗