Biomedical subjects

R J Roman

Publications and source records attributed to R J Roman.

At least 163 records · Page 9Linked to original sources

PubMed1988

Influence of eicosanoids on renal function of DOCA-salt hypertensive rats.

The present study examined the contribution of changes in the synthesis or degradation (or both) of renal eicosanoids to the alterations in renal hemodynamics observed in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Renal blood flow and glomerular filtration rate were markedly reduced in DOCA-salt hypertensive rats compared with values observed in control rats given water or saline to drink. The abnormalities in renal hemodynamics in the hypertensive rats were associated with an increase in the excretion of thromboxane B2, an increase in the release of thromboxane B2 from renal cortical tissue slices, and a diminished release of prostaglandin E2 (PGE2) from renal medullary tissue. Additionally, the urinary excretion of PGE2 and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and the release of 6-keto-PGF1 alpha from renal cortical and medullary tissue were elevated in rats with DOCA-salt hypertension. Since the excretion of PGE2 and 6-keto-PGF1 alpha and the release of 6-keto-PGF1 alpha by medullary tissue were also elevated in normotensive rats given 1% NaCl solution to drink, these latter changes probably were related to an elevation of sodium intake rather than to the development of hypertension. The functional significance of the alterations in the renal production of thromboxane in DOCA-salt hypertensive rats was evaluated by comparing the effects of a thromboxane synthesis inhibitor and a receptor antagonist on renal function in normotensive and DOCA-salt hypertensive rats. The administration of the thromboxane synthetase inhibitor furegrelate and the thromboxane receptor blocker SQ 29548 had no effect on renal hemodynamics in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Massive colonic dilatation as initial presentation of mesenteric vein thrombosis.

The case of a patient with primary mesenteric venous thrombosis presenting with massive dilatation of almost the entire colon is described. The differential diagnosis suggested by this presentation is briefly discussed with special attention to the diagnosis of acute colonic pseudoobstruction. Possible reasons for the atypical presentation of acute mesenteric venous thrombosis should, therefore, be considered in the differential diagnosis of all patients presenting with colonic distention and pseudoobstruction.

Acute Disease↗

PubMed1987

Renal function and sodium balance in conscious Dahl S and R rats.

Renal transplantation studies have indicated that some form of renal dysfunction underlies the development of hypertension in Dahl salt-sensitive (S) rats. In the present study, we compared renal hemodynamic and tubular function of conscious Dahl S and salt-resistant (R) rats. Prehypertensive Dahl S rats had a blunted natriuretic response to an intravenous isotonic sodium chloride load compared with the responses of normotensive Dahl R or hypertensive Dahl S rats. This difference was probably not related to a generalized defect in renal tubular handling of sodium and water, since prehypertensive Dahl S rats excreted quantities of sodium comparable to those of R or hypertensive S rats when infused with hypertonic sodium chloride solutions. Dahl S rats also elevated free water clearance and lowered urine osmolality similar to R rats when challenged with a hypotonic saline load. Renal blood flows and glomerular filtration rates were similar in prehypertensive Dahl S, hypertensive Dahl S, and Dahl R rats. The possible link between sodium retention and the development of hypertension in Dahl S rats was examined further by measuring the changes in sodium and water balance, extracellular fluid volume (ECV), and blood pressure after exposure to an 8% sodium chloride diet. No differences could be detected in the salt and water balances of Dahl S and R rats exposed to a high-salt diet for 14 days. ECV increased significantly by 10% in Dahl S rats on the 1st day of a high-salt diet, whereas no change was observed in Dahl R animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Atriopeptin III alters renal medullary hemodynamics and the pressure-diuresis response in rats.

