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Biomedical subjects

S R Goldsmith

Publications and source records attributed to S R Goldsmith.

69 records · Page 4Linked to original sources
PubMed1983

Comparative hemodynamic effects of antishock suit and volume expansion in normal human beings.

The effects of pneumatic antishock trousers on central venous pressure (CVP) and mean arterial pressure (MAP) were compared with those of volume expansion with normal saline in a group of healthy young men. CVP increased from 4.8 +/- 1.9 to 7.3 +/- 2.5 mm Hg (P less than .001) with the suit and from 4.7 +/- 1.9 to 7.3 +/- 2.2 mm Hg (P less than .001) with volume expansion. During suit use, MAP increased from 85 +/- 6.7 to 93 +/- 6.8 mm Hg (P less than .001), while during volume expansion it did not change. Therefore, despite equivalent increases in CVP, the pneumatic antishock suit significantly increased MAP while volume expansion did not. The data suggest that the increased blood pressure produced by the suit may be at least in part dependent on mechanisms other than increased preload from an "auto transfusion" of blood into the central circulation.

Blood Pressure↗
PubMed1983

Regional blood flow response to orthostasis in patients with congestive heart failure.

To investigate the central and regional circulatory response to orthostasis in congestive heart failure, hemodynamic variables and forearm and hepatic blood flow were measured in 22 patients at supine rest and during a 65 degrees head-up tilt. Results were compared with those in nine normal subjects. Heart rate and mean arterial blood pressure increased during tilt in normal subjects, but not in patients with heart failure. Forearm blood flow decreased in normal subjects from 3.7 +/- 1.1 to 2.7 +/- 1.5 ml/min per 100 g (probability [p] less than 0.02), but did not change from a lower baseline (1.65 +/- 0.78 ml/min per 100 g) in patients. Forearm vascular resistance increased in normal subjects but not in patients. Hepatic blood flow did not change during tilt in either group, but hepatic vascular resistance increased in normal subjects from 0.37 +/- 0.13 to 0.47 +/- 0.15 U, (p less than 0.02). The increase was not seen in patients (1.2 +/- 1.1 to 1.4 +/- 1.0 U, p = not significant [NS] ). Total systemic resistance increased in patients from 1,848 +/- 560 to 2,132 +/- 731 dynes.s.cm-5 (p less than 0.005) indicating that resistance did increase in some vascular beds. Plasma norepinephrine also increased modestly in these patients from 665 +/- 377 to 761 +/- 379 pg/ml (p = 0.035), but individual changes in plasma norepinephrine did not correlate with changes in hepatic or forearm resistance. Thus, both the overall hemodynamic response and the regulation of regional blood flow and resistance differ in several respects in patients with congestive heart failure when compared with normal subjects. Changes in heart rate, blood pressure, forearm flow and forearm and hepatic vascular resistance are all blunted in patients. Reasons for the differences are not yet clear, but may be associated with abnormalities in reflex control of the circulation in patients with congestive heart failure.

Adult↗
PubMed1983

Impaired response of plasma vasopressin to orthostatic stress in patients with congestive heart failure.

Arginine vasopressin, a potent vasoconstrictor and regulator of body water, is frequently increased in the plasma of patients with congestive heart failure. Other neurohumoral control networks, such as the sympathetic nervous system and the renin-angiotensin system, also demonstrate increased activity in congestive heart failure, but fail to respond normally to physiologic stress, such as orthostatic tilt. To assess the response of plasma vasopressin to orthostasis in heart failure, vasopressin was measured before and at 10 and 45 minutes during passive upright tilt in 15 patients with congestive heart failure and their response was compared with that in 9 normal control subjects. Arginine vasopressin was measured by radioimmunoassay. In the normal subjects, plasma arginine vasopressin was 5.3 +/- 2.3 pg/ml at control, was unchanged at 10 minutes, but significantly increased to 7.0 +/- 2.5 pg/ml at 45 minutes (p less than 0.05). In contrast, patients with congestive heart failure showed no significant changes in arginine vasopressin levels from the control levels of 11.6 +/- 5.5 pg/ml. Both plasma norepinephrine and renin activity increased in the normal subjects, but failed to increase from higher baselines in patients with congestive heart failure. Thus, plasma arginine vasopressin, like plasma norepinephrine and renin activity, does not increase in response to upright tilt in patients with congestive heart failure. The explanation is not evident but could involve either abnormalities in reflex control of plasma vasopressin in congestive heart failure or in clearance of the hormone during orthostasis.

