Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased incidence of renal insufficiency is observed in severe damage of liver parenchyma such as fulminant hepatitis, decompensated cirrhosis of the liver, septic cholangitis and the different forms of obstructive jaundice. Functional circulatory disturbances of the kidney, especially of the renal cortex, are of importance in the aetiology of this condition. Dopamine, at a dosage as low as 3 gamma/kg/min leads to an improvement in renal blood flow and also to an increase in hepatic blood flow. These observations are of therapeutic importance. Some important circulatory and functional parameters of both these organs, which influence each other under normal and pathological conditions, were studied in the presence of dopamine and the following results were obtained: 1. An investigation of the intrarenal haemodynamics with 133 Xenon in patients with severe cirrhosis of the liver and in patients with obstructive jaundice resulted in an increase of 91% in the mean renal blood flow. The blood flow in the renal cortex increased by 36.2% and in the renal medulla 18.5%, whereas the renal fat tissue showed no change. Compartment I, which was diminished as compared with the control value, also increased. The percentage contribution of the mean renal blood flow and the blood flow of the renal cortex towards the cardiac output was greater under the influence of dopamine; hence a greater part of the cardiac output flows into the kidney under dopamine. 2. The glomerular filtrate and the renal plasma flow increased under dopamine (13.5% and 43.1%, respectively). The increase was greater in compensated than in decompensated cirrhosis. In patients with obstructive jaundice there was a smaller increase in both these parameters than in patients with cirrhosis in the presence of dopamine. No connection was found between the increase in renal plasma flow with dopamine and the blood levels of bilirubin, cholinesterase, GOT and the Normotest. 3. The urinary output of sodium increased by 191.4% with dopamine. Patients with an initial renal plasma flow value of over 300 ml/min had a higher sodium output. These patients also eliminated more sodium under the influence of dopamine than those with an initial renal plasma flow value of under 300 ml/min. 4. Blood flow determinations in the portal vein and the hepatic artery in man, obtained during operation, showed an increase in portal flow of 28.5% and hepatic artery flow of 6.3% in response to dopamine. The percentage contribution of portal blood flow towards the cardiac output increase on dopamine administration. The functional hepatic blood flow, analyzed with 131-J-BSP, did not change. The wedged hepatic vein pressure, which is a good measure of portal pressure, increased on average by only 7% with dopamine at a dosage of 3 gamma/kg/min, but by 20.3% with twice the dosage. Dopamine did not cause a change in hepatic blood volume; hence, blood sequestration in the liver can be excluded in response to the dopamine-evoked increase in portal blood flow. 5...
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PMID:[Clinical and experimental investigations of the effect of dopamine on haemodynamics and function of kidney and liver (author's transl)]. 27 63

The effect of dopamine on liver function and on renal blood flow and the glomerular filtration rate was studied in 13 patients suffering from liver cirrhosis. Hence, the BSP retention and 131I BSP clearance was determined and also the clearance of 99mTc DTPA and of 125I hippuran in decreasing concentrations, as well as under steady state conditions. Methodological problems arising from the application of the slope clearance technique in cirrhotic patients are discussed. Dopamine did not affect the BSP clearance and BSP retention, but a significant increase in renal plasma flow was observed. The glomerular filtration rate was not significant altered.
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PMID:[The simultaneous investigation of liver and kidney function in the presence of dopamine (author's transl)]. 122 62

