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Biomedical subjects

M Epstein

Publications and source records attributed to M Epstein.

At least 217 records · Page 12Linked to original sources
PubMed1988

Flecainide acetate in the treatment of resistant supraventricular arrhythmias.

Thirty-one patients with a variety of supraventricular tachyarrhythmias resistant to conventional anti-arrhythmic therapy were treated with flecainide acetate, a new class Ic antiarrhythmic drug. The mean follow-up period was 7 months. Control was attained in 19 patients (62%) initially, and the long-term success rate was 39%. In 7 of the 19 controlled patients the drug was subsequently discontinued because of major side-effects, which included negative inotropism and pro-arrhythmia. The mechanisms and implications of these side-effects are reviewed.

Adolescent↗
PubMed1988

Renal hemodynamic effects of calcium antagonists.

Recently, attention has focused on the effects of calcium antagonists on renal function. When administered in vitro to the isolated perfused kidney, calcium antagonists exhibit consistent actions permitting characterization of their renal effects. Calcium antagonists do not affect the vasodilated isolated perfused kidney, but they do dramatically alter the response of the kidney to vasoconstrictor agents. In the presence of norepinephrine, calcium antagonists markedly augment glomerular filtration rate but produce only a modest improvement in renal perfusion. This preferential augmentation of glomerular filtration rate may be attributable to a selective vasodilation of preglomerular vessels. Although the clinical implications of such observations are not yet clear, preliminary studies in experimental animal models indicate that calcium antagonists may exert salutary effects on renal function in clinical settings that are characterized by impaired renal hemodynamics. The possible benefits of calcium antagonists in ameliorating the development of renal dysfunction in patients in whom there is increased risk for the development of acute renal insufficiency remain to be evaluated.

Animals↗
PubMed1988

Bone graft survival in expanded skin.

The effect of tissue expansion on iliac bone graft (onlay) survival was studied on the skulls of 35 New Zealand white rabbits. Wet bone weights at the time of grafting and at sacrifice in control animals (group I) were compared to three experimental groups. Histologic sections of the developing and resolving pseudosheath and skin envelope were performed. A self-inflating 5-mil-thick silicone expander was used for soft-tissue expansion over the rabbit snout. Bone grafts were subsequently placed in this site. Elliptical snout excision without expansion (group II) demonstrated no statistically significant difference in bone graft survival when compared to controls (group I) (p = 0.350). Full tissue expansion followed by immediate bone grafting (group III) within the pseudosheath cavity likewise demonstrated no statistically significant difference in bone graft survival when compared to controls (group I) (p = 0.500); however, when full tissue expansion was followed by delayed (2 weeks) bone grafting to allow for resolution of the giant cell inflammatory reaction of the pseudosheath (group IV), a statistically significant increased bone graft survival was achieved (p less than 0.001). The study demonstrates that the increased vascularity in the pseudosheath and in the expanded soft-tissue envelope significantly increased bone graft survival only when bone grafting was delayed.

Animals↗
PubMed1988

Calcium antagonists and the renal hemodynamic response to vasoconstrictors.

These findings demonstrate that calcium antagonists reverse renal vasoconstriction in a variety of settings. The ability of calcium antagonists to augment GFR of the vasoconstricted kidney is striking and has also been demonstrated in a number of in vivo settings. These observations and others raise the possibility that calcium antagonists have potential utility in the treatment of a number of disorders characterized by renal ischemia and consequent renal insufficiency. Further studies to evaluate this possibility are required. The unique effects of calcium antagonists on GFR reflect a regional heterogeneity within the renal microcirculation and a preferential action of calcium antagonists on the afferent arteriole. Final resolution of the pharmacological basis for the renal hemodynamic actions of calcium antagonists will require a more complete understanding of the divergent activating mechanisms within the renal microcirculation.

Animals↗
PubMed1988

Effects of water immersion on arginine vasopressin release in humans.

