Drugs online research references
Dig Dis Sci. 1996 Nov;41(11):2187-94.
Role of Na(+)-H(+)-antiport in restitution of isolated guinea pig gastric epithelium after superficial injury.
Joutsi T, Paimela H, Bhowmik A, Kiviluoto T, Kivilaakso E.
II Department of Surgery, Helsinki University Central Hospital, Finland.
In addition to its pHi regulatory function Na(+)-H(+)-antiport is also involved in volume regulation of epithelial cells, particularly in neutral conditions. It is also known that the antiport is activated after ligand binding following growth factor receptor activation. The aim of the present study was to evaluate the role of the antiport in restitution of gastric mucosa and whether its activity is dependent on the type of superficial injury. Therefore the fundic epithelium of guinea pig stomach was perfused in an Ussing chamber in neutral conditions. Na(+)-H(+)- and Cl(-)-HCO3(-)-antiports were inhibited with 1.0 mM amiloride, 1.0 mM SITS, or with HCO3- removal and Na(+)-K(+)-2Cl(2-)-cotransporter with 0.3 M furosemide during 4 hr of restitution after superficial injury induced either by 1.25 M NaCl or by 1.0% Triton. Luminal exposure of the epithelium to amiloride had no effect on restitution but serosal application abolished the process completely. The inhibitory effect of amiloride was similar after both NaCl and Triton injury. The inhibition of Cl(-)-HCO3(-)-antiport with SITS interfered with the process as well, while HCO3- removal had no significant inhibitory effect, nor did the inhibition of Na(+)-K(+)-2Cl(-)-cotransporter. The morphologic findings were in accordance with the electrophysiologic measurements in each pair of tissues. It is concluded that the Na(+)-H(+)-antiport is essential for the epithelial cells during restitution even in neutral conditions, but a functional Cl(-)-HCO3(-)-antiport is also required. The activity of Na(+)-H(+)-antiport is sensitive to basolateral amiloride and is necessary regardless of the type of chemical injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8943971&dopt=Abstract
Leber Magen Darm. 1977 Aug;7(4):263-9.
[Renal disorders in hepatic insufficiency - pathogenesis and therapy (author's transl)]
[Article in German]
Thiele KG.
Renal failure in patients with acute or chronic hepatic insufficiency may be caused by prerenal factors (diuretics, hemorrhage), acute renal failure (shock, toxic tubular necrosis) or concurrent primary renal disease. Prerenal (functional terminal or circulatory) insufficiency to the kidneys seems to occur spontaneously; it is characterized by progressive reduction of glomerular filtration rate and renal plasma flow due to vasoconstriction and increase of intrarenal arterial resistance; the pathogenetic mechanisms of these changes are unknown. Reduction of effective plasma volume is especially important. Attempts at pharmacologically influencing renal blood flow have failed up to now. Increase of plasma volume and furosemide medication are therapeutic procedures worthwhile trying. Hemodialysis is indicated only, if restitution of liver function can be expected.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=895328&dopt=Abstract
Br J Cancer. 1997;75(6):829-36.
Interstitial fluid pressure in intracranial tumours in patients and in rodents.
Boucher Y, Salehi H, Witwer B, Harsh GR 4th, Jain RK.
Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA.
Fluid transport parameters in intracranial tumours influence the delivery of therapeutic agents and the resolution of peritumoral oedema. The tumour and cortex interstitial fluid pressure (IFP) and the cerebrospinal fluid pressure (CSFP) were measured during the growth of brain and pial surface tumours [R3230AC mammary adenocarcinoma (R3230AC) and F98 glioma (F98)] in rats. Intratumoral and intracranial pressures were also measured in rodents and patients treated with dexamethasone, mannitol and furosemide (DMF), and hypocapnia. The results show that (1) for the R3230AC on the pial surface, IFP increased with tumour volume and CSFP increased exponentially for tumours occupying a brain volume of 5% or greater; (2) in F98 with volumes of approximately 10 mm3, IFP decreased from the tumour to the cortex, whereas for tumour volumes > 16 mm3 IFP equilibrates between F98 and the cortex; (3) DMF treatment reduced the IFP of intraparenchymal tumours significantly and induced a pressure gradient from the tumour to the cortex; and (4) in 11 patients with intracranial tumours, the mean IFP was 2.0 +/- 2.5 mmHg. In conclusion, the IFP gradient between intraparenchymal tumours and the cortex decreases with tumour growth, and treatment with DMF can increase the pressure difference between the tumour and surrounding brain. The results also suggest that antioedema therapy in patients with brain tumours is responsible in part for the low tumour IFP.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9062403&dopt=Abstract
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