Unlike other pituitary hormones, PRL is under tonic inhibition by the hypothalamus by way of the PRL inhibitory factor, dopamine. GAP and GABA may also be inhibitory. PRL-releasing factors include TRH and VIP and possibly others. Circulating PRL is predominantly monomeric, although some patients with hyperprolactinemia appear to have increased quantities of the less biologically active polymeric forms. PRL is secreted episodically, with an increase in the amplitude of the secretory pulses with sleep. A transitory increase also occurs in response to the protein component of meals. Basal PRL levels increase in response to the hormonal milieu of pregnancy, and suckling postpartum triggers PRL release. Pathologic increases of PRL owing to hypothalamic dysregulation occur with a variety of medications, including the neuroleptics, metoclopramide, antidepressants, methyldopa, reserpine and verapamil, abuse of opiates and cocaine, renal insufficiency, cirrhosis, hypothyroidism, adrenal insufficiency, neurogenic stimulation, and idiopathically. Hyperprolactinemia also may occur from structural lesions of the stalk and hypothalamus, which cause disinhibition with or without maintenance of PRF activity, ectopic neoplasm production, and, most commonly, from prolactinomas. Diagnostic testing consists of routine chemistry and thyroid testing and imaging with MRI or CT. Dopamine agonists are the treatment of choice of prolactinomas of all sizes. Transsphenoidal surgery is an alternative for the patient who does not respond to medical therapy or who wishes definitive tumor removal, realizing that long-term cure is achieved in only 50% to 60% of patients with microadenomas and a much lower number in those with macroadenomas. Radiotherapy is reserved for patients who do respond to either medical or surgical treatment. Patients wishing to become pregnant usually are treated with bromocriptine, although prepregnancy surgical debulking may be advisable for those with large macroadenomas to reduce problems with tumor enlargement.
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PMID:Pathologic hyperprolactinemia. 148 80

The effects of dopamine on kidney function have not been elucidated in patients with cirrhosis. Moreover, although increased portal pressure has been observed with supradopaminergic doses of dopamine in these patients, the splanchnic hemodynamic effects of low doses of dopamine have not been previously studied. Thus we studied the acute systemic, splanchnic and renal hemodynamic effects of a dopaminergic dose of dopamine (1.5 micrograms/kg body wt min) in nine cirrhotic patients. Plasma dopamine levels increased markedly from 35 +/- 20 pg/ml to 31,400 +/- 4,900 pg/ml during dopamine administration. A significant diastolic pressure decrease of 10% was associated with a 15% increase in heart rate. Cardiac output was not altered. Although dopamine significantly increased azygos blood flow by 16%, wedged and free hepatic venous pressures were not altered. Dopamine significantly increased renal blood flow by 31%, but did not change the glomerular filtration rate. We conclude that a dopaminergic dose of dopamine increases azygos blood flow but not the hepatic venous pressure gradient. Finally, although it increases renal blood flow, dopamine does not seem to have any beneficial effects on glomerular filtration rate in cirrhotic patients.
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PMID:Systemic, splanchnic and renal hemodynamic effects of a dopaminergic dose of dopamine in patients with cirrhosis. 187 93

To 11 patients with liver cirrhosis (5 with ascites) and 6 controls a one-hour dopamine infusion, 1.5 micrograms/kg/min., was administered. In all before administration of the infusion catheterization of the hepatic veins and lesser circulation was performed with concurrent assessment of the cardiac minute volume by thermodilution, and haemodynamic measurements were repeated also after the dopamine infusion. Before the dopamine administration and after termination of the infusion the plasma renin activity was assessed (PRA), plasma aldosterone, the atrial natriuretic factor (ANF), prolactin and in some patients also plasma catecholamines. Dopamine administration was not associated with an increase of the cardiac output, heart rate or peripheral resistance; the infusion had only purely dopaminergic effects. Plasma prolactin declined after dopamine administration significantly in controls (from 29.17 +/- 7.01 to 11.83 +/- 3.22, p less than 0.05, in patients with liver cirrhosis without ascites) from 18.16 +/- 2.44 to 8.64 +/- 2.01, p less than 0.01) in patients with ascites liver cirrhosis (from 23.5 +/- 9.3 to 15.2 +/- 7.47, p less than 0.05). In the controls after the dopamine infusion PRA suppression occurred (from 2.37 +/- 0.81 to 0.9 +/- 0.27, p less than 0.05), while in patients with compensated liver cirrhosis (from 0.97 +/- 0.41 to 0.85 +/- 0.34, n.s.) and in patients with decompensated liver cirrhosis the PRA did not change significantly either (from 4.56 +/- 1.67 to 5.065 +/- 2.29, n. s.). After the dopamine infusion in none of the investigated patient groups changes of plasma aldosterone and ANF were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of dopamine on hemodynamic and hormonal parameters in liver cirrhosis]. 214 Sep 56

