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Biomedical subjects

M L Smith

Publications and source records attributed to M L Smith.

At least 325 records · Page 18Linked to original sources
PubMed1989

Right hippocampal impairment in the recall of spatial location: encoding deficit or rapid forgetting?

The recall of spatial location in patients with left or right temporal-lobe lesions was studied in two experiments, in which recall was tested either immediately after presentation of an array of objects, or after an intervening verbal task, a spatial task or an unfilled interval. Deficits were found only in patients with right temporal-lobe lesions that included extensive removal of the hippocampal region, and only when recall was tested after a delay. The presence of an intervening task in the delay interval did not accentuate the deficit. The results show that, despite a normal ability to encode location, patients with large right hippocampal lesions demonstrate an abnormally rapid forgetting of such information.

Adolescent↗
PubMed1989

Hyperinsulinism associated with primary renal cell carcinoma.

A case is reported of a patient with symptomatic hyperinsulinism associated initially with a renal cell carcinoma and then later, with secondary deposits from the same tumor. Evidence points to a strong possibility of renal tumor involvement in the production of insulin hypersecretion.

Carcinoma, Renal Cell↗
PubMed1989

Subnormal heart period variability in heart failure: effect of cardiac transplantation.

Heart period variability and arterial baroreceptor-cardiac reflex function were studied in cardiac transplant patients to determine if correction of heart failure restores parasympathetic control mechanisms toward normal. Heart period variability (standard deviation [SD] of 120 consecutive RR or PP intervals) was measured at supine rest in 34 patients with congestive heart failure (23 patients receiving diuretics, digoxin or vasodilators and 11 patients weaned from all medications), 30 cardiac transplant patients (both innervated recipient and denervated donor atrial rates) and 16 age-matched healthy control subjects. Arterial baroreflex gain was evaluated with intravenous bolus injections of phenylephrine in 22 transplant patients. Mean heart period variability (+/- SEM) was significantly lower (p less than 0.05) in the heart failure groups (22 +/- 3 ms for medicated and 17 +/- 3 ms for nonmedicated) than in the transplant patients (41 +/- 5 ms) or control subjects (58 +/- 5 ms). Heart period variability of the transplant patients was less than that of the control patients (p less than 0.05). A stepwise regression model revealed that heart period variability was inversely related to systolic arterial pressure and directly related to time after transplantation (R2 = 0.39; p = 0.03) in the transplant patients. Baroreflex gain of normotensive transplant patients was normal (11.7 +/- 1.0 ms/mm Hg) and correlated directly with heart period variability (r = 0.62; p less than 0.001). These data suggest that subnormal levels of cardiac parasympathetic activity at rest associated with congestive heart failure can be restored progressively toward normal by correction of congestive heart failure after cardiac transplantation. Post-transplant hypertension opposes this correction of baseline parasympathetic activity.

Adult↗
PubMed1989

Enhancement of sympathetic nerve activity by single premature ventricular beats in humans.

This is the first systematic study of the effects of ventricular premature beats on sympathetic nerve activity in humans. Microneurographic techniques were used to record efferent sympathetic activity from the peroneal nerve, and an intracardiac electrode catheter was used to introduce ventricular premature beats after every 6 to 10 sinus heartbeats. Studies were performed in eight patients, aged 22 to 74 years (mean 57), undergoing cardiac electrophysiologic studies. Three patients did not have apparent heart disease and five had coronary artery disease. During sinus rhythm, 19 to 93% (mean 42%) of heartbeats were followed by a pulse-synchronous burst of sympathetic activity. Provoked ventricular premature beats had obvious effects on this activity. Premature beats with coupling intervals less than 80% of sinus cycle length were consistently followed by a burst of sympathetic activity, and this activity was greater in amplitude, duration and area (all p less than 0.05) than were burst of such activity during sinus rhythm. The magnitude of this burst of activity increased as the coupling interval of the ventricular premature beat decreased (p less than 0.0001). In contrast, postextrasystolic beats were followed by nearly complete neural silence. These effects were seen in all patients regardless of baseline burst incidence and the presence or absence of heart disease. Total nerve activity per 10 heartbeats was 6,520 +/- 770 U during ventricular extrastimulation and 5,720 +/- 440 U during normal sinus rhythm (difference not significant). It is concluded that single ventricular premature beats provoke fluxes of muscle sympathetic nerve activity in humans, comprising surges of sympathetic activity larger than those occurring during sinus rhythm, followed by neural silence.

