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Biomedical subjects

M F Roizen

Publications and source records attributed to M F Roizen.

At least 163 records · Page 9Linked to original sources
PubMed1979

Uterine blood flow and plasma norepinephrine changes during maternal stress in the pregnant ewe.

Because maternal stress may adversely affect the fetus, the authors tested the effects of brief episodes (15-60 sec) of maternal stress in 18 awake pregnant ewes. Maternal agitation and stuggling occurred either following non-painful stimuli such as loud noises or sudden movements of personnel (ten animals) or following the brief application of the ewe's skin of a uniform electrical stimulus of 30 volts with a frequency of 167 Hz for 30-60 sec (eight animals). Stimulation of either type produced a 45-50 per cent increase in mean maternal arterial blood pressure and a concomitant 32-52 per cent decrease in uterine blood flow (P less than 0.05). The decreases in uterine blood flow were brief, lasting less than 3 min, and were not associated with fetal asphyxia. Maternal plasma norepinephrine levels were measured following electrically induced maternal stress and were increased 25 per cent. The authors conclude that maternal stress may decrease uterine blood flow secondary to release of endogenous norepinephrine.

Acid-Base Equilibrium↗
PubMed1978

Pancuronium bromide.

Pancuronium bromide is a nondepolarizing muscle relaxant approved to induce skeletal muscle relaxation during anesthesia and to facilitate the management of patients undergoing mechanical ventilation. The use of pancuronium bromide during surgery led to the appreciation that it has advantages over drugs previously used for muscle relaxation. Patients in whom pancuronium bromide is of value are (1) hypoxemic patients resisting mechanical ventilation and so cardiovascularly unstable that use of sedatives is precluded, (2) patients with bronchospasm unresponsive to conventional therapy, (3) patients with severe tetanus or poisoning where muscle spasm prohibits adequate ventilation, (4) patients with status epilepticus unable to maintain their own ventilation, (5) shivering patients in whom metabolic demands for oxygen should be reduced, and (6) patients requiring tracheal intubation in whom succinylcholine administration is contraindicated. Without concomitant sedation, use of pancuronium bromide is associated with psychological risks. Other risks are undetected ventilator disconnection, tachyarrythmias, prolonged paralysis and drug interactions.

Animals↗
PubMed1978

Effect of general anesthetics on handling- and decapitation-induced increases in sympathoadrenal discharge.

The effect of five anesthetics--cyclopropane, pentobarbital, urethane, chloralose or ketamine hydrochloride--on handling- or decapitation-induced increases in adrenergic tone were studied in the intact rat. The anesthetic agents tested prevented or markedly reduced stress-induced increases in levels of plasma total catecholamines and norepinephrine. Similar changes in norepinephrine were seen in corticosterone- treated adrenalectomized rats in which this catecholamine seemed to be the only one present in plasma. During anesthesia with cyclopropane, blood pressure fell; there was no additional decrease in total plasma catecholamines when the concentration of the inhaled anesthetic agent was increased. With increased length of cyclopropane anesthesia, however, total catecholamine and norepinephrine concentrations increased. Thus, the different effects of anesthetics on the cardiovascular system cannot be solely explained by their effects on stress-induced increases in sympathetic neuronal activity as reflected by circulating catecholamine levels.

Adrenal Medulla↗
PubMed1977

Effect of prolonged treatment with adrenergic neuron blocking drugs on sympathoadrenal reactivity in rats.

The effects of repeated high doses of the adrenergic neuron blocking drug guanethidine or a hexahydropyrazinoindole compound (2-guanyl-1,2,3,10,10a, hexahydro-1,2,a-pyrazinoindole, EMD 21192) (30 mg/kg i.p., 21.5 mg/kg i.p. respectively, equimolar doses) on sympathoadrenal activity were investigated in normotensive adult rats. During treatment for 5 weeks with either guanethidine or EMD 21192 the systemic blood pressure fell steadily. Noradrenaline content in the heart and vas deferens were decreased markedly by guanethidine and to a much less degree by EMD 21192. EMD 21192 markedly lowers the catecholamine content of the adrenal medulla, presumably as a result of inhibition of dopamine-beta-hydroxylase. The plasma catecholamine concentrations reflected the different sites of action of the drugs in the sympathoadrenal system, i.e. guanethidine mainly reduced circulating norepinephrine and dopamine-beta-hydroxylase by more than 50%, whereas EMD 21192 decreased considerably by the total catecholamines (mainly epinephrine) without altering significantly in the plasma norepinephrine. Disappearance or reduction of fluorescent nerve endings in the iris and the heart and a decrease of the intensity of fluorescence in chromaffin cells of the adrenal gland caused by the drugs were consistent with the biochemical alteration. Whereas the repeated doses of guanethidine caused degeneration of sympathetic nerves, destruction of adrenergic neurons was not found after prolonged treatment with EMD 21192.

