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Biomedical subjects

L C Lee

Publications and source records attributed to L C Lee.

64 records · Page 4Linked to original sources
PubMed1976

Petit mal status in a patient with chronic renal failure.

A 39-year-old woman with traumatic spinal paraplegia and chronic renal failure had peritoneal dialysis for acute renal failure precipitated by a bout of urinary tract infection. Two weeks after the dialysis she lapsed into coma for a few days. An electroencephalogram indicated petit mal stupor as it showed generalized epileptic discharges during the initial period of her coma.

Adult↗
PubMed1976

Epileptic discharges triggered by blinking and eye closure.

Two children manifested EEG discharges which were triggered by blinking and/or eye closure in light and in darkness. The first case demonstrated single focal posterior discharges with eye blinks and repetitive focal posterior sharp wave discharges with eye closures. No photoparoxysmal responses were obtainable. Case 2 manifested generalized epileptic discharges triggered by eye closure which were sometimes associated with clinical seizures. In addition she showed photoconvulsive responses. Since the discharges triggered by eye blink and by eye closure occurred in both bright light and in darkness it is suggested that sensory afferents arising from contraction of the orbicularis oculi muscles may have been the epileptic trigger in Case 1 and could have contributed to the epileptic triggering mechanism in Case 2.

Adolescent↗
PubMedDate not supplied

Antihypertensive and hypothalamic depressant effects of tripamide in spontaneously hypertensive rats.

When tripamide was added to the food of spontaneously hypertensive rats (SHR), there were no appreciable effects on heart rate, body weight, or food intake. Tail-cuff systolic pressures measured weekly were also unaffected in normotensive control rats (WKY), but the elevation expected in SHR was significantly reduced. Pressor responses to hypothalamic stimulation were also reduced selectively only in SHR. A peripheral inhibition of cardiovascular reactivity was considered unlikely, since pressor responses to injected norepinephrine, tyramine, or vasopressin were unaltered. Diminished pressor responsiveness was considered to be due to concurrent reduction of central sympathetic vasomotor activity, because sympathetic nerve responses to hypothalamic stimulation were appreciably lessened in tripamide-treated SHR. Although neither the site nor the mechanism causing sympathetic inhibition was determined exactly, our results are in accord with the interpretation that antihypertensive effects of tripamide in SHR depend, at least partly, on sympathetic inhibition.

Animals↗