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Biomedical subjects

B D Levine

Publications and source records attributed to B D Levine.

70 records · Page 4Linked to original sources
PubMed1993

Traumatic myocardial infarction during competitive volleyball: a case report.

A previously asymptomatic physically active 41-yr-old Caucasian male was hit in the chest by a spiked volleyball. Following the impact of the ball he developed substernal chest pain, which persisted during and after the game. Despite the administration of thrombolytic therapy, he suffered an extensive anteroapical myocardial infarction; subsequent cardiac catheterization revealed the presence of a 70% occlusion in his mid left anterior descending coronary artery. We hypothesize that this patient sustained a traumatic coronary artery thrombosis resulting in acute myocardial infarction. The presence of underlying coronary artery disease may predispose an individual to traumatic myocardial infarction.

Adult↗
PubMed1992

The effect of vasodilators on pulmonary hemodynamics in high altitude pulmonary edema: a comparison.

High altitude pulmonary edema is characterized hemodynamically by a markedly restricted pulmonary vascular bed. Pulmonary vascular resistance is six to eight times higher than control values at altitude, and mean pulmonary pressure is generally elevated two to four-fold over control values. We wished to compare the effect of various vasodilators on the hemodynamics of HAPE, both to gauge their potential effectiveness in treatment of HAPE, and also to gain clues as to the mechanism of the altered pulmonary circulation. In a series of field experiments using a total of 16 subjects with HAPE and 10 well controls, we measured pulmonary hemodynamics by non-invasive Doppler echocardiography. The per cent reduction in pulmonary vascular resistance and mean pulmonary artery pressure, respectively, were 46 and 33 for oxygen, 30 and 29 for nifedipine, 29 and 25 with hydralazine, 57 and 42 with phentolamine, and 72 and 52 when oxygen and phentolamine were combined. All the vasodilators improved gas exchange, suggesting a link between edema formation and pulmonary vasoconstriction. A number of vasodilators may be useful in the treatment of HAPE; the superiority of an alpha adrenergic blocker may implicate the sympathetic nervous system in the pathophysiology of high altitude pulmonary edema.

Altitude Sickness↗
PubMed1992

A practical approach to altitude training: where to live and train for optimal performance enhancement.

Altitude training may improve performance by a number of mechanisms. Acclimatization may improve both oxygen delivery and extraction. Hypoxic exercise may increase the training stimulus thus magnifying the effects of endurance training. Conversely, high altitude decreases VO2max and reduces the workloads at which training occurs. At altitude, base training is performed at a slower velocity and lower oxygen uptake (lower absolute workload) compared to sea level, though heart rate is similar and lactate is higher (probably greater relative workload). Interval workouts are performed at a lower absolute workload at altitude and are associated with lower peak heart rates and blood lactate concentrations. Red cell volume is increased during altitude training, as long as iron stores are normal. We suggest that for performance at altitude, acclimatization and/or hypoxic exercise is preferable; for performance at sea level, living at altitude (acclimatization) with sea level training may be the optimal strategy. However neither approach is a substitute for a carefully designed training program including appropriate rest and nutrition.

Acclimatization↗
PubMed1992

The cerebral hemodynamics of normotensive hypovolemia during lower-body negative pressure.

Although severe hypovolemia can lead to hypotension and neurological decline, many patients with neurosurgical disorders experience a significant hypovolemia while autonomic compensatory mechanisms maintain a normal blood pressure. To assess the effects of normotensive hypovolemia upon cerebral hemodynamics, transcranial Doppler ultrasound monitoring of 13 healthy volunteers was performed during graded lower-body negative pressure of up to -50 mm Hg, an accepted laboratory model for reproducing the physiological effects of hypovolemia. Middle cerebral artery flow velocity declined by 16% +/- 4% (mean +/- standard error of the mean) and the ratio between transcranial Doppler ultrasound pulsatility and systemic pulsatility rose 22% +/- 8%, suggesting cerebral small-vessel vasoconstriction in response to the sympathetic activation unmasked by lower-body negative pressure. This vasoconstriction may interfere with the autoregulatory response to a sudden fall in blood pressure, and may explain the common observation of neurological deficit during hypovolemia even with a normal blood pressure.