Adrenal Glands↗
PubMed1976

The effect of two anesthetic agents on norepinephrine and dopamine in discrete brain nuclei, fiber tracts, and terminal regions of the rat.

Catecholaminergic neurons have been implicated in the mechanism of general anesthesia, but previous attempts at measuring changes in adrenergic neuron function during anesthesia have been limited by techniques to whole brain. Microdissection techniques and sensitive radioisotopic-enzymatic assays were used to measure levels of catecholamines in 20 different nuclei, fiber tracts or nerve terminal regions in brains of rats anesthetized for 90-105 min with 1% halothane or 18% cyclopropane. These two anesthetics were chosen because of their diverse effects on the electroencephalogram and on the cardiovascular and respiratory systems. Of the areas examined, significant increases in norepinephrine content with both anesthetic agents were found only in the nucleus accumbens, locus coeruleus and central gray catecholamine areas. Only in the nucleus accumbens was the dopamine level increased by both anesthetics; cyclopropane, but not halothane anesthesia, also increased the dopamine content of the caudate nucleus, while halothane, but not cyclopropane anesthesia, significantly decreased the dopamine level of the ventral nucleus of the thalamus. Changes in levels of transmitters do not distinguish cause from effect of anesthesia, and further experiments are needed to delineate what role, if any, the specific areas play in muscle relaxation, analgesia, sleep or anesthesia. This study shows that a drug can affect one nucleus or region without significantly affecting other regions that contain the same transmitter substance, and that changes in transmitter levels can occur selectively in different regions of brain even if the nerve endings are derived from contiguous cell bodies.

Animals↗
PubMed1976

Peripheral and central catecholaminergic neurons in genetic and experimental hypertension in rats.

1. Activity of peripheral and central catecholaminergic neurons was studied in spontaneously hypertensive rats (SHR) and deoxycorticosterone (DOCA)-salt hypertensive rats. 2. In young SHR (4 weeks) the plasma values of bpth noradrenaline and dopamine-beta-hydroxylase activity were increased compared with those of normotensive rats of the Wistar/Kyoto strain. Total catecholamines (mostly adrenaline) were not significantly different. 3. In the adrenal glands of 2-weeks-old and 4-weeks-old SHR activities of tyrosine hydroxylase, dopamine-beta-hydroxylase, phenylethanolamine-N-methyl transferase were decreased, compared to Wistar/Kyoto rats. 4. The adrenaline-forming enzyme was elevated in the A1 and A2 regions of the brain stem of 4-weeks-old SHR and in the A1 region of adult DOCA-salt hypertensive rats. 5. In the adrenal glands of adult DOCA-salt hypertensive rats tyrosine hydroxylase activity was increased. 6. These results implicate peripheral noradrenaline-containing neurons and central adrenaline-containing neurons in the development of genetic and experimental hypertension in rats.

Adrenal Glands↗
PubMed1976

Inhibition by cyclopropane of release od norepinephrine, but not dopamine-beta-hydroxylase, from the guinea-pig vas deferens.

Like halothane, cyclopropane reduces stimulation-induced release of norepinephrine, but not release of dopamine-beta-hydroxylase, from the isolated guinea-pig vas deverens. The dissociation between transmitter release and enzyme release in the presence of cyclopropane may be the result of either an increase in the affinity of norepinephrine for binding sites on the vesicular membrane produced by cyclopropane, or a direct effect of cyclopropane on a mechanism of release of norepinephrine that could be controlled independently of release of dopamine-beta-hydroxylase.

Animals↗
PubMed1975

The effect of two diverse inhalation anesthetic agents on serotonin in discrete regions of the rat brain.

Sensitive radioisotopic enzymatic methods were used to determine 5-HT levels in 16 different regions of brain from rats anesthetized for 90-105 min with 1% halothane or 18% cyclopropane. These two anesthetics were chosen because of their differing effects on the electroencephalogram and on the cardiovascular and respiratory systems. 5-HT levels in the nucleus amygdaloideus centralis, substantia nigra, and nucleus centralis superior were increased after administration of either anesthetic, but only anesthesia with cyclopropane was associated with an increase in 5-HT level in the nucleus raphe dorsalis. The changes in levels of transmitter does not distinguish cause from effect of anesthesia, and further experiments are needed to delineate what role, if any, the specific areas play in muscle relaxation, analgesia, sleep or anesthesia.

Amygdala↗