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Biomedical subjects

M D Johnson

Publications and source records attributed to M D Johnson.

At least 289 records · Page 16Linked to original sources
PubMed1981

Circulating catecholamines in control of renal electrolyte and water excretion.

Graded physiological doses of norepinephrine or epinephrine were infused either intravenously or directly into the renal artery of conscious dogs previously prepared with chronic indwelling catheters. Infusion rates ranged from 5 to 125 ng . kg-1 . min-1, and aortic plasma catecholamine concentrations were measured during intravenous infusion to determine the actual levels achieved. Even when the renal arterial plasma norepinephrine concentration was raised to 5,000 pg/ml by either intravenous or intrarenal infusion, only a modest sodium and potassium retention was observed. Only intravenous norepinephrine increased urinary flow rate. Increments of epinephrine concentration from 120 to 2,000 pg/ml decreased sodium and potassium excretion only when delivered intravenously. The concentrations of norepinephrine or epinephrine required to alter urinary sodium and potassium excretion and flow rate were in the upper physiological range or higher and the responses were small except for intravenous epinephrine, which decreased sodium excretion at very low physiological concentrations (120-400 pg/ml). We conclude that circulating epinephrine may play an important physiological role in renal sodium conservation. This effect of epinephrine is not due to a direct intrarenal mechanism.

Animals↗
PubMed1980

In vivo nitrosation of morpholine in mice by inhaled NO2.

Groups of 3-5 mice were gavaged with aqueous solutions of 2 mg morpholine and immediately exposed to 2-50 ppm levels of NO2 in inhalation chambers for periods of up to 3 hours. After exposure, mice were frozen and pulverized in liquid nitrogen, and aliquots of frozen powder (congruent to 8 g) were extracted with cold 35% aqueous methanol and methylene chloride. Concentrated methylene chloride solutions were analyzed for N-nitrosomorpholine (NMOR), using gas chromatography with a Thermal Energy analyzer detector. NMOR levels in controls (exposed to NO2 alone, or dosed with morpholine without subsequent NO2 exposure) were less than 5 ng/mouse. NMOR yields in test mice were time-dependent with respect to duration of NO2 exposure and dose-dependent with respect to NO2 levels. These preliminary studies demonstrate the in vivo nitrosating potential of nitrogen oxides.

Animals↗
PubMed1979

Circulating catecholamines and control of plasma renin activity in conscious dogs.

Uninephrectomized dogs were prepared with indwelling catheters in the aorta, inferior vena cava (IVC), and renal artery, and after recovery they were studied in the conscious state. Basal aortic epinephrine and norepinephrine concentrations were 57 +/- 11 and 101 +/- 18 pg/ml, respectively. Elevation of epinephrine concentration to over 2,000 pg/ml by IVC infusion resulted in a sustained 3.5-fold increase in plasma renin activity (PRA), with only a transient decrease in arterial blood pressure. The PRA response to epinephrine was completely blocked by l-propranolol; isoproterenol increased PRA more than did epinephrine. Increasing norepinephrine concentration to 1,600 pg/ml by IVC infusion resulted in only a 1.5-fold increase in PRA. Infusion of epinephrine or norepinephrine directly into the renal artery to achieve similar increments of renal arterial concentration did not increase PRA. Insulin injection or hemorrhage resulted in elevations of arterial epinephrine (but not norepinephrine) concentration greater than the concentrations achieved during IVC infusion in these studies. We conclude that circulating epinephrine in the physiologic range plays a role in the control of PRA by activation of an extrarenal beta-receptor.

Animals↗
PubMed1979

Plasma epinephrine and control of plasma renin activity: possible extrarenal mechanisms.