Adult↗
PubMed1992

The effect of normoxic or hypobaric hypoxic endurance training on the hypoxic ventilatory response.

Cross-sectional studies in endurance athletes have demonstrated a diminished hypoxic ventilatory response (HVR) compared with mountaineers or sedentary controls. Conversely, short-term altitude acclimatization may increase the HVR. The longitudinal effect of training, either at sea level or altitude, on HVR has not been previously reported. We therefore studied 21 untrained men and women before and after 5 wk of cycle ergometer training at either sea level or 2,500 m. HVR was determined using the steady-state method (16). Minute ventilation (VE) was measured with a Tissot spirometer during the last minute of 5 min breathing room air, 8% and 12% O2, administered in random order. CO2 was added at the mouth in an effort to maintain end-tidal CO2 at baseline levels. Oxyhemoglobin saturation was measured directly from arterial blood with a hemoximeter (OSM 3). HVR was defined as the positive slope of the line relating VE to O2 saturation in l.min-1%-1. One group of subjects trained at sea level at 70% maximal oxygen uptake (VO2max; N = 7). A second group trained at 2,500 m in a hypobaric chamber, at the same relative exercise intensity (i.e., 70% altitude VO2max) or same absolute intensity (same power output) as group 1 (N = 14). Both groups trained on a bicycle ergometer for 45 min.d-1, 5 d.wk-1 for 5 wk.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Physical fitness and cardiovascular regulation: mechanisms of orthostatic intolerance.

We studied three groups of eight men each--high, mid, and low fit (peak O2 consumption 60.0 +/- 0.8, 48.9 +/- 1.0, and 35.7 +/- 0.9 ml.min-1.kg-1)--to determine the mechanism of orthostatic intolerance in endurance athletes. Tolerance was defined by progressive lower body negative pressure (LBNP) to presyncope. Maximal calf vascular conductance (Gmax) was measured. The carotid baroreflex was characterized using both stepwise R-wave-triggered and sustained (2 min) changes in neck chamber pressure. High-fit subjects tended to have lower LBNP tolerance than mid- and low-fit subjects but similar baroreflex responses. Subjects with poor LBNP tolerance had larger stroke volumes (SV) (120 +/- 6 vs. 103 +/- 3 ml) and greater decline in SV with LBNP to -40 mmHg (40 +/- 2 vs. 26 +/- 4%). Stepwise multiple linear regression analysis revealed that Gmax and steady-state gain of the carotid baroreflex contributed significantly toward explaining interindividual variations in LBNP tolerance. Thus endurance athletes may have decreased LBNP tolerance, but apparently not as a simple linear function of aerobic fitness. Orthostatic tolerance depends on complex interactions among functional characteristics that appear both related (Gmax and SV) and unrelated (baroreflex function) to fitness or exercise training.

Adult↗
PubMed1991

Left ventricular pressure-volume and Frank-Starling relations in endurance athletes. Implications for orthostatic tolerance and exercise performance.

