Sodium retention in dogs with cirrhosis and ascites: efferent mechanisms

Levy, Mortimer

doi:10.1152/ajprenal.1977.233.6.f586

Cited by 24 publications

(26 citation statements)

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“…It has been shown that chronic aldosterone-receptor blockade prevents sodium retention in rats with cirrhosis induced by CCl 4 22 or common bile duct ligation. 8 However, the present study, as well as studies by others [4][5][6][7][8]23,24 shows that plasma levels of aldosterone are normal during early sodium retention in cirrhosis. This argues against hyperaldosteronism and increased collecting-duct sodium reabsorption as a major factor in early sodium retention.…”

Section: Renal Function During Early Sodium Retention In Cirrhosissupporting

confidence: 46%

“…2,3,9 It is well described that the renal sympathetic nerve activity is increased at early stages of cirrhotic liver disease, 2 and when challenged with a sodium load, cirrhotic rats have an impaired ability to excrete sodium, which can be normalized by renal denervation. 2 However, in a micropuncture study in cirrhotic dogs with sodium retention but without ascites, Levy 4 found that single-nephron GFR and delivery of fluid from the late convoluted proximal tubule were unaltered, suggesting that proximal tubular function was normal in these dogs. Similarly, in the present study, as we previously have described in rats with cirrhosis induced by common bile ligation, 5-8 renal lithium handling was normal in rats with early sodium retention.…”

Section: Renal Function During Early Sodium Retention In Cirrhosismentioning

confidence: 99%

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Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

et al. 2000

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The authors examined the natriuretic efficiency of furosemide in rats with cirrhosis induced by carbon tetrachloride (CCl 4 ). Rats were treated for 17 weeks with intraperitoneal injections of CCl 4 in groundnut oil twice a week throughout the study. Control rats were treated with vehicle (groundnut oil). Studies in metabolic cages showed that sodium retention was present from week 14. Renal clearance experiments were performed in chronically, instrumented conscious rats at the end of week 14 and at the termination of the study (end week 16) when ascites and hyponatremia were present. After 14 weeks, cirrhotic rats had sodium retention along with increased renal plasma flow, normal GFR, normal renal lithium handling, and a significantly increased diuretic (؉41% vs. control) and natriuretic (؉56% vs. control) response to a test dose furosemide (7.5 mg/kg b.w., intravenously). The natriuretic efficiency of furosemide, i.e., the natriuresis expressed relative to the furosemide excretion rate (⌬U Na V/U FUR V) was increased by 51% versus control. After 17 weeks, ascites and hyponatremia had developed, and significant decreases in renal plasma flow (؊33%), GFR (؊30%), and fractional lithium excretion (؊44%) were observed. At this stage urinary recovery of furosemide was significantly decreased and the diuretic (؊27% vs. Control) and natriuretic (؊38% vs. control) responses to furosemide were significantly impaired. However, the increased natriuretic efficiency of furosemide was still present (؉34% vs. control). Together these results suggest that increased sodium reabsoprtion in the thick ascending limb of Henle's loop is involved in the renal sodium retention in cirrhosis in rats that eventually results in decompensation with the

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Section: Renal Function During Early Sodium Retention In Cirrhosissupporting

confidence: 46%

Section: Renal Function During Early Sodium Retention In Cirrhosismentioning

confidence: 99%

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

et al. 2000

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“…As the severity of the liver disease progresses, the cirrhotic dog develops increasing amounts of ascites; shows progressive gastrointestinal hemorrhage; develops elevated plasma levels of renin, aldosterone, and estrogens; and displays signs of vascular underfilling (4,5). Superficial veins collapse and plasma volume contracts as dogs decrease their dietary intake.5 The late, or second-phase, sodium retention now observed presumably represents the sodium retention of a contracted EABV and will subsume the factors responsible for early sodium retention.…”

Section: Resultsmentioning

confidence: 99%

“…First, the dog with chronic biliary cirrhosis must be similar, especially in regard to renal physiology, to the dog with portal cirrhosis that served as the model for previous investigations in this laboratory (4)(5)(6)(7)(8). This appears to be so.…”

Section: Resultsmentioning

confidence: 99%

“…In experiments designed to exclude portal venous hypertension or ascites sequestration from being determinants of urinary sodium retention, extensive studies in our laboratory (4)(5)(6)(7)(8) demonstrated that this first phase, or early sodium retention in canine cirrhosis, is unrelated to arterial hypovolemia, altered systemic hemodynamics, or hyperaldosteronism. As the liver disease progresses, new factors lead to persistent sodium retention.…”

Section: Introductionmentioning

confidence: 99%

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Dogs with experimental cirrhosis of the liver but without intrahepatic hypertension do not retain sodium or form ascites.

Unikowsky¹,

Wexler²,

Levy³

1983

J. Clin. Invest.

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A B S T R A C T Dogs with portal cirrhosis but without portal hypertension (end-to-side portacaval anastomosis) retain sodium and expand plasma volume before ascites formation. In our study, dogs were subjected to bile duct ligation and simultaneous side-toside portacaval anastomosis (PCA) in order to create a canine model of hepatic cirrhosis without intrahepatic or portal hypertension. The effect of normalizing intrahepatic pressures in the face of venous outflow block on sodium handling was studied. 13 dogs survived the surgical procedures and were followed. Two dogs developed sodium retention and ascites at 5-6 wk (livers were cirrhotic) when the PCA spontaneously closed. 11 dogs were free of sodium retention and ascites for as long as 12 wks after surgery, while ingesting 35 meq/d of sodium. In this group glomerular filtration rate remained normal throughout the period of observation and there was no expansion of plasma volume. Nine of these dogs were then fed 85 meq/d of sodium; eight remained in sodium balance and one retained sodium and went on to develop ascites. When 10-15 mg i.m. of desoxycorticosterone acetate (DOCA) was given daily, five dogs developed sodium retention and ascites, while four escaped from DOCA. Dogs who developed ascites had either a partially occluded PCA (4/5) or a patent PCA, but with a significant portacaval pressure gradient of 9.5 cm H20

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Hepatorenal Syndrome

et al. 1993

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Hepatorenal syndrome is a life-threatening complication of severe liver disease. It is generally accepted that the syndrome is the final stage of complex hemodynamic derangements associated with portal hypertension, ie, peripheral arterial vasodilation, effective hypovolemia, and hyperkinetic status. In spite of reduced systemic resistances, intrarenal vascular resistances are increased. This is probably the consequence of the activation of systemic vasoactive factors, such as the renin-angiotensin system, the sympathetic nervous system, and vasopressin aimed at restoring arterial filling pressure. Recently, it has been shown that intrarenal vasoconstrictors, such as leukotrienes and endothelins, are activated with the progression of liver disease. The renal vasoconstriction is counterbalanced by the intrarenal hyperproduction of vasodilating prostaglandins and kallikreins. When this balance is lost, for whatever mechanism, the renal vascular resistances dramatically increase and the hepatorenal syndrome develops. In spite of increased knowledge about pathogenesis, the treatment of hepatorenal syndrome remains unresolved. Low-dose dopamine or ornipressin are currently employed in many liver units to avoid further deterioration of renal function in patients with severe liver disease who are waiting for liver transplantation that remains, at present, the only effective treatment for hepatorenal syndrome.

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Sodium retention in dogs with cirrhosis and ascites: efferent mechanisms

Cited by 24 publications

References 0 publications

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

Dogs with experimental cirrhosis of the liver but without intrahepatic hypertension do not retain sodium or form ascites.

Hepatorenal Syndrome

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