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PubMedDate not supplied

[Effect of osmotic diuretics and saluretics on intracranial pressure in posttraumatic brain edema].

The effect of osmotic diuretics (mannite and glimarite, 29 studies), colloid-osmotic diuretic (algurin, 22 studies), and saluretic (lasix, 58 studies) on intracranial pressure (ICP) was studied in 30 patients in the acute period of severe craniocerebral injury. It was found that the hypotensive effect of the diuretics depended on the state of the water-electrolyte homeostasis, the time of medication with the agents, the severity of the patient's condition, and the initial ICP. The effect of osmotic diuretics was highest in normoosmia and normonatriemia in ICP of 20-45 mm Hg. Medication with osmotic diuretics and algurin in the first 2-3 days after the injury as usually attended by the "yield phenomenon"; the hypotensive effect of algurin in this period was less manifest. The effect of lasix was higher in hyperosmia caused by hypernatriemia but lower in patients who were in a terminal and extremely severe state.

Brain Edema↗
PubMed1989

Difference between hypertonic NaCl and NaHCO3 as osmotic diuretics in dog kidneys.

To compare the osmotic inhibitory effects of NaCl and NaHCO3 on proximal tubular fluid reabsorption, plasma osmolality was raised by 40 mosmol kg-1 H2O by infusing hypertonic NaCl and NaHCO3 in volume-expanded dogs receiving ethacrynic acid. In five dogs studied at constant plasma pH 7.5, both NaCl and NaHCO3 reduced water reabsorption by 29 +/- 2%. However, NaCl infusion reduced bicarbonate reabsorption by 31 +/- 2%, whereas bicarbonate reabsorption remained unchanged during NaHCO3 infusion. In six dogs, bicarbonate reabsorption was kept constant during NaCl and NaHCO3 infusion by adjustments of plasma pH. At similar glomerular filtration rates (42.4 +/- 2.9 ml min-1), water reabsorption was 28.7 +/- 1.7 ml min-1 in the control period, 29.4 +/- 2.5 ml min-1 during hypertonic NaCl infusion and 20.6 +/- 1.2 ml min-1 during hypertonic NaHCO3 infusion. Therefore, NaCl did not reduce proximal tubular water reabsorption by a direct osmotic effect. By calculating the regression coefficient for the relationship between measured chloride reabsorption and maximal convective chloride flux, the effective reflection coefficient for NaCl averaged 0.11 +/- 0.01. The combination of a low reflection coefficient and high permeability may explain why hypertonic NaCl is not an osmotic diuretic.

Animals↗
PubMed2004

Osmotic diuretics induce adenosine A1 receptor expression and protect renal proximal tubular epithelial cells against cisplatin-mediated apoptosis.

Osmotic diuretics are used successfully to alleviate acute tubular necrosis (ATN) produced by chemotherapeutic agents and aminoglycoside antibiotics. The beneficial action of these agents likely involves rapid elimination of the nephrotoxic agents from the kidney by promoting diuresis. Adenosine A1 receptor (A1AR) subtype present on renal proximal tubular epithelial and cortical collecting duct cells mediates the antidiuretic and cytoprotective actions of adenosine. These receptors are induced by activation of nuclear factor (NF)-kappaB, a transcription factor reported to mediate hyperosmotic stress-induced cytoprotection in renal medullary cells. In this study, we tested the hypothesis that induction of the A1AR in renal proximal tubular cells by NF-kappaB contributes to the cytoprotection afforded by osmotic diuretics. Exposure of porcine renal proximal tubular epithelial (LLC-PK1) cells to mannitol or NaCl produced a significant increase in A1AR. This increase was preceded by adenosine release and NF-kappaB activation. Expression of an IkappaB-alpha mutant, which acts as a superrepressor of NF-kappaB, abrogated the increase in A1AR. Cells exposed to mannitol demonstrated increased reactive oxygen species (ROS) generation, which was attenuated by inhibiting xanthine oxidase with allopurinol. Allopurinol attenuated both the increase in A1AR expression and NF-kappaB activation produced by osmotic diuretics, indicating a role of adenosine metabolites in these processes. Treatment of LLC-PK1 cells with cisplatin (8 microm) resulted in apoptosis, which was attenuated by mannitol but exacerbated by selective A1AR blockade. Administration of mannitol to mice increases A1AR expression and activation of NF-kappaB in renal cortical sections. Taken together, these data provide novel mechanisms of nephroprotection by osmotic diuretics, involving both activation and induction of the A1AR, the latter mediated through activation of a xanthine oxidase pathway leading to ROS generation and promoting activation of NF-kappaB.

Allopurinol↗
PubMed2004

Mannitol and other osmotic diuretics as adjuncts for treating cerebral malaria.

BACKGROUND: The main treatment for cerebral malaria is parenteral antimalarials. Mannitol and urea are used as adjunct therapy for cerebral malaria, but the World Health Organization does not recommend them. OBJECTIVES: To compare mannitol or urea to placebo or no treatment for treating children and adults with cerebral malaria. SEARCH STRATEGY: We searched the Cochrane Infectious Diseases Group Specialized Register (June 2004), CENTRAL (The Cochrane Library Issue 2, 2004), MEDLINE (1966 to June 2004), EMBASE (1974 to June 2004), LILACS (1982 to June 2004), and reference lists of articles. We contacted relevant organizations and researchers. SELECTION CRITERIA: Randomized and quasi-randomized controlled trials comparing mannitol or urea to placebo or no treatment in children and adults with cerebral malaria. DATA COLLECTION AND ANALYSIS: No trials met the inclusion criteria. MAIN RESULTS: No trials met the inclusion criteria. REVIEWERS' CONCLUSIONS: We identified no randomized or quasi-randomized controlled trials to support or refute the use of mannitol or urea as adjuncts for treating cerebral malaria in clinical practice. This is likely to require a multicentre trial.

Adult↗
PubMedDate not supplied

[The influence of inhibitors of kinin and prostaglandin formation on the vascular and tubular effects of osmotic diuretics in the kidney].

Mannit was shown to increase the blood flow in the external, middle and internal zone of the renal cortex in anesthetized rats but exerts no effect on the blood supply to the external zone of the medullary layer. A preliminary administration of contrykal fails to influence the diuretic and natriuretic effects of the preparation and to change the character of the hemodynamic shift at the action of the diuretic in the middle zone of the cortical layer. Indomethacin completely eliminates the blood flow increase in the middle zone of the cortex but it does not prevent the diuretic and natriuretic reaction to mannit administration. It is concluded that realization of the vascular and tubular effects of the diuretic is not related to the increase of kinin biosynthesis in the kidneys. Prostaglandins formed in the kidneys under the influence of mannit are involved in the mechanism of dilatation of the vessels of the cortical layer but do not play the significant role in the formation of its tubular effect.

Animals↗