Since suppression of arginine vasopressin (AVP) appears to be a determinant of the diuresis of water immersion (WI) in humans, a further understanding of its responsiveness has important implications for normal physiology, pathophysiology, and space physiology. In recent years, discrepant measurements of AVP in plasma during WI have led to conflicting conclusions. In studies in which the subjects ingested water before or during WI, plasma AVP was reported to be unchanged or even increased. In contrast, plasma AVP was suppressed in studies in which the subjects remained hydropenic. A critical review discloses that water intake before and/or during the experiments introduces several new stimuli for AVP release. Furthermore the lower base-line levels of AVP in hydrated subjects complicate detection of small changes in plasma AVP. Although the mechanisms of AVP suppression during WI are incompletely defined, it appears that not only cardiopulmonary mechanoreceptors but also arterial baroreceptors mediate the response. Additional studies are proposed to delineate further the mechanisms governing AVP release during WI.

Arginine Vasopressin↗
PubMed1988

Management of magnesium depletion.

In addition to the well-known complexities inherent in the recognition of hypomagnesemia and/or magnesium depletion, the management of magnesium deficiency oftentimes is not straightforward and requires the understanding of several important principles. Among these is that the avoidance of ineffective undertreatment of patients with symptomatic severe depletion may require parenteral administration of quite large amounts of magnesium for several days. This point is evident in the included case example describing a patient in whom the small amounts of magnesium given initially were entirely ineffective. The use of the various protocols to provide a patient with magnesium by the parenteral route requires consideration of several factors. The purpose of this paper is to provide the practitioner with a comprehensive, clinically useful review of the oral and parenteral therapy of patients with magnesium depletion.

Administration, Oral↗
PubMed1988

Atrial natriuretic peptide reverses afferent arteriolar vasoconstriction and potentiates efferent arteriolar vasoconstriction in the isolated perfused rat kidney.

The intrarenal sites of action of atrial natriuretic peptide (ANP) have not been resolved fully. Although ANP relaxes in vitro preparations of smooth muscle and exerts profound effects on renal hemodynamics, the effects of ANP on resistance vessels remain a subject of controversy. In the present study, we utilized an in vitro perfused hydronephrotic rat kidney model to assess directly the actions of ANP on renal microvessels during norepinephrine (NE)-induced renal vasoconstriction. Perfusion pressure was maintained constant, and perfusate flow to the kidney was monitored while the afferent arteriole (AA) and efferent arteriole (EA) were visualized using videomicroscopy. Renal AA and EA diameters were measured by computer-assisted image analysis. NE (0.3 microM) decreased renal perfusate flow from 11.8 +/- 1.7 (S.E.) to 5.8 +/- 1.2 ml/min (P less than .005), decreased AA diameter from 20.2 +/- 0.7 to 14.3 +/- 0.8 mu (P less than .005) and decreased EA diameter from 18.6 +/- 1.2 to 15.1 +/- 1.2 mu (P less than .005). ANP (human ANF-(4-28), anaritide, Wyeth) completely reversed the NE-induced AA vasoconstriction with an IC50 of 9.3 +/- 5.6 nM. In contrast, ANP caused a further decrease in EA diameter at concentrations up to 10(-8) M, and elicited a slight dilation of the EA at 10(-7) M. In normal rat kidneys perfused under identical conditions, NE decreased renal perfusate flow, glomerular filtration rate and filtration fraction. ANP increased glomerular filtration rate and filtration fraction above control levels, with maximal effects at 10(-8) M.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Echocardiographic and hemodynamic correlates of diastolic closure of mitral valve and diastolic opening of aortic valve in severe aortic regurgitation.

Acute severe aortic regurgitation (AR) is characterized by a steep increase in left ventricular end-diastolic pressure, exceeding left atrial pressure and occasionally equilibrating with aortic diastolic pressure. These pressure phenomena correlate with the M-mode echocardiographic (echo) findings of diastolic closure of the mitral valve (DCMV) and diastolic opening of the aortic valve (DOAV). Six men, aged 23 to 48 years, with recent-onset, severe AR were evaluated by M-mode echo and pressures at cardiac catheterization. DCMV was seen in all 6 patients and DOAV in 4. Near-constant time intervals from the preceding R wave of the electrocardiogram to DCMV and DOAV were seen, even in 3 patients with varying RR intervals (1 with atrial fibrillation and 2 with asynchronous and demand atrial pacing). When the RR intervals were shorter than these intervals, DCMV and DOAV did not occur. Increasing the heart rate in the 2 patients by atrial pacing resulted in a marked decrease in left ventricular end-diastolic pressure. In conclusion, DCMV and DOAV have a near constant relation to the preceding R wave of the electrocardiogram, DCMV with competence of the mitral valve must be present for DOAV to occur, DOAV indicates that the diastolic blood pressure equals left ventricular end-diastolic pressure, and heart rate is an important factor influencing the hemodynamic and echocardiographic parameters in recent-onset, severe AR.