Previous work from our laboratory has shown that physiological increments of circulating epinephrine concentration increase plasma renin activity (PRA) by an extrarenal beta-receptor mechanism. In the present experiments, epinephrine was infused intravenously at 125 ng.kg-1.min-1 for 45 min in trained, conscious dogs. PRA rose 3 to 5-fold, as previously described, and was accompanied by a transient decline of mean arterial pressure, decreased plasma potassium concentration, and increased hematocrit. Prior splenectomy to maintain hematocrit constant did not attenuate the PRA response to epinephrine. The kidneys of 4 dogs were denervated and constrictor cuff was placed around the renal artery. Renal denervation did not alter the PRA response to intravenous epinephrine infusion. A transient decline in renal perfusion pressure produced by cuff constriction only transiently increase PRA. Neither maintenance of a constant plasma potassium concentration nor oral administration of indomethacin altered the PRA response to epinephrine. We conclude that intravenous epinephrine increases PRA by a mechanism independent of the renal nerves, changes in renal perfusion pressure, hematocrit, plasma potassium concentration, and plasma prostaglandins.

Animals↗
PubMed1979

Effects of AVP and DDAVP on plasma renin activity and electrolyte excretion in conscious dogs.

Uninephrectomized adult female dogs with chronic indwelling catheters were maintained on a low sodium diet and studied without anesthesia. Following hydration with 3% dextrose, an intravenous infusion of either arginine vasopressin (AVP) or of 1-desamino-8-D-arginine vasopressin (DDAVP) was begun. The dose was calculated to achieve a near maximal physiological plasma concentration of AVP, or an equimolar concentration of DDAVP. Both AVP and DDAVP increased urinary osmolality from less than 60 to over 800 mosmol/kg H2O within 1 h. AVP infusion increased mean arterial pressure and renal electrolyte excretion and decreased heart rate and plasma renin activity (PRA), while DDAVP was without effect on these parameters. AVP infused into the renal artery at doses which did not alter systemic pressure and heart rate caused kaliuresis and reduced PRA. We conclude that the AVP-induced inhibition of renin secretion and increase in renal electrolyte excretion are not secondary to increased tubular permeability to water, but must represent a more specific action of AVP which is not shared by DDAVP.

Animals↗
PubMed1977

Altered amounts of hemoglobin synthesis in livers of dystrophic hamsters.

In liver supernatants similar amounts of leucine are incorporated into proteins of normal and dystrophic hamsters. However, using a dual labeling technique, a protein fraction is detected which shows different levels of leucine incorporation between normal and dystrophic animals in an age-dependent fashion. The major protein in this fraction comigrates with hemoglobin or its subunits under various conditions of polyacrylamide gel electrophoresis. In animals younger than 3 days there is more synthesis of this protein fraction in dystrophic animals, while at 6 days there is considerably less synthesis of this protein. These changes are paralleled by differences in the number of erythroid foci in histological sections of the livers. There is no evidence for structurally altered hemoglobin in dystrophic hamsters. The significance of this finding and its possible relation to the dystrophy process are not known at present.

Aging↗
PubMed1977

Renin release and pressor response to renal arterial hypotension: effect of dietary sodium.

Changes in plasma renin activity (PRA) and mean arterial pressure (MAP) produced by renal arterial hypotension were studied in conscious, adrenalectomized dogs maintained on low-, normal-, or high-Na diet during constant steroid replacement therapy. In animals maintained on a low-Na diet, reduction of renal perfusion pressure to 50 mmHg for 45 min increased MAP 40 +/- 3 (SE) mmHg, while PRA rose rapidly by 36.5 +/- 6 ng ml-1 h-1. Similar renal hypotension in dogs maintained on a normal-Na diet increased MAP only 21 +/- 3 mmHg while PRA rose 5.5 +/- 0.9 ng ml-1 h-1; dogs on high-Na intake had a 6 +/- 1 mmHg pressure rise without a significant change in PRA. The rise in MAP correlated well with the log deltaPRA. Calculated open-loop gain was -1.2, -0.7, and -0.1 in dogs on low-, normal-, and high-Na diets, respectively. Nonpeptide angiotensin I converting enzyme inhibitor (CEI) reversed the elevated MAP observed during reduction of renal perfusion pressure in dogs on low- and normal-Na diets, but had little effect in dogs on high-Na intake. These observations suggest that the renin-angiotensin system becomes quantitatively more important in the regulation of blood pressure as Na intake is reduced.

