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E H Rubinstein

Publications and source records attributed to E H Rubinstein.

44 records · Page 3Linked to original sources
PubMedDate not supplied

Midlatency auditory evoked responses: differential effects of a cholinergic agonist and antagonist.

The effects of a cholinergic antagonist (scopolamine) and agonist (physostigmine) on the auditory middle latency evoked responses (MLRs) were studied in 7 normal male volunteers. Scalp recordings were made from a central (Cz) electrode referenced to linked ear lobes on one channel and to a non-cephalic, sternovertebral reference on a second channel. Three components were statistically analyzed for changes in latency and amplitude: Pa, with peak positivity in the 25-40 msec latency range, Nb, with peak negativity 40-50 msec, and P1, with peak positivity 50-65 msec. Control recordings included responses to click rates of 1, 5, 8 and 10/sec; as has been previously reported, P1 showed a marked decrease and disappeared at the faster rates of stimulation whereas Pa showed no change in amplitude. Intravenous injections of scopolamine resulted in a rapid and complete disappearance of P1 and a slight increase in Pa; concurrently, the subjects reported feeling drowsy but were awake with eyes open through the recordings. Subsequent injections of physostigmine resulted in a rapid reversal of the scopolamine effects so that the subjects became alert, Pa decreased, and P1 reappeared and increased to control amplitudes. Rapid click rates caused P1 to diminish, as in the control period, indicating a common P1 recovery cycle in both the control and physostigmine conditions. These data are discussed in terms of the hypothesis that the P1 generator system is comprised of a cholinergic brain-stem-thalamic component of the ascending reticular activating system.

Adult↗
PubMedDate not supplied

Enhancement of cerebrovascular effect of CO2 by hypoxia.

Internal carotid blood flow, taken as an index of cerebral blood flow (CBF); arterial pressure; and respiratory O2 and CO2 concentrations, were measured in halothane (1%)-anesthetized, paralyzed and mechanically ventilated rabbits. CBF was determined at end-tidal CO2 of 4% (normocapnia) and 8%, as inspired O2 [O2]I) was varied stepwise over the range of 6.5 to 92%. Normocapnic CBF was constant over the range of 15 to 92% [O2]I, but it increased significantly to 240% and 380% of control when [O2]I was at 10% and 6.5%, respectively. Cerebrovascular response to CO2 was constant over the range of [O2]I tested, except for a significant elevation to 180% of control at [O2]I of 10%.

Animals↗
PubMedDate not supplied

Effect of ketamine on cerebral cortical blood flow and metabolism in rabbits.

The effects of intravenous ketamine (1 mg/kg) on cerebral cortical blood flow and O2 uptake were evaluated in 13 anesthetized, ventilated rabbits. Blood flow was measured either directly (Group 1) or by the H2 clearance method (Group 2). In those animals of Groups 1 and 2 with normal control arterial pH (pHa), ketamine produced a significant increase in cerebral cortical blood flow of 18 and 34%, respectively, but had no effect on cerebral cortical O2 uptake. However, in rabbits with low control pHa, ketamine caused an increase in blood flow (30%) accompanied by a significant increase in O2 uptake (22%). Ketamine produced nonsignificant changes in mean arterial blood pressure and arterial blood gases, except for a significant reduction in pressure in animals with low pHa. It is concluded that ketamine is a cerebral vasodilator without cerebral metabolic effect when mean arterial blood pressure and arterial PCO2, PO2, and pH are held constant at physiologic levels. The vasodilator effect of ketamine is probably due to direct dilating action or activation of a cholinergic cerebral vasodilator system.

Animals↗
PubMedDate not supplied

Cholinergic cerebral vasodilator effect of ketamine in rabbits.

To analyze the mechanism of the cerebral vasodilator effect of ketamine in anesthetized rabbits, we measured the internal carotid blood flow with an electromagnetic flowmeter, the arterial pressure, intracranial pressure, end-tidal CO2, and the electroencephalogram. Ketamine injection (1 mg/kg) induced a significant cerebral vasodilatation that was blocked by scopolamine, a cholinergic antagonist. In contrast, the increase in cerebral blood flow after ketamine was additive to the cerebral vasodilator actions of inhaled CO2 and of physostigmine infusion, two procedures that activate cholinergic mechanisms. These observations suggest that in rabbits, ketamine activates a cholinergic cerebral vasodilator system.

Animals↗
PubMedDate not supplied

Cerebrovascular CO2 reactivity: role of a cholinergic mechanism modulated by anesthesia.

Cerebral cortical blood flow was measured in rabbits with the hydrogen clearance technique. The reactivity to CO2, tested by changing the end tidal CO2 (ETCO2) in steps from 2 to 6 volumes %, was highly dependent on the kind of anesthesia, being greatest under halothane and least under nitrous oxide. Reactivity to CO2 in halothane-anesthetized animals also depended on arterial blood pressure, being greatest when pressure was below 70 mm Hg. Intravenous atropine blocked the increase in reactivity in halothane-anesthetized animals at low blood pressures. Conversely, intravenous eserine (physostigmine) greatly increased the reactivity to CO2 in nitrous oxide-anesthetized animals. Precollicular decerebration considerably decreased CO2 reactivity of halothane-anesthetized rabbits, while partial brain stem lesions that spared midline structures had no effect on CO2 reactivity. It is concluded that a central neurogenic mechanism with a cholinergic link may be responsible, at least in part, for the cerebrovascular effect of CO2. Moreover, the cerebrovascular effects of halothane may result from stimulation of the same system.

Anesthesia↗