Adult↗
PubMed1987

Renal hemodynamic effects of calcium antagonists.

Although the cardiovascular actions of calcium antagonists have been studied extensively, it is only recently that attention has focused on the effects of calcium antagonists on renal function. Variable actions of calcium antagonists on renal hemodynamics have been observed when these agents are used in experimental animal models. In contrast, when administered in vitro to the isolated perfused kidney, calcium antagonists demonstrate more predictable actions. Calcium antagonists do not affect the vasodilated isolated kidney, but they do dramatically alter the response of the kidney to vasoconstrictor agents. In the presence of norepinephrine, calcium antagonists produce a modest improvement in renal perfusion and significantly augment glomerular filtration rate. This preferential augmentation of glomerular filtration rate may be attributable to a selective vasodilation of pre-glomerular vessels. Although the clinical implications of such observations are not yet clear, preliminary studies indicate that calcium antagonists may exert salutary effects on renal function in clinical settings that are characterized by impaired renal hemodynamics. The possible benefits of calcium antagonists in ameliorating the development of renal dysfunction in patients in whom there is increased risk for the development of acute renal insufficiency remain to be evaluated.

Animals↗
PubMed1987

Inhibition by diltiazem of pressure-induced afferent vasoconstriction in the isolated perfused rat kidney.

The renal hemodynamic response to calcium entry blockade depends on the neural, hormonal and physiologic determinants influencing basal renal vascular tone. The effects of perfusion pressure per se on the renal vascular response of the rat kidney to diltiazem were evaluated using normal kidneys and hydronephrotic kidneys perfused extracorporally. In isolated perfused normal kidneys, diltiazem did not alter perfusate flow or glomerular filtration rate (GFR) when administered at a perfusion pressure of 100 mm Hg. In contrast, when diltiazem was administered at a perfusion pressure of 150 mm Hg, the calcium antagonists caused a striking increase in GFR, which was accompanied by an increase in renal perfusate flow. In the isolated perfused hydronephrotic rat kidney, elevation of perfusion pressure was associated with an increase in renal vascular resistance and a reduction in afferent arteriolar diameter. Diltiazem abolished the pressure-induced constriction of afferent arterioles and caused an increase in renal perfusate flow in hydronephrotic kidneys perfused at pressures above 100 mm Hg. These findings suggest that in the setting of increased renal perfusion pressure, diltiazem's effects on GFR are mediated in part by an inhibition of pressure-induced constriction of the afferent arteriole.

Animals↗
PubMed1987

Detailed characterization of a tank used for head-out water immersion in humans.

Water immersion has long been known to produce marked diuresis, natriuresis, and kaliuresis and suppression of the renin-aldosterone system. These effects are mediated primarily by an increase in central blood volume. Immersion has therefore gained increased acceptance in human physiology for the investigation of the effects of central volume expansion on renal function and hormonal responsiveness without altering the composition of the extracellular fluid. An immersion tank used for studies in humans is described. Requisite features to ensure study reproducibility include a constant temperature, capability to alter the depth of immersion by adjusting water height, and the ability to maintain hygienic quality by means of constant circulation of the water through a sand filter. A constant temperature of 34.5 +/- 0.2 degrees C is maintained by thermostatically controlling the heat exchange to a unidirectional closed-circuit water system in the bottom of the immersion tank coursing through a stream source. The level of the water may be adjusted to any desired level by means of a waste line or an inlet of tap water.

Equipment Design↗
PubMed1987

Modification of the renal hemodynamic response to vasoconstrictors by calcium antagonists.