The effects of atriopeptin III on the renal response to changes in renal perfusion pressure (RPP) were examined in uninephrectomized and adrenalectomized rats. Neural influences on the kidney were eliminated by renal denervation. Plasma levels of antidiuretic hormone (ADH), angiotensin II, aldosterone, corticosterone, and norepinephrine were controlled by intravenous infusion. Infusion of atriopeptin III at a dose of 30 or 100 ng X kg-1 X min-1 increased plasma levels of atrial natriuretic peptide from 101 +/- 8 pg/ml to 424 +/- 16 and 2,553 +/- 308 pg/ml, respectively. In control rats, increasing RPP in two steps from 100 to 125 to 150 mmHg produced sixfold increases in sodium and water excretion. The slopes of the relationships between fractional sodium and water excretion and RPP were enhanced by approximately 10, 20, and 40% in the rats infused with the 30, 100, and 500 ng X kg-1 X min-1 dose of atriopeptin III. Renal blood flow and glomerular filtration rate were not significantly different in vehicle- and atriopeptin III-infused rats at any RPP studied. Papillary blood flow measured with a laser-Doppler flowmeter increased 15% within the first 5 min of infusion of atriopeptin III at a dose of 100 ng X kg-1 X min-1. Cortical blood flow was not significantly altered. The rise in papillary blood flow during atriopeptin III infusion, however, may be a consequence and not the cause of the natriuresis and diuresis, since urine flow increased before significant changes in papillary blood flow were detected. These studies suggest that atrial natriuretic factor could influence the long-term control of arterial pressure by altering renal medullary hemodynamics and promoting the elimination of sodium and water. The plasma levels of atrial natriuretic peptide needed to alter the pressure-natriuresis relationship, however, may exceed levels that can be attained in vivo with endogenous release.

Animals↗

PubMed1987

Altered pressure-natriuresis relationship in young spontaneously hypertensive rats.

In the present study, the pressure-natriuretic responses of 3- to 5- and 6- to 9-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were characterized to determine whether the relationship between sodium excretion and renal perfusion pressure is altered during the development of hypertension. Differences in the neural tone and renal hormone levels in SHR and WKY were minimized by denervating the kidney and fixing plasma concentrations of aldosterone, vasopressin, norepinephrine, and cortisol by intravenous infusion. Renal perfusion pressure was varied using adjustable occluders on the lower aorta. The slopes of the relationships between sodium excretion and renal perfusion pressure were not significantly different in 3- to 5-week-old SHR and WKY (0.31 +/- 0.05 vs 0.42 +/- 0.06 microEq/min/g kidney weight); however, the x-intercept of this relationship was significantly shifted to the right by 15 mm Hg in SHR compared to WKY. Blood pressure was moderately elevated even in the 3- to 5-week-old SHR in comparison to WKY (98 +/- 5 vs 81 +/- 6 mm Hg). As the degree of hypertension became more severe, the slope of the pressure-natriuresis relationship became significantly lower in 6- to 9-week-old SHR compared to the corresponding slope observed in age-matched WKY (0.16 +/- 0.02 vs 0.31 +/- 0.04 microEq/min/g kidney weight). These results indicate that the relationship between sodium excretion and renal perfusion pressure is altered even in very young SHR. Thus, the resetting of kidney function occurs very early and may be necessary for the development of hypertension in SHR.

Aging↗

PubMed1987

Fluctuations of alpha cell calcium, potassium and sodium during amino acid perifusion of rat pancreatic islets.

Perifusion of rat pancreatic islets with a physiologic, 6-mM amino acid mixture resulted in typical acute and second phase glucagon secretion over 30 min. At various intervals, islets were acutely fixed and processed for scanning electron microscopy, identification of alpha cells, and measurements of single alpha cell content of calcium (Ca), potassium (K) and sodium (Na) with energy-dispersive x-ray analysis. Biphasic glucagon secretion was attended by corresponding biphasic Ca accumulation and a reciprocal, biphasic suppression of K content and acute phase suppression of Na in alpha cells. All secretory and cellular events were preceded by an evanescent upward spike in alpha cell K at 1 min. These results indicate that alpha cell glucagon secretion in response to amino acid mixtures may be initiated by a K signal and is coupled subsequently to phasic changes in alpha cell Ca content. Fluctuations of alpha cell K and Na appear to relate inversely to Ca, suggesting that transmembrane fluxes of the three cations are interrelated.