Adult↗
PubMed1983

The neurohumoral and hemodynamic response to orthostatic tilt in patients with congestive heart failure.

Thirty-five patients with varying degrees of congestive heart failure were subjected to 60 degrees upright tilt. Eight of the patients with normal resting hemodynamics had elevated resting plasma norepinephrine levels (PNE) (p less than 0.001), but their response to upright tilt was similar to that in normal subjects: All had increases in heart rate, plasma norepinephrine (from 263 +/- 32 to 483 +/- 78 pg/mg, p less than 0.02) and plasma renin activity (from 4.8 +/- 0.9 to 13.7 +/- 7.6 ng/ml/hour, p less than 0.05). In 27 patients with high resting pulmonary wedge pressure and low cardiac index, resting PNE was higher (668 +/- 71 ng/ml), but PNE, plasma renin activity and heart rate did not increase significantly during tilt despite a fall in pulmonary capillary wedge pressure and cardiac index. In 18 of these patients, PNE rose during tilt, whereas in nine it did not change or fell; the resting hemodynamics and the hemodynamic response to tilt were not significantly different in these two groups. These data suggest that an abnormality of mechanoreceptor or baroreceptor function is common in patients with CHF. This abnormality corresponds in part to the severity of the resting hemodynamic abnormality, but among patients with severe CHF, the reflex neurohumoral abnormality may provide independent information about the severity of the disease.

Adult↗
PubMed1982

Response of plasma norepinephrine and epinephrine to dynamic exercise in patients with congestive heart failure.

The activity of the sympathetic nervous system is increased at rest in patients with congestive heart failure. To determine whether this augmentation is carried over during dynamic upright exercise, 14 patients with congestive heart failure were stressed maximally during upright bicycle ergometry. Plasma norepinephrine and epinephrine levels were measured in the basal upright (sitting) posture before and during maximal exercise. The results were compared with those in six healthy control subjects before and during maximal exercise. Plasma norepinephrine increased during exercise from a mean (+/- standard error of the mean) of 650 +/- 95 to 1,721 +/- pg/ml in the group with heart failure. This increase was significantly less (p less than 0.001) than that in the control group (from 318 +/- 36 to 3,230 +/- 418 pg/ml). However, for equivalent levels of total body oxygen consumption (VO2), the group with heart failure had higher levels of plasma norepinephrine than the control group. Plasma epinephrine was similar in the two groups in the basal upright position (92 +/- 18 and 92 +/- 26 pg/ml), but it increased more during exercise in the normal subjects (743 +/- 210 pg/ml) than in the group with heart failure (167 +/- 67 pg/ml) (p less than 0.001). The percent increase in norepinephrine correlated with the percent change in VO2 in the group with heart failure (r = 0.62, p less than 0.02), but the percent change in epinephrine did not. There is, therefore, a disturbance in the sympathetic nervous system during exercise in patients with congestive heart failure. Although norepinephrine increases in such patients to a greater extent than in normal subjects at lower levels of exercise, the extremely high levels of norepinephrine and epinephrine generated by normal subjects during maximal upright exercise do not occur in patients with heart failure.

Adult↗
PubMed1982

Relationship of exercise capacity to resting left ventricular performance and basal plasma norepinephrine levels in patients with congestive heart failure.