BACKGROUND: Endurance athletes have a high incidence of orthostatic intolerance. We hypothesized that this is related to an abnormally large decrease in left ventricular end-diastolic volume (LVEDV) and stroke volume (SV) for any given decrease in filling pressure. METHODS AND RESULTS: We measured pulmonary capillary wedge (PCW) pressure (Swan-Ganz catheter), LVEDV (two-dimensional echocardiography), and cardiac output (C2H2 rebreathing) during lower body negative pressure (LBNP, -15 and -30 mm Hg) and rapid saline infusion (15 and 30 ml/kg) in seven athletes and six controls (VO2max, 68 +/- 7 and 41 +/- 4 ml/kg/min). Orthostatic tolerance was determined by progressive LBNP to presyncope. Athletes had steeper slopes of their SV/PCW pressure curves than nonathletes (5.5 +/- 2.7 versus 2.7 +/- 1.5 ml/mm Hg, p less than 0.05). The slope of the steep, linear portion of this curve correlated significantly with the duration of LBNP tolerance (r = 0.58, p = 0.04). The athletes also had reduced chamber stiffness (increased chamber compliance) expressed as the slope (k) of the dP/dV versus P relation (chamber stiffness, k = 0.008 +/- 0.004 versus 0.031 +/- 0.004, p less than 0.005; chamber compliance, 1/k = 449.8 +/- 283.8 versus 35.3 +/- 4.3). This resulted in larger absolute and relative changes in end-diastolic volume over an equivalent range of filling pressures. CONCLUSIONS: Endurance athletes have greater ventricular diastolic chamber compliance and distensibility than nonathletes and thus operate on the steep portion of their Starling curve. This may be a mechanical, nonautonomic cause of orthostatic intolerance.

Adult↗
PubMed1989

Dexamethasone in the treatment of acute mountain sickness.

Cerebral edema occurs in fatal cases of acute mountain sickness. Dexamethasone, commonly used to treat cerebral edema due to other causes, also reduces the symptoms of acute mountain sickness when given prophylactically. However, the efficacy of dexamethasone in the treatment of established acute mountain sickness remains uncertain. To investigate this question, we exposed six men in a hypobaric chamber to a simulated altitude of 3700 m (barometric pressure, 64 kPa [481 mm Hg]) for 48 hours on two occasions. Acute mountain sickness was diagnosed with use of a symptoms questionnaire, and dexamethasone (4 mg every six hours) or placebo was then given in a randomized, double-blind, crossover fashion. Dexamethasone reduced the symptoms of acute mountain sickness by 63 percent (P less than 0.05), whereas placebo had a minimal effect (reduction by 23 percent; P not significant). In spite of this response, one subject had mild cerebral edema on brain CT after both placebo and dexamethasone. Dexamethasone had no effect on fluid shifts, oxygenation, sleep apnea, urinary catecholamine levels, the appearance of chest radiographs or perfusion scans, serum electrolyte levels, hematologic profiles, or the results of psychometric tests. Dexamethasone treatment was complicated by mild hyperglycemia in all subjects (mean [+/- SE] glucose level, 7.3 +/- 1.3 mmol per liter [132 +/- 23 mg per deciliter]). We conclude that dexamethasone effectively reduces the symptoms of acute mountain sickness. However, it did not improve objective physiologic abnormalities related to exposure to high altitudes. We therefore recommend that dexamethasone be used only when descent is impossible, or to facilitate cooperation in evacuation efforts.

Acute Disease↗
PubMed1989

Day to day variability of Doppler color flow jets in mitral regurgitation.

Doppler color flow mapping offers the potential to assess serial changes in mitral regurgitation associated with therapeutic interventions such as surgical valve repair or after-load reduction. However, the day to day variability of color flow jets in mitral regurgitation must be established to distinguish therapeutic responses from random variation. Therefore, 14 patients with mitral regurgitation were each studied on 5 sequential days by color flow velocity mapping. Instrument settings were kept constant for each patient, and no patient had a significant change in heart rate, blood pressure, left ventricular end-diastolic dimension or circumferential wall stress between studies. To assess day to day variability, the area of the Doppler color flow map was carefully measured in multiple views by an experienced echocardiographer. Mitral regurgitant jet area by color flow mapping tended to be greater from apical rather than parasternal views (5.6 +/- 4.0 versus 2.9 +/- 2.1 cm2, respectively, p less than 0.03). The maximal jet area in any view ranged from 0.4 to 15.0 cm2 in individual subjects. Variability of maximal jet area within subjects was not statistically significant by repeated measures analysis of variance (F = 1.88, p = 0.13); however, the coefficient of variation was approximately 15%. Thus, a reduction in jet area of greater than or equal to 30% would be needed to predict a therapeutic response at the 95% confidence level. These data have important implications regarding the use of color flow mapping to assess the efficacy of therapeutic interventions in mitral regurgitation.