Theoretical considerations suggest that the renal response to calcium antagonists may vary depending on the factors influencing basal vascular tone. Studies were conducted using the isolated perfused rat kidney to determine the response to calcium antagonists under conditions in which the determinants of renal vascular tone were accurately defined. With this model, calcium antagonists elicit vasodilation only in the presence of a vasoconstrictor. In this setting, however, the degree of vasodilation elicited depends on the nature of the vasoconstrictor employed. Thus, the reduction in renal perfusate flow (RPF) elicited by KCl-induced depolarization was completely reversed by the calcium antagonist, nitrendipine. In contrast, identical levels of vasoconstriction elicited by norepinephrine or angiotensin II were only partially reversed, suggesting that these agonists activate the renal vasculature by mechanisms that are more complex than membrane depolarization. Examination of the response of glomerular filtration rate (GFR) revealed that in the presence of norepinephrine and angiotensin II, nitrendipine exerted a preferential augmentation of GFR. Thus, concentrations that produced only modest effects on RPF increased GFR to levels equal to or exceeding control values. This selective augmentation of GFR did not occur during the renal vasoconstriction elicited by KCl. It is proposed that renal microvessels exhibit regional heterogeneity in regard to activation mechanisms and sensitivity to calcium antagonists. Calcium antagonists may selectively attenuate agonist-induced vasoconstriction of preglomerular vessels.

Animals↗
PubMed1987

Left ventricular mechanics in the normal newborn.

The transition from fetal to neonatal circulatory status is accompanied by marked alteration in relative right and left ventricular systolic and diastolic pressure. These alterations would be expected to influence both global and regional performance of the left ventricle. To address this issue, sequential two-dimensional echocardiographic studies were performed in normal newborns during the first days of life. Global and regional left ventricular wall motion were quantified by computer digitization with the use of an automated edge detection algorithm and a floating-center-of-mass model. Comparison was made with a control group of normal infants and young children and the sequential change over the first 5 days of life was assessed. Newborns were found to have a circular left ventricular configuration at end-diastole beginning on day 1. At end-systole, however, there was significant left ventricular distortion due to septal flattening, which persisted until day 3 and resolved entirely by day 5 of life. Regional wall motion analysis demonstrated a corresponding augmentation of septal and contralateral left ventricular free wall systolic movement during the first days of life, with a normal pattern attained by day 4. Due to the nonhomogeneity of the left ventricular wall motion in the first few days of life, standard single-dimension shortening fraction provided an unreliable measure of global left ventricular performance before day 4. Thus, systolic right ventricular hypertension at a level sufficient to distort the left ventricular configuration is present until day 4 or 5 of life, resulting in altered left ventricular regional wall motion. As a result, usual M mode echocardiographic assessment of left ventricular function is unreliable in this age group.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1987

Relationship of increased plasma atrial natriuretic factor and renal sodium handling during immersion-induced central hypervolemia in normal humans.

Although maneuvers augmenting atrial volume and/or stretch also augment plasma levels of atrial natriuretic factor (ANF), the role of ANF in modulating renal sodium and water handling has not been defined. Water immersion to the neck (NI) was employed to assess the ANF response to acute volume expansion in 13 seated sodium-replete normal subjects. ANF increased promptly and markedly from 7.8 +/- 1.8 to 19.4 +/- 3.8 fmol/ml, then declined to 6.3 +/- 1.4 fmol/ml after 60 min recovery. Concomitantly, NI increased urine flow rate (V) (2.0 +/- 0.6 to 7.0 +/- 0.9 ml/min; P less than 0.001) and sodium excretion (UNaV) (92 +/- 12 to 191 +/- 15 mu eq/min; P less than 0.001), and decreased PRA (-66 +/- 3%) and plasma aldosterone (-57 +/- 6%). Increases of plasma ANF ranged from less than 20% to over 12-fold. Similarly, the natriuretic response to NI varied markedly from none to 500%. There was a strong correlation between peak ANF and peak UNaV (r = 0.67; P less than 0.025), but none between peak V and peak plasma ANF (r = -0.10; P greater than 0.5). These findings suggest that an increase in plasma ANF contributes to the natriuretic response to NI, implying a physiological role for ANF in modulating volume homeostasis in humans.

Adult↗