Amino Acids↗

PubMed1986

Laser-Doppler determination of papillary blood flow in young and adult rats.

Renal hemodynamics and renal blood flow autoregulatory ability differ in young (body wt 100 g) and adult (body wt 300 g) rats. Possible age-dependent changes in inner medullary hemodynamics have not been examined because it has not been possible to expose the papilla of adult rats for direct study of the vasa recta circulation. This study presents a technique for exposure of the papilla in any size rat. Seven days before an acute experiment, a small amount of cortical tissue overlying the papilla on the dorsal surface of the kidney was removed. The creation of this papillary window allowed for exposure of the papilla in adult rats after removal of the ureter. Using this preparation, we compared papillary blood flow in young and adult rats using a Periflux differential laser-Doppler flowmeter (Perimed, Stockholm, Sweden). The meter was calibrated by comparing the signal obtained from the papilla of 28 rats with papillary flow measured from the accumulation of 51Cr-labeled erythrocytes in the papilla. The laser-Doppler flow signal was linearly related and highly correlated (r = 0.92) to the red cell flow into the papilla. Comparisons of laser-Doppler flow signals obtained from the papilla of young and adult animals indicated that papillary blood flow was approximately 2-fold greater in the adult rats than in the young animals. This finding was associated with an enhanced maximal urine concentrating ability found in the younger rats. These studies demonstrate the utility of the laser-Doppler flowmeter for the assessment of papillary blood flow and suggest that inner medullary hemodynamics differ in young and adult rats.

Aging↗

PubMed1986

Abnormal renal hemodynamics and pressure-natriuresis relationship in Dahl salt-sensitive rats.

The renal responses to changes in renal perfusion pressure (RPP) were compared in Dahl salt-resistant (R) rats and in prehypertensive and hypertensive Dahl salt-sensitive (S) rats to determine whether an abnormality in the pressure diuresis response is involved in the development of this form of hypertension. Possible differences in the neural and endocrine background to the kidney of S and R rats were eliminated by denervating the kidney and by holding plasma levels of vasopressin, aldosterone, corticosterone, and norepinephrine fixed by intravenous infusion. Arterial pressure averaged 124 +/- 1 mmHg in R rats, 133 +/- 1 mmHg in prehypertensive S rats, and 158 +/- 2 mmHg in hypertensive S rats. Control renal blood flows (RBF) and glomerular filtration rates (GFR) were not significantly different in the three groups. RBF was autoregulated over a range of pressures from 80 to 160 mmHg in normotensive S and R rats. GFR was autoregulated at pressures greater than 100 mmHg in R rats and greater than 120 mmHg in prehypertensive S rats. In contrast, RBF was only autoregulated at pressures greater than 110 mmHg in hypertensive Dahl S rats, and GFR was significantly reduced from control when RPP was lowered below 150 mmHg. In R rats, increasing RPP from 100 to 150 mmHg produced a fivefold increase in urine flow and sodium excretion. In prehypertensive or hypertensive Dahl S rats the slopes of the relationships between urine flow, sodium excretion, and RPP were less than half of those seen in R rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Evaluation of laser-Doppler flowmetry as a measure of tissue blood flow.

In this study the technique of laser-Doppler flowmetry was evaluated for the measurement of tissue blood flow by comparing laser-Doppler flow (LDF) signal in the renal cortex, gracilis muscle, and cremaster muscle of anesthetized rats to whole-organ blood flow measured with an electromagnetic flowmeter or radioactive microspheres. In vitro, LDF signal was closely correlated (r = 0.99) to changes in erythrocyte velocity generated with a rotating wheel. Although individual LDF readings varied in situ, mean LDF signal calculated from multiple readings on the tissue surface were significantly correlated (r = 0.74-0.95) with tissue blood flows measured at various perfusion pressures. However, significant differences in the slope of the LDF signal vs. blood flow relationship were observed in different tissues and with different methods of measurement in the same tissue. This study indicates that mean laser-Doppler flow signal provides a good estimate of tissue blood flow, provided a sufficient number of points is scanned. However, there appears to be no universal calibration factor for the method.

