Unilateral pulmonary changes in acute respiratory distress syndrome of the adult.
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Biomedical subjects
Publications and source records attributed to M Epstein.
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The relationship between systemic and renal hemodynamics was studied in 20 patients with advanced cirrhosis of the liver. Cardiac output was assessed by an indicator dilution technique, and both mean renal blood flow and intrarenal blood flow distribution were determined by the 133Xe washout method. Ten patients had elevated cardiac outputs (7.14 to 13.58 L/min; HCO group), seven patients had normal cardiac ouptputs (5.16 to 6.78; NCO group), and three had low cardiac outputs (3.65 to 4.1; LCO group). Renal hemodynamics did not correlate with cardiac output (r = 0.051; N.S.), since comparable reductions in mean renal blood flow occurred in both the LCO and HCO patients. Similarly, the degree of cortical ischemia, as assessed by percentage flow to the rapid flow component (C1%), did not correlate with cardiac output (r = 0.007; N.S.). Vasomotor instability as assessed by intrapatient variability of sequential xenon washout studies occurred frequently, and its magnitude did not correlate with cardiac output (r = -0.069; N.S.). These studies demonstrate that the abnormalities of intrarenal blood flow in cirrhosis are independent of alterations in cardiac output. Furthermore, the finding of marked intrarenal hemodynamic instability in the majority of patients with cirrhosis suggests that caution should be exercised in interpreting studies assessing the efficacy of vasoactive agents on renal hemodynamics in this disease, since the changes attributed to treatment may merely reflect spontaneous change.
A 23-year-old-man had true erythrocytosis and the nephrotic syndrome. A renal biopsy specimen showed focal sclerosing glomerulonephritis and nephrosclerosis. Both serum and urinary erythropoietin levels were increased, and plasma renin activity was in the high normal range. The association of erythrocytosis and glomerulonephritis with the nephrotic syndrome is reviewed, and the uniqueness of this association is proposed. Finally, a dissociation between these hormones was demonstrated using water immersion to the peck as a suppressive maneuver.
Utilizing the rebreathing of a gas mixture containing C2H2, C180, He O2, and N2, we obtained serial measurements of the pulmonary capillary blood flow (Qc), diffusing capacity per unit of alveolar volume (DL/VA), functional residual capacity (FRC), pulmonary tissue plus capillary blood volume (VTPC), and O2 comsumption (VO2) in five normal subjects under the following conditions: 1) 6 h of sitting, 2) 4 h of sitting while immersed in thermoneutral water to the neck, and 3) 4 h of lying in thermoneutral water to the neck. Water immersion (NI) was preceded and followed by 1-h prestudy and 1-h recovery periods. The measurements were made at 30-min intervals. Seated NI produced a fourfold increase in sodium excretion (UNaV), a 25-36% increase in Qc, a 45-59% increase in DL/VA, and a 30-36% decrease in FRC. This occurred as early as the 1st h of NI and persisted throughout the 4-h period of study. Throughout the seated control and NI periods, VO2, heart rate, and VTPC remained constant. During supine NI, Qc, HR, DL/VA, FRC, and VO2 did not differ significantly from supine prestudy. These date demonstrate that seated NI causes a significant increase of Qc and DL/VA which persists throughout the immersion period. Furthermore, the lack of change of VTPC suggests that the central vascular engorgement induced by seated NI is not accompanied by extravasation of fluid into the pulmonary interstitial space.
Although previous studies have demonstrated that water immersion to the neck (NI) results in a significant natriuresis and diuresis, the mechanisms are incompletely delineated. Since recent studies have demonstrated that NI induces a marked increase in cardiac index, it is possible that, as a consequence, renal hemodynamics may be augmented markedly during NI thereby mediating the encountered renal changes. The present study was undertaken to delineate the effects of NI on renal plasma flow and glomerular filtration rate as assessed by the clearance of PAH (CPAH) and inulin (CIn), respectively. Nine normal male subjects were studied on two occasions, control and NI. The conditions of seated posture and time of day were identical. Immersion did not alter CIn or CPAH at a time when sodium excretion was increasing markedly. The constancy of CPAH during NI suggests that renal blood flow is unaltered and that the natriuresis of NI is mediated independently of alterations in overall renal perfusion. The sluggish decline of a naturiuresis during recovery is consistent with the presence of a humoral factor contributing to the encountered natriuresis.