Dopamine may be used in cirrhotic patients with renal or circulatory failure, but this drug can also increase the degree of portal hypertension. Hence, the systemic and splanchnic hemodynamic effects of dopamine have been studied in portal hypertensive rats with secondary biliary cirrhosis. The dose-response curves showed that dopamine significantly increased portal pressure at the same dose (80 micrograms min-1 kg-1 body wt.) in normal and biliary cirrhotic rats. Arterial pressure only increased with higher doses of dopamine in rats with biliary cirrhosis (160 micrograms min-1 kg-1 body wt.) while in normal animals it increased (80 micrograms min-1 kg-1 body wt.). Dopamine (160 micrograms min-1 kg-1 body wt.) significantly increased mean arterial pressure in normal and biliary cirrhotic rats. It significantly increased cardiac output in biliary cirrhotic rats from 134 +/- 6 to 153 +/- 7 ml/min but not in normals. Accordingly, systemic vascular resistance increased significantly in normal rats but not in cirrhotics. Portal pressure increased significantly in normal rats from 8.0 +/- 0.3 to 12.1 +/- 0.6 mmHg and in rats with biliary cirrhosis from 15.9 +/- 1.0 to 19.0 +/- 1.3 mmHg. Portal tributary blood flow increased significantly in normal and biliary cirrhotic rats (14.1 +/- 1 to 20.9 +/- 2.3 ml/min and 18.0 +/- 0.9 to 25.5 +/- 1.8 ml/min, respectively). This study shows that an elevated dose of dopamine increases the hyperkinetic syndrome in rats with secondary biliary cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of dopamine in conscious rats with secondary biliary cirrhosis. 225 34

Dopamine (DA) is known to increase diuresis and natriuresis through its action on renal dopaminergic receptors. Augmentation of intra-renal DA concentration by enhancement of its in situ production is greatly dependent on the availability of its precursor L-DOPA to the sites of its renal decarboxylation. Vicia faba (Vf) is a ubiquitous plant rich in easily absorbable L-DOPA. Following ingestion of 40 g freshly chopped Vf containing 120-130 mg of L-DOPA, plasma L-DOPA and urinary sodium and DA excretion increased significantly. The DA/Cre ratio reached a maximum level (280 +/- 58 micrograms/g) 60 minutes after Vf ingestion. This was significantly higher than the DA/Cre ratio after a control meal (1.8 +/- 0.2 micrograms/g; P < 0.0005). The Na/Cre ratio reached the maximal level (2.85 +/- 0.42 mmol/g) 90 minutes after Vf ingestion. This was significantly higher than the Na/ Cre ratio after the control meal (1.4 +/- 0.24 mmol/g; P < 0.005). We suggest that Vf might be of value in treating conditions such as hypertension, heart failure, renal failure, and liver cirrhosis in which natriuresis and diuresis are medically beneficial.
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PMID:The influence of Vicia faba (broad bean) seedlings on urinary sodium excretion. 922 6

