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Biomedical subjects

A P Chang

Publications and source records attributed to A P Chang.

8 recordsLinked to original sources
PubMed1998

Focal conduction block in n-hexane polyneuropathy.

A 19-year-old man with an asymptomatic history of recreational gasoline vapor inhalation presented with subacute progressive quadriparesis. For 2 weeks, he had intensely inhaled Coleman fuel oil vapor, which contains n-hexane. Nerve conduction studies including near-nerve needle stimulation showed focal conduction block in the bilateral median and ulnar nerves. Sural nerve biopsy was consistent with giant axonal neuropathy. Conduction block as seen in this case has not heretofore been described in n-hexane polyneuropathy.

Administration, Inhalation↗
PubMed1990

Role of plasma catecholamines in eliciting cardiovascular changes seen during naloxone-precipitated withdrawal in conscious, unrestrained morphine-dependent rats.

Rats given morphine (8 mg/kg i.v.) followed after 2 hr by infusions of morphine (4 mg/kg i.v.) every 2 hr for 24 hr (total infusion time of 2 min for each infusion) became dependent on morphine. Injection of the opiate antagonist naloxone (5 mg/kg) precipitated a withdrawal response including an increase in mean arterial blood pressure (BP), biphasic heart rate response and an increase in plasma norepinephrine (NE) and Epinephrine (Epi). Plasma Epi was also higher after abrupt withdrawal from morphine. After removal of adrenal glands from morphine-dependent rats, naloxone injection produced no change in the BP or plasma Epi. However, naloxone injection to morphine-dependent rats treated with phentolamine to block the alpha receptor-mediated effects of circulating catecholamines led to a significant decrease in BP even though plasma Epi increased 8-fold. In morphine-dependent rats in which NE levels in sympathetic nerves have been reduced by prior exposure to 6-hydroxydopamine, naloxone produced a biphasic BP response, an initial decrease followed by an increase along with a 3-fold increase in plasma Epi. These results suggest that Epi released from the adrenal medulla of morphine-dependent rats mediates, in large part, the autonomic withdrawal responses elicited by naloxone. Naloxone injection to control and morphine-dependent rats produced similar increases in plasma NE (2-fold) indicating that the increase in plasma NE is not responsible for the withdrawal response.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1989

Effect of naloxone on blood pressure responses and plasma catecholamine levels following clonidine injection in conscious, unrestrained rats.

Intravenous injection of clonidine produces a biphasic blood pressure response, a transient increase followed by a prolonged decrease. Significant increases in plasma norepinephrine (NE), epinephrine (EPI), and dopamine (DA) levels occur 5 min following injection, corresponding to the hypertensive phase. Thirty minutes after clonidine injection, blood pressure, NE, EPI, and DA levels had returned to control levels. However, at 60 min, when the blood pressure had decreased to below control levels, a significant decrease in plasma NE was found. This finding confirms that clonidine decreases blood pressure, in part, by reducing sympathetic nerve activity. Naloxone, an opiate antagonist, when given prior to clonidine, abolished the hypotensive phase as well as preventing the decrease in plasma NE levels. The hypertensive phase was potentiated. Naloxone, when given alone, increased plasma NE levels at 15, 40, and 70 min following injection, indicating that naloxone increases sympathetic nerve activity peripherally, and may prevent clonidine's hypotensive phase by also increasing sympathetic activity in the central nervous system through blockade of opiate receptors. Therefore, the hypotensive effect of clonidine may involve interactions with endogenous opiate peptides.

Animals↗