Animals↗

PubMed1986

Pressure diuresis mechanism in the control of renal function and arterial pressure.

Precise knowledge of the interrelationships between arterial pressure and urinary excretion of sodium and water is crucial to understanding the long-term control of arterial pressure. Although increases in renal perfusion pressure have been known for more than 35 years to inhibit tubular reabsorption, the mechanism of this pressure diuresis response, the humoral or physical factors involved, and even the nephron segments in which the changes in tubular function occur remain relatively unknown. This review focuses on the experimental evidence that supports current hypotheses concerning the mechanism of pressure diuresis. Specifically, it examines the possibility that pressure diuresis is caused by a small increase in glomerular filtration rate, alterations in the humoral or physical factors regulating proximal tubular reabsorption, and/or inhibition of tubular reabsorption in deep nephrons secondary to changes in hemodynamics in juxtamedullary nephrons. The concept originally proposed that the kidney serves as the dominant long-term controller of arterial pressure is largely based on the assumptions that the pressure diuresis phenomenon exists and that it occurs via a nonadaptive mechanism. It has been proposed that hypertension can develop only if the relationship between arterial pressure and sodium excretion is shifted toward higher pressures. The remainder of this review examines recent evidence indicating that an abnormality in the pressure natriuresis relationship may be associated with the development of hypertension in humans and in the genetic rat models of the disease.

Absorption↗

PubMed1985

Role of renal prostaglandins in the fall in urine osmolality after papillary micropuncture.

The effect of micropuncture of the renal papilla through an intact ureter on urinary concentrating ability of rats was examined. Micropuncture of the renal papilla caused a fall in urine osmolality in the punctured kidney from 1718 +/- 106 to 1035 +/- 79 mosmol/kg X H2O. In order to investigate the role of renal prostaglandins in this process, PGE2 excretion was measured and found to increase from 63.4 +/- 14.0 to 205.5 +/- 57.1 pg/min. Urine osmolality and PGE2 excretion from the contralateral kidney were not significantly altered. In animals given meclofenamate (2 mg/kg X hr), renal PGE2 excretion was reduced to 22.3 +/- 5.1 pg/min prior to micropuncture and it remained low at 8.9 +/- 1.8 pg/min after papillary micropuncture. Meclofenamate also blocked the fall in urine osmolality caused by micropuncture of the renal papilla, with urine osmolality averaging 1940 +/- 122 before and 1782 +/- 96 mosmol/kg X H2O after the micropuncture. These results indicated that papillary micropuncture through an intact ureter increased renal PGE2 excretion and that a rise in renal production of PGE2 or some other prostanoid is associated with a fall in urine concentrating ability.

Animals↗

PubMed1985

Mechanisms of antinatriuresis during low-frequency renal nerve stimulation in anesthetized dogs.

The influence of 1.0 Hz renal nerve stimulation (RNS) on the renal excretion of sodium and bicarbonate was determined in anesthetized dogs before and during inhibition of renal bicarbonate reabsorption. RNS decreased both urinary sodium and bicarbonate excretion without changing arterial pressure, renal blood flow, or glomerular filtration rate. Pharmacological blockade of bicarbonate reabsorption with acetazolamide prevented RNS-induced decreases in bicarbonate excretion and reduced the antinatriuretic response. Physiological blockade of tubular bicarbonate reabsorption with intrarenal sodium bicarbonate infusion (1 M) abolished both the antinatriuretic response to RNS and the decrease in bicarbonate excretion. This physiological blockade of neurogenic antinatriuresis resulted from alkalinization of the urine and/or peritubular blood rather than an increase in filtered sodium load, because during intrarenal infusion of 1 M sodium chloride RNS concomitantly decreased sodium and urinary bicarbonate excretion. Since antinatriuretic responses and the decrease in bicarbonate excretion response to RNS were significantly decreased by blockade of bicarbonate reabsorption (with acetazolamide and intrarenal sodium bicarbonate infusion), antinatriuresis during RNS is partly mediated by a mechanism dependent on intact bicarbonate reabsorption. The data suggest that renal nerve activity may participate in the normal regulation of acid-base balance via changes in bicarbonate excretion.