In normal humans, plasma dopamine levels rise during head-out water immersion or saline intravenous infusion. Dopamine inhibits Na+,K+-ATPase activity in the proximal tubule and blunts aldosterone secretion leading to increased diuresis and natriuresis. The aim of this study is to evaluate the role of endogenous dopaminergic activity in the intrarenal sodium handling in patients with compensated liver cirrhosis. We studied nine healthy controls and 12 patients with Child-Pugh A cirrhosis during a normosodic diet for (1) dopaminergic activity, as measured by the incremental aldosterone responses 30 and 60 min after intravenous metoclopramide administration; (2) basal plasma levels of active renin and aldosterone; (3) 4-hr renal clearance of lithium (an index of fluid delivery to the distal tubule), creatinine, sodium, and potassium, first without and then with dopaminergic blockade with intravenous metoclopramide. The patients displayed greater endogenous dopaminergic activity, evidenced by higher incremental aldosterone responses compared with controls (+30 min: 160.2 +/- 68.8 vs 83.6 +/- 35.2 pg/ml, P < 0.01; +60 min: 140.5 +/- 80.3 vs 36.8 +/- 39.1 pg/ml, P < 0.01, respectively). In spite of this, patients and controls did not show significantly different basal aldosterone plasma levels, delivery of sodium to the distal nephron, or urinary excretion of sodium. In both groups the dopaminergic blockade with metoclopramide determined no change in sodium and potassium urinary excretion, but it caused a fall of the fluid and sodium delivery from the proximal tubule to the distal nephron among the patients (from 30.7 +/- 9.3 to 14.4 +/- 4.5 ml/min, P < 0.001; and from 4.25 +/- 1.30 to 2.00 +/- 0.64 meq/min, P < 0.001, respectively). In this group the natriuresis was maintained due to a reduction of the reabsorbed fraction of the distal sodium delivery (from 97.5 +/- 1.9% to 89.8 +/- 12.4%, P < 0.05). In conclusions, compensated cirrhotic patients display an increased endogenous dopaminergic activity compared with controls. This function is critical in maintaining the delivery of sodium to the distal nephron.
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PMID:Dopaminergic control of renal tubular function in patients with compensated cirrhosis. 1185 57

Hepatorenal syndrome is a life-threatening complication occurring commonly in cirrhosis liver and rarely in acute liver failure. It can be precipitated by shock, infection, surgery, large volume paracentesis or nephrotoxic drugs. Type I hepatorenal syndrome which usually develops over acute liver failure is rapidly progressive and has poor outcome. Type II hepatorenal syndrome is usually associated with refractory ascites and is slowly progressive with relatively good prognosis. Peripheral vasodilation with intrarenal vasoconstriction is the main pathophysiologic change. Diagnostic criteria, ascertained by international ascites club, is helpful to reach at a proper diagnosis. Management includes pharmacologic therapy to induce splanchnic vasoconstriction which improve renal circulation. Dopamine, vasopressin analogs (ornipressin and terlipressin), midodrine, noradrenaline have been used mainly as a bridge to the liver transplant or in anticipation of improvement in hepatic function. The molecular adsorbent recycling system (MARS) have been recently used in patients with hepatorenal syndrome. Transjugular intrahepatic portosystemic shunt is also another modality which has been used as a bridge to liver transplant in such patients.
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PMID:Hepatorenal syndrome. 1269 50

Hepatorenal syndrome (HRS) is a type of renal failure that occurs in patients with advanced cirrhosis. It is a result of splanchnic arterial vasodilation, renal vasoconstriction, reduced effective arterial volume, and potentially reduced cardiac output. Often, HRS is a fatal complication, and the only definitive treatment currently available is liver or liver-kidney transplantation. A number of other treatment modalities have been tested for the management of HRS, but most evidence is derived from small noncontrolled studies. The primary role of these treatment options is to provide a bridge to liver transplantation. Treatment may also provide acute reversal of renal failure and some symptomatic relief, but relapse is a common occurrence. The best therapeutic options appear to be those that reverse portal hypertension, splanchnic vasodilation, and/or renal vasoconstriction. Vasopressin analogs, particularly terlipressin, have emerged as the preferred pharmacologic therapies for management of HRS. Albumin is an appropriate adjunctive therapy to terlipressin and can be used to prevent HRS in patients with spontaneous bacterial peritonitis. Transjugular intrahepatic portosystemic shunt may provide a surgical option for qualified patients with HRS. Octreotide is ineffective as monotherapy but may be used as adjunctive therapy to other vasoactive agents. Dopamine agonists, endothelin antagonists, natriuretic peptides, and nitric oxide synthase inhibitors have not been effective for reversing HRS. Artificial hepatic support therapies have demonstrated the ability to improve laboratory abnormalities in patients with HRS, but their effect on clinical outcomes has not been determined. The role of renal replacement therapies or the newer artificial hepatic support therapies need further evaluation before they can be routinely recommended.
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PMID:Treatment of hepatorenal syndrome. 1979 93


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