Adult↗
PubMed1989

Irregular nocturnal breathing patterns high altitude in subjects susceptible to high-altitude pulmonary edema (HAPE): a preliminary study.

We studied nocturnal breathing patterns and symptoms of acute mountain sickness (AMS) during trekking in the Japanese Alps (altitude: 2,760-2,920 m) for 4 d in five subjects susceptible to high-altitude pulmonary edema (HAPE-S-S) and five control volunteers. Breathing patterns were evaluated with the impedance plethysmograph, and symptoms of AMS were evaluated by the environmental symptoms questionnaire-III score for AMS of cerebral type (AMS-C score). In both groups, the percentage of time with periodic breathing significantly increased at high altitude and the percentage in controls was significantly higher than in HAPE-S-S on the second night. In four HAPE-S-S, other disordered breathing patterns, termed "irregular breathing," were observed frequently by night at high altitude. Irregular breathing patterns were characterized by irregularly repeated oscillatory or nonoscillatory clusters of breaths with augmented tidal volume, followed by expiratory pause, apnea, or hypoventilation of various durations. All controls did not show significant changes in AMS-C score, but four HAPE-S-S showed the increase in AMS-C score on the next morning after frequent irregular nocturnal breathing. There was significant correlation between the percentage of time with irregular nocturnal breathing and AMS-C score on the next morning. These results suggest that HAPE-S-S are prone to irregular nocturnal breathing patterns at high altitude, which is associated with the development of AMS, but it was not possible to determine whether these abnormal breathing patterns are a cause or an effect of AMS.

Adult↗
PubMed1988

Effect of increasing heart rate on left ventricular performance in patients with normal cardiac function.

The influence of an increase in heart rate on left ventricular (LV) contractile performance was assessed in patients with normal LV function. In 19 patients (3 men, 16 women) ages 55 +/- 9 years (mean +/- standard deviation) with normal global and segmental LV function and normal coronary arteries, LV dP/dt max was measured at baseline heart rate and during atrial pacing at baseline +5, baseline +25 and baseline +45 beats/min. In 10 of the patients, intravascular volume was not altered during pacing and, as a result, echocardiographically measured LV end-diastolic dimension decreased (5.4 +/- 0.4 at baseline vs 4.9 +/- 0.5 cm at baseline +45 beats/min, p less than 0.05). In these patients, LV dP/dt max increased modestly (1,571 +/- 237 at baseline vs 1,760 +/- 199 mm Hg/s at baseline +45 beats/min, p less than 0.05). In the other 9 patients, intravascular volume was expanded rapidly (by saline infusion) during pacing and, as a result, LV end-diastolic dimension was held constant (5.2 +/- 0.6 at baseline vs 5.1 +/- 0.6 cm at baseline +45 beats/min, difference not significant). In these patients, LV dP/dt max increased substantially with pacing (1,505 +/- 228 at baseline vs 2,050 +/- 258 mm Hg/s at baseline +45 beats/min, p less than 0.05). Thus, an increase in heart rate induces a modest increase in LV dP/dt max in patients in whom LV preload (as reflected by end-diastolic dimension) is allowed to decrease; in contrast, it causes a marked increase in LV dP/dt max in those in whom LV preload is maintained constant.

Adult↗
PubMed1988

Role of barometric pressure in pulmonary fluid balance and oxygen transport.