Animals↗

PubMed1985

Prostaglandins in the sodium excretory response to altered renal arterial pressure in dogs.

Acute variations in renal arterial pressure are associated with corresponding alterations in absolute and fractional sodium excretion even under conditions of highly efficient autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR). Since prostaglandins recently have been implicated in the regulation of sodium excretion, we investigated the hypothesis that the renal prostaglandin system participates in "pressure natriuresis." Anesthetized sodium-replete dogs were subjected to partial carotid artery constriction to elevate systemic arterial pressure. Under these control conditions, sodium excretion was 103 +/- 18 mueq/min (n = 17) and urinary prostaglandin E2 excretion averaged 4.6 +/- 1.5 ng/min (n = 8). Decreases in renal arterial pressure within the auto-regulatory range reduced sodium excretion (2.1%/mmHg) and prostaglandin E2 excretion (1.7%/mmHg), whereas GFR and RBF were not affected. There was a significant correlation between the changes in sodium and prostaglandin E2 excretion rates (r = 0.932, P less than 0.01). In nine dogs treated with indomethacin, sodium excretion was reduced by 70% while GFR and autoregulatory capability were unaffected. There was a marked attenuation of the effect of changes in arterial pressure on sodium excretion, with this parameter exhibiting changes averaging 0.6%/mmHg (P less than 0.001). These observations suggest that the renal prostaglandin system may exert an important influence on the pressure-natriuresis mechanism.

Animals↗

PubMed1985

Characterization of a new model for the study of pressure-natriuresis in the rat.

The acute relationships between the urinary excretion of sodium and water and renal perfusion pressure were characterized in the rat using a new in vivo model of pressure diuresis. Neural and hormonal influences on the kidney were held constant by denervating the kidney and by maintaining fixed high plasma levels of vasopressin, aldosterone, corticosterone, and norepinephrine levels by intravenous infusion. Renal perfusion pressure (RPP) was varied above and below control using specially designed aortic clamps. Increasing RPP within the autoregulatory range from 90 to 160 mmHg produced 5- to 20-fold increases in urine flow and sodium excretion with no detectable changes in glomerular filtration rate, renal blood flow, or peritubular capillary pressure. The slope of the line relating urine flow and RPP averaged 2 microliter X min-1 X kidney-1 X mmHg-1 rise in RPP. If RPP was first lowered to 90 mmHg, urine flow could be doubled by increasing RPP by as little as 5 mmHg. Uninephrectomy 7-12 days before an experiment did not alter the renal pressure diuresis relationship. The presence of intact renal nerves, however, was found to shift the relationship between urine flow and RPP to the right. The magnitude of the response produced by elevations in pressure using this new model of pressure diuresis was greater than when RPP was increased using carotid occlusion or epinephrine infusion as in previous studies. The results indicate that small changes in arterial pressure may have a greater influence on sodium and water excretion than has been previously recognized.

Animals↗

PubMed1985

Abnormal pressure-diuresis-natriuresis response in spontaneously hypertensive rats.

The renal responses to changes in perfusion pressure (RPP) were studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to determine whether an abnormality in the pressure-diuresis phenomenon could be involved in the resetting of kidney function in hypertension. Differences in the neural and endocrine background to the kidneys were minimized by denervating the kidney and by holding plasma vasopressin, aldosterone, corticosterone, and norepinephrine levels constant by intravenous infusion. In WKY, increasing renal perfusion pressure 54 mmHg, from 103 to 157 mmHg, produced a ninefold increase in urine flow and sodium excretion with no measurable change in renal blood flow (RBF) or glomerular filtration rate (GFR). In SHR, increasing renal perfusion pressure 54 mmHg, from 133 to 187 mmHg, produced only a fourfold increase in urine flow and sodium excretion. GFR, RBF, and peritubular capillary pressures were well autoregulated and were similar in the SHR and WKY at pressures above 110 mmHg. These results indicate the presence of intrinsic changes in the kidney of SHR that enhance fractional tubular reabsorption and impair the pressure-diuresis response. This blunting of the renal pressure-diuresis phenomenon in SHR may represent the functional resetting of the kidney that is necessary for sustained hypertension.

