Richard A. Theye

Bio: Richard A. Theye is an academic researcher from University of Minnesota. The author has contributed to research in topics: Cerebral blood flow & Halothane. The author has an hindex of 6, co-authored 8 publications receiving 217 citations.

The effects of morphine and N-allylnormorphine on canine cerebral metabolism and circulation.

Abstract: The effects of morphine and nalorphine on cerebral metabolism and circulation were examined in 18 dogs. Incremental doses of morphine caused progressive decreases in CMRo2 and CBF to 85 per cent and 45 per cent of control, respectively, until a dose of 1.2 mg/kg had been given in a one-hour period. Subsequent doses had no further significant effect. The decrease in CBF resulted from both a direct action of morphine (approximately 30 per cent) and the effect of time on experimental canine CBF. A single large dose of morphine (2 mg/kg) had similar effects on CMRo2 and CBF. These effects were reversed by nalorphine (0.3 mg/kg), which initially produced overshoots in both CMRo2 and CBF. Subsequent doses of nalorphine had no further effect. EEG changes correlated with CMRo2 changes caused by morphine and nalorphine. Nalorphine given alone (0.3 mg/kg) produced small decreases in both CMRo2 and CBF, an effect not magnified by subsequent larger doses.

The Response of Denervated Skeletal Muscle to Succinylcholine

Abstract: The responses of denervated and normal canine gastroenemius muscle to succinylcholine (SCh) were compared and contrasted in regard to potassium (K+) flux O2, muscle tension, and electrical activity. K+ efflux and O2 of denervated muscle increased 20-fold and fourfold after SCh, respectively, while K

Myocardial and total oxygen consumption with halothane.

Abstract: In paralyzed dogs, with steady systemic flow rates of 2.0 liters/mtnute/m.2 assured by right-heart bypass, increasing halothane from 0.1 to 0.9 per cent resulted in an 8 per cent reduction in rate of whole-body Or consumption (&OV0312;O2) in the presence of vagotomy and spinal anesthesia. The decrease in non-myocardial &OV0312;O2 was 7 per cent and unrelated to changes in arterial pressure. The latter change in &OV0312;O2 is believed due to a direct depressant effect of halothane. Reductions in myocardial &OV0312;O2 were related to decreases in external work of the heart and are considered to represent indirect depressant effects of halothane.

Effects of methoxyflurane on canine cerebral metabolism and blood flow.

Abstract: The rate of cerebral oxygen consumption (CMRo2) and the cerebral blood flow (CBF) were determined in eight dogs at three end-expired concentrations of methoxyflurane (means >0.1, 0.25, and 0.44 per cent). With each increase in concentration above >0.1 per cent, a significant decrease in CMRo2 was observed (approximately 10 and 25 per cent less than the >0.1 per cent value, respectively). The cerebrovascular effects of methoxyflurane were less striking. At 0.25 per cent, a small but significant increase in CBF and a decrease in (cerebral vascular resistance) CVR were observed, compared with the >0.1 per cent values. No further significant change was observed at higher concentrations. The cerebrovascular responses to changes in Paco2 were tested at 0.25 per cent end-expired methoxyflurane. Over a range of Paco2 of approximately 20 mm Hg (30 to 50 mm Hg), the expected responses of CBF and CVR were observed. The authors conclude that methoxyflurane resembles halothane in its overall cerebral metabolic effects but, unlike halothane, produces only modest changes in CVR and CBF.

Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms.

Abstract: Lethal hyperkalemic response to succinylcholine continues to be reported, but the molecular mechanisms for the hyperkalemia have not been completely elucidated. In the normal innervated mature muscle, the acetylcholine receptors (AChRs) are located only in the junctional area. In certain pathologic states, including upper or lower motor denervation, chemical denervation by muscle relaxants, drugs, or toxins, immobilization, infection, direct muscle trauma, muscle tumor, or muscle inflammation, and/or burn injury, there is up-regulation (increase) of AChRs spreading throughout the muscle membrane, with the additional expression of two new isoforms of AChRs. The depolarization of these AChRs that are spread throughout the muscle membrane by succinylcholine and its metabolites leads to potassium efflux from the muscle, leading to hyperkalemia. The nicotinic (neuronal) 7 acetylcholine receptors, recently described to be expressed in muscle also, can be depolarized not only by acetylcholine and succinylcholine but also by choline, persistently, and possibly play a critical role in the hyperkalemic response to succinylcholine in patients with upregulated AChRs.

Nimodipine Improves Cerebral Blood Flow and Neurologic Recovery after Complete Cerebral Ischemia in the Dog

Abstract: Ten minutes of complete ischemia was produced in 11 dogs by temporary ligation of the aorta. Immediately before the ischemic episode, the dogs received nimodipine, a new calcium entry blocker, 10 μ...

Prevention of neurological damage during open-heart surgery.

Abstract: A previous study of neurological damage related to open-heart surgery suggested that the onset of cardiopulmonary bypass is a time of particular hazard, and there is evidence that both microemboli from the extracorporeal circulation and inadequate cerebral perfusion may be contributory factors. Measures to eliminate or minimize these hazards have been introduced, and a clinical survey has been undertaken to evaluate their efficacy. There has been a very highly significant decrease in the incidence of neurological damage as judged by comparison with the results of a similar survey carried out before these measures were introduced. In spite of limitations imposed by differences in workload, perfusion techniques, and methods of data collection, it is concluded that the prophylactic measures have been responsible for the reduction in the incidence of neurological damage.