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Biomedical subjects

B D Miller

Publications and source records attributed to B D Miller.

At least 37 records · Page 2Linked to original sources
PubMed1983

Inhibition of cardiac sympathetic nerve activity during intravenous administration of lidocaine.

The antiarrhythmic action of lidocaine has been attributed solely to its direct electrophysiological effects on the heart. However, lidocaine is particularly effective in treating ventricular arrhythmias associated with increased sympathetic activity, e.g., in myocardial infarction and digitalis toxicity. We tested the hypothesis that lidocaine administered intravenously depressed cardiac sympathetic nerve activity (CSNA). We measured CSNA in six dogs in control state and after lidocaine in doses of 0.625, 1.25, and 2.5 mg/kg i.v. over 2 min. These doses of lidocaine produced graded decreases of CSNA of -8 +/- 2, -18 +/- 1, and -41 +/- 5%, respectively (P less than 0.05, mean +/- SE). In six additional experiments the bolus of lidocaine was followed by an infusion for 20 min (1.25 mg/kg followed by 100 micrograms/kg per min and 2.5 mg/kg followed by 200 micrograms/kg per min). Infusion of lidocaine maintained depression of CSNA at a level that was 23 +/- 3 and 35 +/- 5% less than control (P less than 0.05), respectively, at plasma lidocaine levels of 5.2 +/- 0.6 and 7.5 +/- 1.4 micrograms/ml, respectively. CSNA returned to control during recovery periods. CSNA did not decrease with the passage of time or administration of vehicle. In five dogs with vagi intact, carotid sinuses isolated and held at a pressure of 100 mmHg, and aortic baroreceptors denervated, administration of lidocaine (2.5 mg/kg followed by 200 micrograms/kg per min) decreased renal nerve activity to 71 +/- 8% of control. Increases in left ventricular systolic pressure and maximum derivative of pressure with respect to time (dP/dtmax) resulting from electrical stimulation of preganglionic sympathetic nerves were not significantly altered by lidocaine, but were markedly attenuated by hexamethonium, a ganglionic blocker. In conclusion, lidocaine administered intravenously produces dose-dependent and sustained decreases in cardiac sympathetic nerve activity. These decreases can occur with therapeutic plasma levels. We speculate that this effect is due to central nervous system effects of the drug and that this effect may contribute to the antiarrhythmic actions of lidocaine.

Animals↗
PubMed1982

Baroreflex regulation of renal nerve activity during volume expansion.

Volume expansion could inhibit renal nerve activity by stimulating cardiopulmonary baroreflexes or by increasing arterial pressure (i.e., stimulating the sinoaortic baroreflexes). Our study assessed the relative roles of these two reflexes in the renal nerve activity responses to volume expansion (15 ml/kg 6% dextran in normal saline). With cardiopulmonary and arterial baroreflexes intact, volume expansion resulted in increases in arterial pressure and pulmonary artery wedge pressure and in decreases in renal nerve activity. After sinoaortic denervation, volume expansion resulted in similar decreases in renal nerve activity for similar increases in pulmonary artery wedge pressure. In contrast, after selective vagotomy (sinoaortic baroreflexes intact) volume expansion resulted in increases in arterial pressure and pulmonary artery wedge pressure, but reductions in renal nerve activity were markedly attenuated. After sinoaortic denervation and vagotomy, volume expansion did not result in significant changes in renal nerve activity. We conclude that decreases in renal nerve activity during volume expansion are mediated mainly by cardiopulmonary receptors with afferent vagal fibers. Sinoaortic baroreceptors appear to play a minor role in mediating these responses.

Animals↗
PubMed1982

Sensitization of vagal cardiopulmonary baroreflex by chronic digoxin.

It has been recently reported that intracoronary acetylstrophanthidin injection acutely sensitizes the cardiac baroreflex (vagal afferents). We wondered whether chronic administration of digoxin also augmented the gain of this reflex. We treated seven dogs with digoxin intravenously (40 micrograms/kg loading dose followed by 15 micrograms.kg-1.day-1) for 7 days; eight additional dogs received vehicle for 7 days. With the dogs under chloralose anesthesia, we assessed the changes in renal nerve activity that resulted from stimulation of cardiopulmonary receptors with volume expansion (15 ml/kg of 6% dextran in saline) in digoxin- and vehicle-treated groups under control conditions, after sinoaortic denervation (SAD), and after SAD plus vagotomy. Under control conditions volume expansion resulted in decreases of renal nerve activity of 13.5 +/- 3.5%/mmHg increase in pulmonary artery wedge pressure in digoxin-treated dogs. This tended to be greater than the response of sham-treated dogs (-9.5 +/- 1.5%/mmHg increase). After SAD, renal nerve activity decreased 19 +/- 5%/mmHg increase in pulmonary artery wedge pressure in the digoxin group compared with only 8 +/- 1%/mmHg increase in the vehicle group. These responses were significantly different. The plasma digoxin level in the digoxin-treated group was in the therapeutic range (1.9 +/- 0.4 ng/ml). Vagotomy abolished the responses to volume expansion in both groups. Thus chronic digoxin treatment resulting in therapeutic plasma levels of digoxin sensitizes vagal afferents mediating the cardiopulmonary baroreflex influence on renal nerve activity.

Animals↗
PubMed1978

Nonsensory neglect.

Five monkeys trained to perform with the extremity contralateral to a stimulus had unilateral neglect induced by frontal and reticular formation lesions. Postoperatively the performance of the animals was abnormal only on ipsilateral stimulation, which suggests that the mechanism underlying neglect in these subjects is not deafferentation of sensory inattention but a defect of intention.

Animals↗
PubMed1977

Evoked potential in neglect.

The evoked potential was studied in Macaca speciosa before and after they received a lesion inducing neglect. Significant evoked potential changes associated with neglect were seen only in late components (N2, P3). These observations support the hypothesis of the arousal-attention mechanism of neglect.

Animals↗
PubMed1975

A memory defect in uremic encephalopathy.

It has been demonstrated that anesthesia primarily affects the reticular activating system and psychological studies on patients undergoing anesthesia demonstrated a verbal memory defect. This study was performed in order to determine whether metabolic (uremic) encephalopathy follows the Jacksonian dissolution hypothesis and disrupts cortical function or whether it acts like an anesthetic, causes dysfunction in phylogenetically older systems and thereby produces a memory defect. Twenty-four uremic subjects were tested for memory function, language function, and intellectual function, and compared to 12 control subjects. The greatest difference between the groups was in immediate memory function suggesting that uremia probably acts in a manner similar to anesthesia (by causing dysfunction in the reticular activating system). It is postulated that poor arousal interferes with rehearsal and rehearsal is probably an important component of immediate memory.

Adult↗