Adrenalectomy↗
PubMed1977

Antidiuretic hormone and the distribution of renal cortical blood flow.

The radioactive microsphere method was used to study the distribution of cortical blood flow in anesthetized dogs during water diuresis and during antidiuresis. Infusion of antidiuretic hormone (ADH) at rates ranging from 0.33 to 0.5 mU/kg-min into dogs previously volume expanded with 3% dextrose resulted in an increase in urinary osmolality and a significant increase in fractional flow in the inner cortex. Mean arterial pressure, glomerular filtration rate, and renal plasma flow were unaltered by the infusion of ADH at these doses, suggesting that absolute, as well as fractional, blood flow to the inner cortex increased in response to ADH. In three additional experiments, termination of an infusion of ADH in hydropenic dogs and subsequent induction of water diuresis was accompanied by a shift in fractional cortical blood flow away from the inner cortex. The redistribution of cortical blood flow in response to ADH at a time when the kidney is producing a more concentrated urine supports the hypothesis that this vascular effect of ADH may have functional significance in the urinary concentration ability of the kidney.

Animals↗
PubMed1977

Stimulation of renal sodium reabsorption by angiotensin II.

Various parameters of renal function were studied before, during, and after the infusion of physiological increments of angiotensin II directly into one renal artery of anesthetized dogs. During water diuresis and during antidiuresis induced with exogenous antidiuretic hormone (ADH), angiotensin II consistently reduced UNaV, UKV, and CPAH, and increased the filtration fraction in the infused kidney. Urinary osmolality was increased only in the presence of ADH, while during water diuresis angiotensin II had no apparent effect on urinary osmolality or flow rate. During saline diuresis, a mean increment of angiotensin II concentration of 14 pg/ml was sufficient to significantly reduce UNaV and urinary flow rate. Changes in CCr, CPAH, and filtration fraction did not correlate with changes in sodium excretion, and intracortical distribution of blood flow remained unaltered. These data support the hypothesis that normal circulating levels of angiogensin II play a direct renal role in the control of sodium, potassium, and water homeostasis, and that angiotensin II exerts a direct, stimulatory effect on tubular sodium reabsorption independent of changes in GFR, RPF, filtration fraction, or intracortical distribution of blood flow.

Angiotensin II↗
PubMed1977

Prognostic indices for survival during postcardiotomy intra-aortic balloon pumping. Methods of scoring and classification, with implications for left ventricular assist device utilization.

To define more clearly a salvageable patient for possible utilization of a left ventricular assist device prior to multiple organ failure and irretrievability during postcardiotomy intra-aortic balloon pumping (IABP), we made prospective and retrospective analyses to determine prognostic indices for survival. Serial left ventricular function curves (IABP on-off), scoring methods, hemodynamic and renal function tracking trajectories, survival versus nonsurvival data envelopes, and classification methods were developed and used. All patients requiring postcardiotomy IABP support who were in Class A survived; 80 percent of the patients in Class B survived. All patients who remained in Class C for 12 hours or more following operation with IABP support died. These preliminary analyses suggest that the postcardiotomy IABP-supported patient with a score of less than 6 who remains in Class C for 12 hours or more is at the highest possible risk and is a probably candidate for more effective support with a left ventricular assist device.

Assisted Circulation↗
PubMed1976

Performance of an abdominal left ventricular assist device during induced tachycardias and dysrhythmias.

Experiments were designed to assess the performance of an intracorporeal (abdominal) left ventricular assist device (ALVAD) in the presence of induced tachycardias, multiple premature ventricular contractions (PVC's), and ventricular fibrillation in calves. Performance criteria were the degree of left ventricular unloading and the per cent cardiac output assumed by the ALVAD. During synchronous pumping, left ventricular unloading was complete and the entire cardiac output was captured by the device. During induced tachycardias up to rates of 120 beats per minute, these degrees of performance were maintained. At rates in excess of 120 beats per minute, performance declined due to decreased biologic stroke volumes and prosthetic filling times. In the presence of induced PVC's, performance during synchronous pumping decreased because of erratic R-wave sensing. Left ventricular unloading was complete but irregular, and the total cardiac output was captured. When asynchronous pumping was utilized, mean left ventricular systolic pressures increased, but total cardiac output was still captured. During induced ventricular fibrillation, ALVAD actuation maintained cardiac outputs equal to control values for periods up to 5 1/2 hours. These experiments indicate that, during normal sinus rhythm, synchronous pumping is optimal; asynchronous pumping is optimal during complex dysrhythmias; and either can be utilized to support the circulation with varying degrees of left ventricular unloading.

