Effects of Dopamine on Renal Function in Patients with Cirrhosis

Barnardo, David E.; Baldus, William P.; Maher, Frank T.

doi:10.1016/s0016-5085(70)80066-x

Cited by 71 publications

(32 citation statements)

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“…Although cardiac output was not measured in the present study, it seems likely that an increase in cardiac output occurred, on the basis of the observations cited. Barnardo et al (1970) administered dopamine to a series of patients with cirrhosis. Patients with advanced renal failure were not assessed: none had an endogenous creatinine clearance of less than 25 ml/min.…”

Section: N K Hollenberg Et Almentioning

confidence: 99%

“…It appears therefore that, although dopamine increases renal blood flow in both patients with cirrhosis and those with congestive heart failure, it does not abolish the vascular factors responsible for sodium retention and decreased glomerular filtration rate in both: the vascular factors must differ. Barnardo et al (1970) hypothesized a parallel effect on pre-glomerular and post-glomerular vessels so that glomerular capillary pressure was not increased pari passu with the increase in flow. Their interpretation seems reasonable.…”

Section: N K Hollenberg Et Almentioning

confidence: 99%

“…A combination of pharmacologic characteristics which includes a positive inotropic action on the heart and a vasodilator action on the splanchnic and renal vascular beds has been considered useful therapeutically. The renal response, since it is associated with a diuresis, has led to exploration of the therapeutic use of dopamine in patients with shock (Talley, Goldberg, Johnson & McNay, 1969), congestive heart failure (Goldberg, McDonald & Zimmerman, 1963), the hepatorenal syndrome (Barnardo, Baldus & Maher, 1970) and acute renal failure (Talley, Forland & Beller, 1970). There are, however, significant species differences in its cardiovascular effects and few reports on the characteristics of the renal vascular response to this agent in normal man (Goldberg, 1972).…”

mentioning

confidence: 99%

“…There are, however, significant species differences in its cardiovascular effects and few reports on the characteristics of the renal vascular response to this agent in normal man (Goldberg, 1972). The demonstration of a decrease in p-aminohippurate (PAH) extraction in association with the vasodilatation has raised the question of a relative increase in medullary flow to account for the diuresis (Breckenridge, Orme & Dollery, 1971). In this study we have investigated the renal vascular effects of dopamine in normal potential kidney donors with radioactive xenon and renal angiography, which provide some insight into intrarenal blood flow distribution.…”

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confidence: 99%

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Renal Vascular Responses to Dopamine: Haemodynamic and Angiographic Observations in Normal Man

et al. 1973

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1. The renal vascular response to intravenously administered dopamine was assessed in normal man by selective renal arteriography and xenon washout. Infusion of 3 pg min-' kg-' induced renal vasodilatation with an increase in the cortical component of blood flow. Arterial blood pressure was not influenced and a systemic effect was not demonstrable. Lower doses did not induce a renal response. Increasing dosage raised arterial blood pressure and induced subjective symptoms, but did not result in a further increase in renal blood flow.2. Renal vascular resistance increased with increasing age in the normal subjects. A significant inverse relationship was found between the initial vascular resistance and the renal vasodilator response to dopamine. It thus appears that the vascular effects of increasing age (nephrosclerosis) may limit the dilator response to dopamine.3. It is concluded that dopamine is an effective renal cortical vasodilator when administered intravenously at doses which are free from other systemic cardiovascular effects. The dose-response relationship must be considered in attempts at reversal of conditions characterized by renal vasoconstriction.

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Section: N K Hollenberg Et Almentioning

confidence: 99%

Section: N K Hollenberg Et Almentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

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Renal Vascular Responses to Dopamine: Haemodynamic and Angiographic Observations in Normal Man

et al. 1973

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“…As potential renal vasodilators, dopamine (in nonpressor dose) [23][24][25][26][27][28][29], prostaglandin A 1 [25], misoprostol (synthetic prostaglandin E 1 ) [30,31], prostaglandin E 2 [31], and prostacyclin (prostaglandin I 2 ) [28] have all been tried without success in the treatment of hepatorenal syndrome. In particular, dopamine has never been shown to improve renal function in hepatorenal syndrome despite its ability to increase renal blood flow [24,26,27].…”

Section: The Rationale Behind Pharmacological Treatment Of Hepatorenamentioning

confidence: 99%

Vasoconstrictor Therapy for Hepatorenal Syndrome in Liver Cirrhosis

Schmidt¹,

Ring‐Larsen²

2006

CPD

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Hepatorenal syndrome is a severe, but not uncommon complication of decompensated liver cirrhosis. In particular, the rapidly progressive form of hepatorenal syndrome (type 1) is associated with a dismal prognosis. Established hepatorenal syndrome has a spontaneous reversibility below 5%. Hepatorenal syndrome is involved in more than 50% of cirrhosis-related mortality. Thus, any treatment capable of reversing hepatorenal syndrome would be expected to reduce morbidity and mortality from liver cirrhosis. A pathophysiological hallmark of hepatorenal syndrome is arterial underfilling due to an extreme splanchnic vasodilatation. Consequently, potent vasoconstrictors capable of reversing this vasodilatation have been investigated in hepatorenal syndrome. Several vasoconstrictors including the alpha-adrenergic agonists, midodrine and noradrenalin, and the vasopressor analogues, ornipressin and terlipressin, have all been associated with a significant improvement in renal function in 57 to 100% of cases and even reversal of hepatorenal syndrome in 42 to 100% of cases. The majority of recent studies are on terlipressin. A randomized, controlled trial showed a significant effect of terlipressin on reversal of hepatorenal syndrome. The contribution of volume expansion to the beneficial effects of vasoconstrictors on hepatorenal syndrome remains to be determined. In general, reversal of hepatorenal syndrome was associated with an improved survival. However, it remains to be determined if vasoconstrictor therapy should be used in hepatorenal syndrome in general, or if it should be reserved for potential candidates for liver transplantation. In conclusion, evidence for a beneficial effect of vasoconstrictor therapy for the treatment of hepatorenal syndrome is steadily accumulating. Confirmation of the preliminary data in larger randomized, controlled trials looking at long-term survival is required.

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