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Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant relative central hypervolemia induced by water immersion to the neck (NI) results in a significant natriuresis which is quantitatively identical to that induced by the acute administration of 2 L. of saline. Since the central hypervolemia induced by NI occurs without concomitant alterations in serum ionized calcium concentration (Ca++), the NI model was utilized to assess the role of volume in the regulation of PTH secretion in man. Seven normal subjects were studied following 11 hours of dehydration on two occasions, control and NI. The conditions of seated posture and time of day were identical. Blood for ionized calcium and PTH was obtained at 30-minute intervals for 6 hours. NI resulted in a significant increase in UNaV from a prestudy value of 78 +/- 12 (S.E.M.) to 222 +/- 20 muEq per minute (p less than 0.001). Concomitantly, Ca++ remained constant, ranging between 4.57 to 4.71 mg. per cent. Despite the volume-induced natriuresis, PTH was not altered throughout 5 hours of NI, ranging from 36 +/- 7 to 45 +/- 5 mul-Eq. per milliliter. Phosphate excretion remained constant. These data indicate that central volume expansion does not alter PTH in normal man when the variables of ionized calcium, posture, and time of day are controlled. Furthermore, the current demonstration of the absence of phosphaturia during immersion despite the probability that the distal delivery of phosphate was enhanced, permits consideration of the possibility that the concept of a distal tubular reabsorptive site for phosphate may be applicable to man.
Age modifies a number of factors which determine renal sodium handling including the rate of glomerular filtration, renal hemodynamics, and the responsiveness of the renin-angiotensin-aldosterone system. This study was carried out, therefore, to examine the effects of age on the capacity of the normal human kidney to respond to restriction of sodium intake. Renal conservation of sodium and response to dietary sodium restriction was assessed in 89 healthy subjects who were free of cardiovascular, renal, or adrenal disease. The daily reduction in urine sodium which followed restriction of intake to 10 mEq. of sodium and 100 mEq. of potassium per day conformed well to an exponential function, defined by an unweighted least-squares fit. The half-time for the reduction in renal sodium excretion in subjects under 30 years was -17.6 +/- 0.7 hours, significantly faster than for subjects aged 30 to 59, who had a relatively constant half-time (23.4 +/- 1.1 hours). In subjects over 60 years of age the half-time was prolonged to 30.9 +/- 2.8 hours, significantly greater than that of the younger age group. These observations indicate that age significantly influences the kidney's capacity to conserve sodium. Age-related change must be considered in the assessment of this function in human disease.
The hepatorenal syndrome following right hemiphepatectomy is reported in a previously healthy patient who sustained a shotgun wound in the abdomen. In spite of the development of severe oliguric renal insufficiency and the administration of massive amounts of volume expanders and furosemide, the urine sodium concentration remained very low, therby excluding the diagnosis of acute tubular necrosis. Although severe hyperbilirubinemia developed, the prothrombin time was only slightly abnormal and the liver doubled in size in the 2 weeks after surgery. The study of functional renal failure in patients with liver disease other than decompensated cirrhosis and with significant preservation of hepatic function may suggest that factors other than a circulating toxin participate in mediating the hepatorenal syndrome.
Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant central hypervolemia induced by water immersion to the neck (NI) results in a significant natriuresis, kaliuresis, and diuresis. The NI model was utilized to assess the role of "effective volume" and hyperaldosteronism in the impairment of sodium and water handling in cirrhosis. Eleven cirrhotic patients were studied twice while in balance on a 10 mEq. Na, 100 mEq. K diet: control and NI. The conditions of seated posture and time of day were identical. UNaV was constant throughout C, ranging from 1 to 2 muEq per minute. During NI, UNaV increased progressively from 1 +/- 1 (S.E.M.) during the prestudy hour to 89 +/- 32 muEq per minute during hour 5 of NI (p less than 0.02), greatly exceeding the comparable value found in normal subjects on an identical diet. (See article).
