Reduction in Severity of Acute Renal Failure in Rats by Beta-Adrenergic Blockade

Iaina, Adrian; Solomon, Sidney; Eliahou, H. E.

doi:10.1016/s0140-6736(75)90060-4

Cited by 30 publications

(10 citation statements)

References 18 publications

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“…The pro tective effect of DMSO in this experimental setting was more pronounced than has been reported for propranolol [5,10] or chronic saline loading [II]. However, the main difference between the present experiment and those re ported previously is that treatment was given after and not during the ischemic episode.…”

Section: Discussioncontrasting

confidence: 51%

“…However, attempts to reduce the residual renal damage in experimental ARF with propranolol [5,10], chronic saline loading [II], infusion of angiotensin antagonist or the vasodilating prostaglandin A, have so far met with partial or no success [5,13]. Furthermore, in most experimental studies, treatment was instituted prior to or concurrently with the induction of renal ischemia, while in a clinical setting one should look for treatment modalities effective when employed some time after the occurrence of the ischemic event.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Alleviation of Experimental Ischemic Acute Renal Failure by Dimethyl Sulfoxide

Kedar¹,

Cohen²,

Jacob³

et al. 1981

Nephron

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Acute, ischemic renal failure was induced in rats by clamping of the renal vessels for 1 h. Following the termination of the ischemic period 5 g/kg of dimethyl sulfoxide (DMSO) were administered intravenously as a 20% solution in saline. Control animals received normal saline. There were no deaths among the DMSO-treated animals. Urine flow began within 15 min of DMSO infusion. 24 h after the experiment the mean blood urea was 73 ± (SEM) 14 mg/100 ml (n = 29). All the control rats died during the week following the experiment. The mean blood urea at 24 h was 276 ± 18 mg/l00 ml (n = 20). In 10 additional animals perfusion of the kidney with DMSO prior to the closure of renal vessels protected the organ from ischemic damage. These experiments have a bearing on the therapeutic approach to ischemic renal failure in man, and on preservation methods of donor kidneys for transplantation.

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Section: Discussioncontrasting

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Alleviation of Experimental Ischemic Acute Renal Failure by Dimethyl Sulfoxide

Kedar¹,

Cohen²,

Jacob³

et al. 1981

Nephron

View full text Add to dashboard Cite

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“…32. 46 [52] and the (3-blocker, propra nolol [53][54][55][56], also improve renal function. It would be interesting to know to what extent the beneficial action of furosemide can be attributed to inadvertent volume expansion, only excluded in one study in which no ben efit was observed [47], It is also interesting to speculate whether calcium channel blockers and other vasodilators can raise the intrarenal perfusion pressure to the congested capil laries and mobilise the aggregated erythro cytes.…”

Section: Unresolved Problemsmentioning

confidence: 99%

The Pathophysiology of Ischaemic Acute Renal Failure

Mason¹

1986

Kidney Blood Press Res

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“…There are reports on the effects of propranolol on postischemic acute renal failure [25,26] and the stabilizing effect of lysosomes in the anoxic myocardium [27], There fore, (3-agonists probably do play a role in the release of lysosomal enzymes, in vivo. These postulations may ex plain the effects seen in our experiments with [3-blockade using d, /-propranolol.…”

Section: Discussionmentioning

confidence: 99%

Intrarenal Beta-Adrenergic Stimulation Enhances Excretion of Urinary Lysosomal Enzyme in Anesthetized Dogs

Akabane¹,

Kawamura²,

Ito³

et al. 1984

Nephron

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The effects of intrarenal administration of isoproterenol on excretion of urinary enzymes were examined in dogs. Urinary N-acetyl-β-D-glucosaminidase (NAG) and glutamyl transpeptidase (γ-GTP) originated from lysosomes and the brush border membrane of the kidney, respectively. NAG excretion was elevated for 10 min by isoproterenol (0.2 µg/kg/min) without a drastic change in glomerular filtration rate and renal blood flow. This elevation was inhibited by pretreatment with d, l-propranolol (0.6 mg/kg bolus injection 0.3 mg/kg/30 min) but less so by d-propranolol. Urinary γ-GTP excretion was little affected by isoproterenol. In light of these findings, the possibility that β-receptors may be involved in the excretion of NAG has to be considered.

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Reduction in Severity of Acute Renal Failure in Rats by Beta-Adrenergic Blockade

Cited by 30 publications

References 18 publications

Alleviation of Experimental Ischemic Acute Renal Failure by Dimethyl Sulfoxide

Alleviation of Experimental Ischemic Acute Renal Failure by Dimethyl Sulfoxide

The Pathophysiology of Ischaemic Acute Renal Failure

Intrarenal Beta-Adrenergic Stimulation Enhances Excretion of Urinary Lysosomal Enzyme in Anesthetized Dogs

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