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Biomedical subjects

L A Arbeit

Publications and source records attributed to L A Arbeit.

10 recordsLinked to original sources
PubMed1989

Cyclosporine nephrotoxicity: blood volume, sodium conservation, and renal hemodynamics.

Glomerular filtration rate (GFR) and renal blood flow (RBF) are depressed by chronic cyclosporine treatment. We examined the hypothesis that depletion of extracellular or intravascular fluid volume contributes to the renal vasoconstriction of early cyclosporine nephrotoxicity (CCN). Control and CCN rats were given 10 mg/kg cyclosporine A or vehicle intramuscularly daily for 7 days. The effects of extracellular volume expansion, both acute (AVE, 10% body wt saline) and chronic (CVE, 10% body wt/day saline ip, 10 days including cyclosporine A treatment period), on renal hemodynamics were measured. In CCN, AVE completely normalized GFR and RBF, whereas CVE partially prevented the development of CCN. Renal autoregulatory ability was depressed in CCN but was largely restored by AVE. Intravascular volumes were measured with Evans blue and 51Cr-labeled red cells. Plasma and red cell volumes were reduced by 24% in CCN, indicating circulatory hypovolemia. Acute repletion of the deficit in blood volume by acute administration of an isoncotic solution (1.8 ml/100 g body wt of 5% albumin in isotonic saline) restored GFR and RBF to levels similar to those in control rats. Extracellular fluid volume, estimated as inulin space, was similar in both CCN and control groups. A metabolic study (7 day) showed stool Na loss in CCN to be twice that in controls but both groups remained in sodium balance. We conclude that the renal vasoconstriction produced in the rat by short-term cyclosporine treatment is, at least in part, prerenal in origin and related to the development of circulatory hypovolemia.

Animals↗
PubMed1987

Cyclosporine nephrotoxicity: sodium excretion, autoregulation, and angiotensin II.

Cyclosporine-induced nephrotoxicity (CIN) was studied in rats treated for 7 days with cyclosporine (10 mg x kg-1 x day-1 im) or vehicle (CON). CIN rats displayed characteristic reductions in glomerular filtration (GFR) and renal blood blood flow (RBF), and electron microscopy showed injury to proximal cells. Metabolic studies (7 day) showed significantly lower renal sodium excretion in conscious CIN rats compared with CON. In anesthetized rats at similar blood pressures, nephron GFR (SNGFR) was lower in CIN than CON, but fractional Na reabsorption was similar. In CIN, SNGFR, measured proximally to block flow to the sensing site of tubuloglomerular feedback (TGF) at the macula densa, was not significantly different than distal SNGFR. The rate of distal fluid delivery was significantly lower in CIN than in CON. Inhibition of the renin-angiotensin system (RAS) with captopril (CAP, 10 mg/kg iv), or saralasin (SAR, 0.3 mg x kg-1 x h-1 iv) caused marked arterial hypotension in CIN and a fall in renal vascular resistance (RVR). With arterial pressure controlled, CAP or SAR increased GFR and RBF, and reduced RVR in CIN, but did not reverse the renal deficits compared with similarly treated CON. RBF autoregulation in CIN was impaired between 90 and 140 mmHg but was partially restored by CAP. We conclude that both the filtered load and excretion rate of sodium in CIN are significantly reduced compared with controls, that SNGFR in CIN is not depressed by TGF in response to elevated distal fluid delivery, and that the RAS is not a primarily mediator of the renal vasoconstriction in CIN.

Angiotensin II↗
PubMed1986

Reduced or absent serum anion gap as a marker of severe lithium carbonate intoxication.

Two patients with life-threatening lithium carbonate intoxication (serum levels, greater than 4 mEq/L [greater than 4 mmol/L]) presented with a reduced or absent serum anion gap. In both subjects, hemodialysis simultaneously removed the excess lithium ion and normalized the anion gap. Conversely, the anion gap was normal in subjects with therapeutic serum lithium ion levels. Severe lithium carbonate intoxication should be added to the category of illnesses (multiple myeloma, bromide intoxication) causing a marked reduction in the anion gap. In the comatose patient, a reduced anion gap may serve as an important clinical clue to the presence of this drug intoxication.

Acid-Base Equilibrium↗
PubMed1985

Renal dysfunction after arteriography.

