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Biomedical subjects

W H Griffith

Publications and source records attributed to W H Griffith.

50 records · Page 3Linked to original sources
PubMed1978

The protective effect of phentolamine against cardiac arrhythmias in the rat.

Norepinephrine was given by continuous infusion at a rate of 80 microgram/kg/min for 2 min. Norepinephrine caused the appearance of cardiac arrhythmias, primarily ventricular extrasystoles. The prior administration of phentolamine, even in a dose which did not antagonize the pressor effect of norephinephrine, prevented extrasystole production by norepinephrine. Tolazoline and yohimbine, in doses which did not affect the vasopressor action of norepinephrine, also suppressed extrasystole production. It is concluded that the antiarrhythmic effect of phentolamine, does not require antagonism of alpha-adrenoceptors of the type found in the vasculature, but may involve effects on a different type of alpha-adrenoceptors in the heart.

Angiotensin II↗
PubMedDate not supplied

Age-related decline in cholinergic synaptic transmission in hippocampus.

Age-dependent changes in central nervous system (CNS) cholinergic synaptic transmission were studied in three age groups of Sprague-Dawley and Fischer 344 rats: 1- to 2-month-old, 8- to 10-month-old, and 18- to 23-month-old. Utilizing intracellular recording techniques and the in vitro hippocampal slice preparation, we report an age-related decline in central cholinergic transmission as a function of age. Slow excitatory postsynaptic potentials (slow EPSPs) were reduced approximately 60% in aged (18- to 23-month-old) compared to younger (1- to 2-month-old) animals. The response of the postsynaptic membrane to the muscarinic agonist, carbachol (0.3 microM), was also reduced with age. These changes were not accompanied by a global decline in muscarinic receptor function since two additional measures of cholinergic function were not changed with age. Both presynaptic inhibition of fast excitatory synaptic transmission and postsynaptic inhibition of the afterhyperpolarization (AHP) following a train of spikes were not changed during aging. Our results suggest that a primary functional decline in central cholinergic mechanisms during aging may be a specific reduction in central cholinergic synaptic transmission.

Aging↗
PubMedDate not supplied

Acute ethanol dependence or long-term ethanol treatment and abstinence do not reduce hippocampal responses to carbachol.

In the hippocampus of human alcoholics, prolonged ethanol treatment reduces the number of muscarinic ligand binding sites present at autopsy suggesting a decrease in functional muscarinic receptors. Whether these changes are due to alcohol-induced brain damage or ethanol dependence and represent a reduced level of cholinergic function is unknown. The present studies tested the impact of ethanol dependence or long-term ethanol treatment and subsequent withdrawal on the function of pre- and postsynaptic muscarinic receptors in the CA1 region of the rat hippocampus. Field excitatory postsynaptic potentials (EPSPs) were inhibited in a concentration-dependent manner by 0.1-100 microM carbachol. This presynaptic inhibitory action of carbachol involving muscarinic receptors was not significantly reduced either by ethanol treatment (12 days), causing physical dependence, or by long-term ethanol treatment (97-120 days) and abstinence (3-6 months). Postspike after hyperpolarizations (AHPs) were inhibited in a concentration-dependent manner by carbachol (6-2000 nM). This postsynaptic excitatory action of muscarinic receptors also was not significantly reduced either by 12-day ethanol treatment or by long-term ethanol treatment. Taken together, these results suggest that neither pre- nor postsynaptic muscarinic receptor function measured electrophysiologically is reduced by either ethanol dependence or long-term ethanol consumption and abstinence in the rat as suggested by reduced muscarinic ligand binding in the hippocampus of human alcoholics.

Alcoholism↗