Adult↗
PubMed1989

Oblique views in thyroid imaging.

To assess the value of oblique thyroid views during routine thyroid scanning 73 sequential euthyroid patients with focal or diffuse thyroid pathology were studied. Oblique thyroid images did not alter the scan report in 37 patients shown to have a multinodular goitre on the anterior image. However, in the remaining 36 patients oblique thyroid images altered scan category in 30% of patients, mainly demonstrating multiple nodules in thyroids which would have been reported as having a solitary nodule on the anterior image alone. Despite the extra imaging time required, both anterior oblique thyroid images should be obtained in all euthyroid patients presenting with focal or diffuse thyroid pathology in whom the anterior image does not clearly demonstrate a multinodular goitre.

Humans↗
PubMed1989

Rheumatoid papules: lesions showing features of vasculitis and palisading granuloma.

Whether palisading granuloma formation occurs with leukocytoclastic vasculitis in rheumatoid nodules and in histopathologically similar conditions is debatable. Patients with high titers for rheumatoid factor and severe erosive rheumatoid arthritis are at risk for both rheumatoid vasculitis and rheumatoid nodules. A patient with all of these features developed a papular eruption. These papules showed clinicopathologic features both of leukocytoclastic vasculitis and of early palisading granuloma. Lesions resolved slowly with low-dose oral corticosteroid therapy. It is proposed that these lesions be called rheumatoid papules and that they may represent a link between vasculitis and the palisaded granulomatous reaction seen in rheumatoid nodules.

Biopsy, Needle↗
PubMed1989

Seizure-induced damage to substantia nigra and globus pallidus is accompanied by pronounced intra- and extracellular acidosis.

Status epilepticus of greater than 30-min duration in rats gives rise to a conspicuous lesion in the substantia nigra pars reticulata (SNPR) and globus pallidus (GP). The objective of the present study was to explore whether the lesion, which encompasses necrosis of both neurons and glial cells, is related to intra- and extracellular acidosis. Using the flurothyl model previously described to produce seizures, we assessed regional pH values with the autoradiographic 5,5-dimethyl[2-14C]oxazolidine-2,4-dione technique. Regional pH values were assessed in animals with continuous seizures for 20 and 60 min, as well as in those allowed to recover for 30 and 120 min after seizure periods of 20 or 60 min. In additional animals, changes in extracellular fluid pH (pHe) were measured with ion-selective microelectrodes, and extracellular fluid (ECF) volume was calculated from the diffusion profile for electrophoretically administered tetramethylammonium. In structures such as the neocortex and the hippocampus, which show intense metabolic activation during seizures, status epilepticus of 20- and 60-min duration was accompanied by a reduction of the "composite" tissue pH (pHt) of 0.2-0.3 unit. Recovery of pHt was observed upon termination of seizures. In SNPR and in GP, the acidosis was marked to excessive after 20 and 60 min of seizures (delta pHt approximately 0.6 after 60 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Decrease of glutamate decarboxylase activity in substantia nigra and caudoputamen following transient hyperglycemic ischemia in the rat.

Glutamate decarboxylase (GAD) activity was determined in caudoputamen (CP), substantia nigra (SN), and cerebral cortex (CCX) after 19-22 h of recirculation following 10 min of transient ischemia in hyperglycemic rats, i.e., under the conditions when previously a pronounced nerve cell damage was demonstrated in both CP and SN. The present results demonstrate a decrease of GAD activity in SN by 30% and in CP by 22% and no change in CCX. No statistically significant change in GAD activity could be detected in SN, CP, or CCX 1,4, and 7 days following 10 min of ischemia in normoglycemic animals. The decrease of GAD activity in SN at the time preceding the onset of postischemic seizures suggests that there may be an imbalance between augmented excitatory and decreased inhibitory transmission in SN. We tentatively conclude that this may increase the probability of generalized seizures in the postischemic period following ischemia in hyperglycemic animals.

Animals↗
PubMed1989

Preischemic hyperglycemia enhances postischemic depression of cerebral metabolic rate.