Acute renal failure has been observed in patients undergoing angiography in which a hypertonic triiodinated contrast medium is used. To ascertain the incidence of renal dysfunction and the clinical risk factors, we did a prospective study in which creatinine clearance was measured before and immediately after 120 arteriographic procedures. Thirty-seven patients (31%) sustained a significant reduction in creatine clearance after arteriography. No specific risk factor could be determined. Our findings, however, indicate that patients with preexisting renal insufficiency or diabetes mellitus are not at a higher risk for sustaining a fall in creatinine clearance after angiography.

Acute Kidney Injury↗
PubMed1985

Decreased total and active urinary kallikrein in normotensive Dahl salt susceptible rats.

Abnormalities in the kallikrein-kinin system have been found in human and animal models of essential hypertension. The purpose of this study is to assess the kallikrein-kinin system in normotensive Dahl salt sensitive (S) and salt resistant (R) rats on a zero sodium diet. Urinary kallikrein was measured at 7 and 12 wk of age by different techniques. When kallikrein activity was assessed, by a kininogenase assay, S rats excreted 66% (P less than 0.001) and 75% (P less than 0.01) as much kallikrein as R rats at 7 and 12 wk of age. Using an artificial substrate method (Kabi S-2266), S rats excreted 30% (P less than 0.001) and 56% (P less than 0.05) as much kallikrein as R rats at 7 and 12 weeks, respectively. Using a technique to measure total kallikrein, S rats excreted 53% (P less than 0.001) and 65% (P less than 0.05) as much kallikrein as R rats at 7 and 12 wk of age. Normotensive S rats failed to increase maximally kallikrein activity or total kallikrein when the diet was switched from a .4% to a .0064% sodium chloride diet. There was no difference in inhibitors, as measured by the recovery of purified kallikrein added to S and R urine (56 +/- 21% vs. 53 +/- 13%). Km values for S and R urinary kallikrein were similar (3.1 +/- .5 X 10(-5) vs. 2.6 +/- .5 X 10(-5) M/liter). Trypsin-activatable kallikrein was equivalent in the S and R rats on the .0064% and .4% sodium chloride diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Independent action of prostaglandins and kinins on vasopressin-stimulated water flow.

The kallikrein-kinin and the prostaglandin systems are both important modifiers of vasopressin action. This study examines whether the systems are dependent on one another for their action. Four groups of toad hemibladders were examined. In groups 1 and 2 animals the endogenous prostaglandin system was inhibited. Inhibition of kallikrein by aprotinin caused vasopressin-stimulated water flow to increase further (24.8 +/- 4.9 to 34.5 +/- 4.8 microliters/min) while potentiation of kinins by captropril caused vasopressin-stimulated water flow to decrease (45 +/- 6.3 to 30.5 +/- 5.4 microliters/min). In groups 3 and 4 endogenous kallikrein was inhibited by aprotinin. The addition of prostaglandin E2 caused vasopressin-stimulated water flow to decrease (17.5 +/- 2.7 to 5.71 +/- 1.0 microliter/min) while the inhibition of endogenous prostaglandins caused vasopressin-stimulated water flow to increase (26.7 +/- 3.4 to 39.2 +/- 3.5 microliters/min). Thus, the inhibitory effects of prostaglandins and kinins on vasopressin-stimulated water flow are independent of one another.

Animals↗
PubMed1981

Role of the endogenous kallikrein-kinin system in modulating vasopressin-stimulated water flow and urea permeability in the toad urinary bladder.

This study investigates the endogenous kallikrein-kinin system's role as a modulator of vasopressin action in the toad urinary bladder. Kalli-krein inhibition by aprotinin, which results in decreased kinin production, significantly increased both vasopressin and 8-Br-cyclic (c) AMP-stimulated water flow. Kinin potentiation by the kininase II inhibitor captopril (SQ 14225) significantly decreased vasopressin and 8-Br-cAMP-stimulated water flow. In contrast to water flow, vasopressin-stimulated urea permeability was decreased by aprotinin and increased by captopril. We conclude that the endogenous kallikrein-kinin system represents a significant modulator of vasopressin action and it permits separate control of vasopressin-stimulated water flow and solute transport.

8-Bromo Cyclic Adenosine Monophosphate↗