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The ability of short-term furosemide administration to alter intrarenal hemodynamics and to modify the clinical course of acute renal failure was assessed in six patients 2 to 9 days after the onset of acute renal failure. Following renal arterial catheterization, the intraarterial administration of furosemide at a dose of 9.6 mg/min for 30 minutes failed to improve renal function as assessed either by an increase in urine output or a decrease in serum creatinine during the 4 days after administration in the five oliguric patients. In a sixth patient with nonoliguric acute renal failure, urine volume increased with a gradual decrease in blood urea nitrogen and creatinine during the week after study. Furosemide failed to alter either mean renal blood flow or its intrarenal distribution as determined at intervals of 3 to 40 minutes after its infusion. These studies demonstrate that the short-term administration of furosemide in large doses does not improve renal hemodynamics or alter the clinical course of patients with established acute oliguric renal failure.
Since previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant relative central hypervolemia induced by water immersion to the neck causes a profound natriuresis and a suppression of the renin-aldosterone system, it was of interest to assess whether the diuresis induced by immersion was mediated by an analogous inhibition of ADH. The effects of water immersion on renal water handling and urinary ADH excretion were assessed in 10 normal male subjects studied following 14 h of overnight dehydration on two occasions, control and immersion. The conditions of seated posture and time of day were identical. During control ADH persisted at or above prestudy values. Immersion resulted in a progressive decrease in ADH excretion from 80.1 plus or minus 7 (SEM) to 37.3 plus or minus 6.3 muU/min (P smaller than 0.025). Cessation of immersion was associated with a marked increase in ADH from 37.3 +/- 6.3 muU/min to 176.6 +/- 72.6 muU/min during the recovery hour (P smaller than 0.05). Concomitant with these changes urine osmolality decreased significantly beginning as early as the initial hour of immersion from 1044 +/- 36 to 542 +/- 66 mosmol/kg H2O during the final hour of immersion (P smaller than 0.001). Recovery was associated with a significant mean increase in Uosm of 190 +/- 40 mosmol/kg H2O over the final hour of immersion (P smaller than 0.001). The suppression of ADH occurred without concomitant changes in plasma tonicity. These studies are consistent with the suggestion that in hydrated subjects undergoing immersion suppression of ADH release contributes to the enhanced free water clearance, which has been previously documented.
Although previous studies have demonstrated that water immersion to the neck (NI) results in both central hypervolemia and a significant natriuresis, it is unclear whether the magnitude of the "volume stimulus" of NI is comparable to that induced by the extracellular fluid volume expansion (ECVE) induced by acute saline administration. The present study was undertaken therefore to compare the natriuresis induced by these two different stimuli. All subjects were studied on four occasions while in balance on a diet containing 150 meq of sodium and 80 meq of potassium daily: seated control; seated immersion; and saline administration in both the seated and recumbent posture. The increment in UNaV during NI was indistinguishable from that of seated saline. Similarly, the kaliuretic response during NI was similar to that induced by seated saline infusion. In contrast, supine saline infusion resulted in a greater increment in UNaV than either NI or seated saline. The present data indicate that the "volume stimulus" of immersion is identical with that of standard saline-induced ECVE in normal seated subjects. Furthermore, the ability of NI to induce a natriuresis without a concomitant increase in total blood volume and with a decrease in body weight, rather than the increase which attends saline infusion, suggests that NI may be a preferred investigative tool for assessing the effects of ECVE in man.
Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant relative central hypervolemia induced by water immersion to the neck (NI) results in a significant natriuresis which is quantitative identical to that induced by the acute administration of 2 liters of saline. Since the central hypervolemia induced by NI occurs without concomitant alterations in serum sodium and potassium concentration, the NI model was utilized to assess the role of volume in the regulation of both plasma renin (PRA) and plasma aldosterone (PA) in man. Nine normal subjects were studied on two occasions while in balance on a 10 meq Na, 100 meq K diet; Control and NI. The conditions of seated posture and time of day were identical. Blood for PRA and PA was obtained at 30-min intervals for 6 h. NI produced a profound suppression of PRA as early as 30 min with maximal suppression (62%) by 180 min (P less than 0.001). Recovery from NI was associated with a prompt return to pre-study levels. The changes in PA paralleled those of PRA with regard to both the rapidity and magnitude of the suppression (r = 0.993: P less than 0.001). These data emphasize the importance of central volume per se as a primary determinant of PRA and PA regulation in normal man. Furthermore, the current studies confirm the importance of the renin-angiotensin axis in the control of volume-related changes in PA in normal man. The ability of NI to induce a prompt and parallel suppression of PRA and PA without concomitant alterations in plasma composition, suggests that NI may be a preferred investigative tool for assessing the effects of volume expansion on renin-aldosterone.
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