Animals↗

PubMed1985

Cat scratch disease. Report of a case with hepatic lesions and a brief review of the literature.

An unusual case of cat scratch disease with large hepatic defects is presented. We describe a previously healthy 16-yr-old black man presenting with a neck mass, hepatosplenomegaly, and systemic symptoms. Pathology of the neck mass revealed a lymph node with chronic inflammation and focal necrosis. An abnormal computed tomography scan showed large hepatic defects which were confirmed at peritoneoscopy; biopsy specimens are described. Routine and special stains for bacteria and fungi were all negative. Serologic studies were unremarkable but a cat scratch skin test was positive. Follow-up examinations revealed resolution of all findings. Cat scratch disease should be considered in the differential diagnosis of diseases causing lymphadenopathy, systemic symptoms, and hepatic (and splenic) defects.

Adolescent↗

PubMed1984

Analysis of picogram quantities of protein in subnanoliter-size samples.

The ability to measure protein concentration in subnanoliter volumes would be helpful in many biological studies. A microassay for measuring nanogram protein quantities in nanoliter-size samples and an ultramicroassay for measuring picogram quantities in picoliter samples were developed to measure lymphatic protein concentration. Aliquots of a sample solution were mixed with an o-phthalaldehyde mercaptoethanol reagent using micropipetting techniques. Reaction product fluorescence was measured using a modified Leitz MPV-1 microscope as a microfluorometer. Fluorescence varied linearly with albumin concentrations between 1 and 8 g/100 ml. A typical microassay measuring albumin standards at 0.0, 1.0, 2.0, and 4.0 g/100 ml yielded a linear regression of y = 207x + 60 (r = 0.99). Minimum detectable protein concentration was 0.125 g/100 ml. The SE for the albumin standards varied from 0.02 to 0.17 g/100 ml. An ultramicroassay measuring similar standards yielded a linear regression of y = 1180x + 109 (r = 0.96). Minimum detectable protein concentration was 0.028 g/100 ml. The SE for the standards varied from 0.01 to 0.32 g/100 ml.

Albumins↗

PubMed1984

Prostaglandin-vasopressin interactions on the renal handling of calcium and magnesium.

The role of prostaglandins in the regulation of sodium and water excretion has been widely studied, but little is known about the influence of prostaglandins (PGs) on the tubular handling of calcium, magnesium or phosphorus. Recent observations have suggested that PGE2 and vasopressin may interact and influence reabsorption of calcium and phosphorus in the cortical collecting duct. The present study investigated the effect of meclofenamate (2 mg/kg), and inhibitor of PG synthesis, on the excretion of calcium, magnesium and phosphorus. Experiments were performed in antidiuretic and water diuretic rats to examine potential PG-vasopressin interactions on the reabsorption of these ions by renal tubules. In antidiuretic rats given meclofenamate, urine osmolality increased whereas urine flow and the fractional excretion of water, urea, sodium, calcium and magnesium decreased by 30 to 50%. In water diuretic animals, urine osmolality and urea excretion were unaltered after meclofenamate administration. Fractional excretion of sodium, water, calcium and magnesium declined approximately 50% in water diuretic rats given meclofenamate. Urinary excretion of PGE2 was not significantly different in water diuretic and antidiuretic rats averaging 262 +/- 78 vs. 167 +/- 35 pg/min, respectively. Meclofenamate significantly reduced urinary excretion of PGE2 in both groups. The results indicate that renal PGs modulate renal tubular reabsorption of calcium and magnesium, as well as sodium and water.

Absorption↗