To examine the role of barometric pressure in high-altitude pulmonary edema, we randomly exposed five unanesthetized chronically instrumented sheep with lung lymph fistulas in a decompression chamber to each of three separate conditions: hypobaric hypoxia, normobaric hypoxia, and normoxic hypobaria. A combination of slow decompression and/or simultaneous adjustment of inspired PO2 provided three successive stages of simulated altitudes of 2,600, 4,600, and 6,600 m during which hemodynamics and lymph flow were monitored. Under both hypoxic conditions we noted significant and equivalent elevations in pulmonary arterial pressure (Ppa), cardiac output, and heart rate, with left atrial and systemic pressures remaining fairly constant. Normoxic hypobaria was also accompanied by a smaller but significant rise in Ppa. Lymph flow increased to a highly significant maximum of 73% above base line, accompanied by a slight but significant decrease in lung lymph-to-plasma protein ratio, only under conditions of combined hypobaric hypoxia but not under equivalent degrees of alveolar hypoxia or hypobaria alone. Arterial hypoxemia was noted under all three conditions, with arterial PO2 being uniformly lower under hypobaric conditions than when identical amounts of inspired PO2 were delivered at normal atmospheric pressure. We therefore hypothesize that alveolar pressure significantly alters the Starling forces governing transcapillary fluid flux in the lung and may affect the alveolar-arterial gradient for O2 as well.

Altitude↗
PubMed1987

In vivo induction and reversal of nitroglycerin tolerance in human coronary arteries.

The mechanism by which tolerance to the clinical effects of organic nitrates develops has not been elucidated. This study was done to determine whether an intravenous infusion of nitroglycerin induces tolerance in the coronary vascular bed and whether such tolerance is reversed by the sulfhydryl-group donor N-acetylcysteine. We studied 19 subjects--17 with coronary artery disease and 2 without it--who had a mean age (+/- SD) of 54 +/- 9 years. Coronary sinus blood flow, which approximates blood flow to the left ventricle, was measured before and during intracoronary injections of nitroglycerin (10, 25, 50, and 100 micrograms). The patients then received a 24-hour intravenous infusion of saline (n = 7) or of nitroglycerin, 45 +/- 13 micrograms per minute (n = 12), after which the responses of coronary sinus flow to the same doses of intracoronary nitroglycerin used earlier were measured. In the seven patients given saline, the four doses of intracoronary nitroglycerin caused similar percentage increases in coronary sinus flow before and after the saline infusion. In the 12 patients given intravenous nitroglycerin, the four intracoronary doses caused percentage increases in coronary flow before the infusion of 30 +/- 9, 35 +/- 14, 41 +/- 12, and 52 +/- 15, respectively. After the infusion, the same doses of nitroglycerin caused smaller (P less than 0.05) percentage increases (16 +/- 6, 21 +/- 11, 23 +/- 12, and 27 +/- 11, respectively), indicating the development of partial tolerance. Subsequently, 7 of the 12 patients received N-acetylcysteine, after which intracoronary nitroglycerin caused percentage increases in coronary sinus flow similar to the values measured before the intravenous nitroglycerin was given (34 +/- 13, 32 +/- 8, 38 +/- 11, and 44 +/- 16, respectively). We conclude that the coronary vasodilator effect of nitroglycerin is attenuated by an intravenous infusion of nitroglycerin (that is, partial tolerance develops) and that tolerance to the agent can be reversed by administration of the sulfhydryl-group donor N-acetylcysteine. The mechanism by which N-acetylcysteine reverses tolerance will require further investigation.

Acetylcysteine↗
PubMedDate not supplied

Myositis ossificans of traumatic origin in the foot.

This case reviews a myositis ossificans of traumatic origin discovered beneath the fifth metatarsal in an adult male. Details of its anatomic appearance are illustrated with the assistance of plane film roentgenography and magnetic resonance imaging. Histologic sections are included to support the diagnosis and present characteristic cellular patterns. A review of the literature including etiology, clinical classification, and diagnostic criteria are also presented.

Aged↗