Seventeen patients with chronic congestive heart failure (CHF) were studied to assess the relationship of resting left ventricular function, as measured by noninvasive and invasive methods, to maximal exercise capacity, as measured by peak total body oxygen consumption (VO2). Supine basal plasma norepinephrine (NE) was also measured to evaluate its relationship to the severity of heart failure and to determine whether it may be a better predictor of exercise capacity in patients with CHF than the more commonly employed noninvasive and invasive tests of left ventricular function. Fourteen of the 17 patients underwent upright bicycle exercise (average peak VO2 10.60 +/- 1.40 ml/kg/min, +/- SEM) to their symptomatic maximum. There was no significant correlation between peak VO2 and the noninvasive measurements of left ventricular performance obtained at rest, including cardiothoracic ratio, left ventricular internal dimension by M-mode echo, percent shortening of the minor axis by M-mode echo, and radionuclide ejection fraction. Hemodynamic measurements were performed in 16 patients. The hemodynamic measurements at rest also failed to correlate with exercise capacity. The supine basal plasma NE, which was elevated in these 17 patients (612 +/- 100 pg/ml), had an inverse relationship with stroke work index (r - -0.70, p less than 0.01) and stroke index (r = -0.83, p less than 0.001) and a positive correlation with right atrial pressure (r = 0.81, p less than 0.001). Although both noninvasive and invasive measurements at rest failed to correlate significantly with peak VO2 during exercise, the plasma NE had a significant inverse correlation with peak exercise VO2 (r = -0.50, p less than 0.05). The basal supine plasma NE is therefore elevated in patients with CHF, is a marker for the severity of CHF as measured by hemodynamics performed at rest, and is a better predictor of exercise capacity than standard noninvasive and invasive tests performed at rest.

Adult↗
PubMed1982

Response of vasopressin and norepinephrine to lower body negative pressure in humans.

To examine the contributions of cardiopulmonary and sinoaortic baroreceptors to the nonosmotic release of arginine vasopressin (AVP) in normal humans, we subjected nine individuals without evidence of hypertension or heart disease to graded, lower body negative pressure (LBNP). We also studied the effects of this maneuver on sympathetic nervous system activity using plasma norepinephrine (NE) as an index. Heart rate (HR), mean arterial pressure (MAP), pulse pressure (PP), and central venous pressure (CVP) were measured in the control state and during two consecutive levels of increasingly intense LBNP. At each stage blood was sampled for AVP and NE. AVP was analyzed by radioimmunoassay, NE by a radioenzymatic method. During the first level of LBNP, CVP decreased with no change in HR, MAP, or PP. NE increased from 147 +/- 47 to 212 +/- 53 (SD) pg/ml, P less than 0.01, whereas AVP (5.0 +/- 1.0 pg/ml) did not change. With increased suction CVP fell further, HR increased, and PP narrowed, but MAP did not change. NE further increased to 291 +/- 58 pg/ml (P less than 0.01), but AVP still did not change significantly. One subject became markedly hypotensive, and his AVP increased from 2.6 to 81 pg/ml. A fall in CVP that results in sympathetic activation presumably via cardiopulmonary receptors does not therefore increase AVP levels; a further fall in CVP that leads to modest unloading of the sinoaortic baroreceptor and further increased sympathetic activity also fails to stimulate AVP. Hypotension, however, is accompanied by a rapid and profound increase in circulating AVP.

Arginine Vasopressin↗
PubMed1975

Lymphocyte depletion induced by cholera toxin; relationship to adrenal cortical function.

Intravenous injection of cholera toxin (choleragen) into mice caused a profound lymphocytopenia associated with marked cellular depletion of the lymph nodes, spleen, and thymus. After administration of 1 mu g of choleragen, lymphocytopenia was mot marked at 24 hr; recovery occurred 6 to 10 days later. Similarly depletion of lymph nodes and spleen was maximal at 24 hr with recovery by 14 days. Choleragen also caused a marked elevation of serum corticosterone and lymphocyte depletion was not observed in adrenalectomized mice. These results suggested that the lymphocytopenic effect of choleragen was mediated by increased production and secretion of adrenal cortical hormones secondary to a rise in intracellular cAMP induced by cholera toxin. The site of action of choleragen may be the adrenal cortex itself and/or the hypothalamic-pituitary system.

Adrenal Cortex↗