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Biomedical subjects

G P Cooper

Publications and source records attributed to G P Cooper.

32 records · Page 2Linked to original sources
PubMed1977

Catalytically and noncatalytically treated automobile exhaust: biological effects in rats.

Chronic exposure to catalytically treated or noncatalytically treated automobile exhaust significantly depressed the spontaneous locomotor activity (SLA) of rats. Exposure to H2SO4 alone or CO at comparable levels did not alter the SLA. Exposure to noncatalytically treated exhaust resulted in significant reductions in growth rate and food and water intake. However, these effects were not evident in the exposure to catalytically treated exhaust or in the control H2SO4 and CO exposures. Blood acid-base analyses indicated that exposure to either catalytically treated exhaust or H2SO4 elicits a metabolic alkalosis, while exposure to CO alone results in a metabolic acidosis. All acid-base parameters were within the normal range several weeks after the termination of exposure.

Acid-Base Equilibrium↗
PubMed1977

Effects of cadmium and lead on adrenergic neuromuscular transmission in the rabbit.

The effects of inorganic lead (PbCl2) and cadmium (DdCl2) on the pressor response of rabbit saphenous arteries produced by sympathetic nerve stimulation were examined. A 1- to 3-cm length of artery was removed, placed in a bath containing mammalian Ringer solution, and perfused with the same solution at a constant rate sufficient to maintain a 40-60 mmHg perfusion pressure. Increases in perfusion pressure resulting from electrical stimulation -f periarterial nerve endings were reduced or completely blocked by the addition of 5-20 muM lead or cadmium to the bathing solution for a period of 15-30 min. Responses to norepinephrine or to direct electrical stimulation of the muscle remained relatively unaffected. During lead or cadmium blockade, the response to nerve stimulation could be restored by a fourfold increase in calcium concentration. It is concluded that lead and cadmium reduce the response to sympathetic nerve stimulation primarily through an effect on presynaptic nerve terminals.

Action Potentials↗
PubMed1975

Effects of formaldehyde and ozone on the trigeminal nasal sensory system.

The effects of formaldehyde and ozone on the electrical activity of the nasopalatine nerve were studied in anesthetized rats. The response (increase in action potential frequency) of nasopalatine and ethmoidal nerves to brief presentations of formaldehyde, ozone, or amyl alcohol was a power function of stimulus concentration. When formaldehyde was presented continuously for one hour, it produced a decrease in nasopalatine nerve response to amyl alcohol that varied directly with the formaldehyde concentrations employed. Perfusion of the nasal cavities with air for one hour following the formaldehyde exposure resulted in a partial recovery of the neural response to amyl alcohol. Ozone exposures of 5 ppm lasting one hour produced an increase in nasopalatine nerve response to amyl alcohol. Air perfusion following the ozone exposure reduced the neural response to amyl alcohol, but not to preexposure levels.

Analysis of Variance↗
PubMed1970

Response of olfactory bulb neurons to x-rays as a function of nasal oxygen concentration.

Responses of single olfactory bulb neurons in rats to x-irradiation of the head were examined during the perfusion through the nasal cavities of gas containing various concentrations of oxygen. Response to x-ray was unchanged with oxygen concentrations of from 100 percent down to about 5 percent. Progressively larger response decrements were observed with oxygen concentrations of 2 percent and less.

Animals↗
PubMedDate not supplied

Differential effects of triethyllead on synaptosomal [3H]dopamine vs. [3H]acetylcholine and [3H]gamma-aminobutyric acid release.

In vitro exposure to tetraethyllead (Et4Pb, 10 microM) did not alter the release of [3H] dopamine (DA), [3H]acetylcholine (ACh), or [3H]gamma-aminobutyric acid (GABA) from superfused synaptosomes isolated from rat brain striatum, hippocampus, and cortex, respectively. On the other hand, a concentration-dependent increase in the spontaneous release of these transmitters was observed following exposure to triethyllead (Et3Pb, 0.1-10 microM). The magnitude of 1 microM Et3Pb-induced [3H]DA release was 5-fold greater than that observed for [3H]ACh or [3H]GABA release. Removal of [Ca2+]e did not alter the Et3Pb-induced increase in the release of these three transmitter substances, nor did Et3Pb alter synaptosomal 45Ca efflux. EtePb-induced [3H]ACh and [3H]GABA release, but not [3H]DA release, was blocked by lowering [Na+]e from 140 to 50 mM. Similarly, the release of [3H]ACh and [3H]GABA, but not [3H]DA, induced by either Na,K-ATPase inhibition or veratridine (a Na(+)-ionophore), was attenuated by lowering [Na+]e from 140 to 50 mM. However, Et3Pb did not inhibit isolated synaptic membrane Na,K-ATPase, nor did the magnitude or temporal patterns of Et3Pb-induced transmitter release resemble transmitter release induced by Na,K-ATPase inhibition. Et3Pb and veratridine, but not Na,K-ATPase inhibition, produced an increase in synaptosomal [3H] deoxyglucose phosphate (dGluP) efflux, suggesting that both compounds increase membrane permeability. A Et3Pb-induced increase in membrane permeability is further supported by electrophysiological studies using the frog neuromuscular junction in which Et3Pb was found to reduce both the input resistance and membrane potential of muscle cells. As with [3H]ACh and [3H]GABA release, the Et3Pb-induced increase in synaptosomal [3H]dGluP efflux was attenuated by lowering [Na+]e.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