Animals↗
PubMed1975

Plasma renin activity during pentobarbital anesthesia and graded hemorrhage in dogs.

Six dogs were implanted with chronic arterial and venous catheters and were trained to lie quietly on a padded table. The effect of pentobarbital anesthesia and of graded hemorrhage on plasma renin activity (PRA) was then examined in the absence of surgical stress. Pentobarbital anesthesia resulted in a fivefold increase in PRA within 15 min, followed by a slow decline to a level 3 times control at 1.5 h. Mean arterial pressure (MAP) fell transiently but returned to control values. In the unanesthetized dog, graded hemorrhage to 12 ml/kg resulted in a twofold increase in PRA with no change in MAP or heart rate. The same hemorrhage in pentobarbital-anesthetized dogs resulted in a similar increase in PRA, accompanied by a substantial increase in heart rate. It is concluded that 1) pentobarbital anesthesia in the dog results in a rapid and sustained increase in PRA, and 2) in the conscious dog, increased PRA in response to graded hemorrage appears to be independent of an arterial baroreceptor mechanism and of generalized increased sympathetic nervous system activity.

Anesthesia↗
PubMed1974

Studies on the pathogenesis of type I (distal) renal tubular acidosis as revealed by the urinary PCO2 tensions.

This study was designed to investigate the pathogenesis of type I (distal) renal tubular acidosis. Urinary and blood Pco(2) tensions were determined when the pH of the urine was equal to or exceeded the corresponding blood pH. This provided an indication of net hydrogen ion secretion in the distal nephron. In 16 normal subjects, the Pco(2) of the urine exceeded blood values (U-B Pco(2)) by 32.7+/-3.1 mm Hg. In contrast, the urinary Pco(2) tensions in 10 patients with type I (distal) renal tubular acidosis were not significantly greater than blood values (U-B Pco(2) = 2.0+/-2.2 mm Hg). These results indicate that type I (distal) renal tubular acidosis is caused by failure of the cells of the distal nephron to secrete hydrogen ions rather than to gradient-limited hydrogen ion addition to the urine. This is suggested by the fact that urinary Pco(2) levels should be higher than blood Pco(2) levels when hydrogen ions are secreted into urine containing bicarbonate in the distal nephron and they were not in this study despite the presence of a favorable hydrogen ion gradient (tubular fluid pH exceeded blood pH).

Acidosis, Renal Tubular↗
PubMedDate not supplied

Role of central epinephrine in regulation of anterior pituitary hormone secretion.

Hypothalamic regulation of anterior pituitary hormones is thought to be mediated by the release of stimulatory and/or inhibitory peptides that are, in turn, regulated by catecholaminergic neurons. The recent development of selective epinephrine (EPI) synthesis inhibitors has made it possible to disrupt central EPI neurotransmission without affecting norepinephrine or dopamine. These compounds were used in the present investigation to assess the involvement of brain EPI systems in regulation of GH, LH, and prolactin (PRL) in male and ovariectomized female rats. Inhibition of central EPI synthesis (1) inhibited episodic and morphine-, but not clonidine-induced GH release, and (2) blocked the LH surge induced by estrogen and progesterone, but did not affect episodic LH release in hormonally untreated rats. Inhibition of peripheral (adrenal) EPI synthesis had no effect on these hormones. Results of these studies suggest an excitatory role for EPI in regulation of GH and LH secretion, mediated by stimulation of GH-releasing hormone and LHRH, respectively. EPI does not appear to have a major function in regulation of PRL secretion.

Animals↗