The objective of the present study was to explore metabolic correlates to the appearance of postischemic seizures and the enhancement of brain damage observed in subjects that are made hyperglycemic prior to the induction of ischemia. To that end, transient forebrain ischemia of 10-min duration was induced in normo- and hyperglycemic rats, with subsequent measurements of local CMRglc (LCMRglc) after 3, 6, 12, and 18 h of recirculation. We posed the questions of whether postischemic depression of LCMRglc is exaggerated by preischemic hyperglycemia and whether there are signs of localized increases in LCMRglc in hyperglycemic rats, reflecting subclinical seizure activity. The results confirmed the presence of a long-lasting postischemic depression of LCMRglc in normoglycemic rats. This depression was partially but not tightly related to the degree of reduction of local CBF during ischemia. The depression was most pronounced in neocortical areas and in the hippocampus, but notably it was less pronounced in the densely ischemic caudoputamen. Little or no reduction of LCMRglc was observed in moderately or mildly ischemic structures such as the hypothalamus, red nucleus, and cerebellum. Preischemic hyperglycemia markedly accentuated the postischemic depression of LCMRglc. For example, although the subjects quickly regained wakefulness and motility, they had LCMRglc values in neocortical areas that remained below 50% of control. Corresponding but quantitatively less pronounced reductions in LCMRglc were observed in other areas. Notably, preischemic hyperglycemia reduced postischemic LCMRglc also in areas that showed only moderate to mild reductions in CBF during the ischemia. The results thus demonstrate that preischemic hyperglycemia has pronounced metabolic effects in the postischemic recovery period. The data provide no indication that postischemic seizures, which develop after a recovery period of approximately 24 h, are preceded by the appearance of hypermetabolic "seizure" foci.

Animals↗
PubMed1989

Time course of early brain edema following reversible forebrain ischemia in rats.

Cerebral ischemia is known to be accompanied by brain edema. This increase in brain tissue water content probably influences the final outcome of an ischemic insult negatively. Despite extensive investigations on different aspects of brain edema, information on edema development during the early recirculation period following ischemia is sparse. We assessed changes in brain water content, as reflected by changes in tissue density, during the early recirculation period following severe forebrain ischemia. Fasted rats were subjected to 5, 15, or 30 minutes of ischemia and 5 to 180 minutes of recirculation. The specific gravity of specimens from the caudoputamen, frontoparietal cortex, hippocampus, and mesencephalon were measured with a Percoll linear density gradient. Five minutes of ischemia followed by recirculation did not produce any significant regional brain edema. However, following 15 minutes of ischemia, transient edema developed in the caudoputamen, frontoparietal cortex, and hippocampus. This edema was maximal after 30 minutes of reperfusion and was normalized after 180 minutes of reperfusion. Similar edema was seen following 30 minutes of ischemia. In the mesencephalon (where blood flow is approximately 50% of control during the ischemic insult) no brain edema was noted following 5, 15, or 30 minutes of ischemia. We discuss to what extent this transient regional brain edema may influence the selective neuronal vulnerability and cell damage observed in rats subjected to reversible forebrain ischemia and how these findings may correlate with neurochemical alterations observed during the early recirculation period.

Animals↗
PubMed1989

Exercise training bradycardia: the role of autonomic balance.

We used an algebraic model of resting heart rate (HRr), HRr-mn (HRo), to compare resting parasympathetic (n) and sympathetic (m) influence, intrinsic heart rate (HRo), and resting autonomic balance (Abal) in ten endurance-trained (ET) and ten nontrained (NT) men. The values of m, n, and Abal were determined by selective pharmacological blockade with atropine and metoprolol. HRo was obtained during double blockade with atropine and metoprolol. HRo and HRr were significantly lower (P less than or equal to 0.04 and P less than or equal to 0.01, respectively) in the ET subjects (79.5 +/- 2.8 beats.min-1 and 54.7 +/- 3.0 beats.min-1, respectively) when compared to the NT subjects (86.6 +/- 2.5 beats.min1 and 70.2 +/- 3.1 beats.min-1, respectively). Parasympathetic influence (n) was greater in the ET subjects (P less than or equal to 0.04), while sympathetic influence (m) was slightly (P less than or equal to 0.05) less in the ET subjects. Consequently, the value of Abal was significantly less in the ET subjects (P less than or equal to 0.02), indicating that resting parasympathetic predominance was significantly greater in the ET subjects. We concluded that the exercise training bradycardia, observed in this group of subjects, was due to both a lower HRo and an Abal with an augmented parasympathetic dominance.

Adult↗
PubMed1989

Percutaneous transluminal coronary angioplasty: update 1988.

This report updates the current indications, techniques and investigational devices used in a busy interventional cardiology practice. Specific attention is devoted toward the problem areas of thrombolytic treatment of acute myocardial infarction, restenosis after angioplasty and the use of angioplasty in the treatment of multivessel coronary artery disease.

Angioplasty, Balloon, Coronary↗