Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have examined the effects of 25 min of ischemia in the isolated erythrocyte-perfused rat kidney (IEPK). We have previously shown that, in this model, perfusate flow rate is close to blood flow rates in vivo and morphology is normal. The functional and morphological consequences of both warm ischemia (at 37 degrees C) and ischemia induced during mild hypothermia (27 degrees C) were compared. (1) Warm ischemia resulted in a 51% increase in renal vascular resistance (RVR) during the reflow period, while glomerular filtration rate (GFR) was reduced to 24% of control levels. (2) Kidneys subjected to warm ischemia showed marked morphological damage localized to the proximal tubule. There was dilatation of the proximal segments and widespread loss of the proximal brush border due both to shedding into the lumen and interiorization into the cell. In contrast to the proximal tubular damage, the cells of the medullary thick ascending limb segments were intact. However, the lumena of many of these segments were filled with cytoplasmic blebs and necrotic cell debris. There was also pronounced vascular congestion of the capillary plexus in the inner stripe of the outer medulla. (3) Hypothermia to 27 degrees C resulted in almost complete protection against ischemic injury: RVR and GFR were not different from control values. Also, kidneys subjected to cold ischemia showed only isolated areas of mild brush border damage; no evidence of tubular obstruction or vascular congestion was present. (4) Thus, warm ischemia in the IEPK results in functional and morphological effects comparable to those found in vivo. Post-ischemic vasoconstriction as well as medullary congestion occur in the absence of systemic hormones and renal nerves. These consequences of ischemia are prevented by modest hypothermia.
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PMID:Ischemia in the isolated erythrocyte-perfused rat kidney. Protective effect of hypothermia. 324 34

Using in vitro microperfusion of rabbit nephron segments we measured the effects of osmotically induced water flow on net transport of HCO3 and Cl. Measurements were made in superficial and juxtamedullary proximal convolutions and in superficial pars recta. In addition, measurements were taken in the presence and absence (hypothermia) of active transport. Using osmotic gradients of 25 mM raffinose in superficial and 50 mM in juxtamedullary segments, we observed increases in water flow equal to or greater than the normal rates of volume reabsorption observed in these tubule segments. However, there were no significant changes in HCO3 and Cl flux. This lack of significant solvent drag was seen both when osmotic water flow was in the lumen-to-bath direction and when osmotic flow was in the bath-to-lumen direction. The results of these studies suggest that solvent drag does not contribute significantly to NaCl and NaHCO3 reabsorption in proximal tubules. The lack of significant solvent drag of these salts can be interpreted as indicating either that osmotically induced transepithelial water flow in proximal tubules almost exclusively traverses transcellular pathways or that proximal tubule tight junction reflection coefficients for these salts are close to unity.
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PMID:Lack of solvent drag of NaCl and NaHCO3 in rabbit proximal tubules. 628 75

Procainamide is an organic cation and commonly prescribed drug that is actively secreted into the urine by renal proximal tubules. In order to elucidate further the mechanisms involved in this secretion, [3H]procainamide uptake into dissected S2 segments of superficial proximal tubule cells was studied. Uptake of [3H]procainamide was reduced by hypothermia and in a dose-related manner by the organic cations nonradiolabeled procainamide, cimetidine and quinidine and also by the carbonic anhydrase inhibitors acetazolamide and benzolamide, but not by ouabain. All these drugs were shown previously to inhibit transtubular secretion of [3H]procainamide in isolated perfused proximal tubules. The results of these and our previous studies suggest that 1) organic cations reduce the tubular secretion of each other, in part, by competing for uptake across the basolateral membrane of renal tubule cells, 2) acetazolamide and benzolamide reduce urinary excretion of organic cations, in part, by inhibiting proximal tubular secretion and 3) the potential difference across the basolateral cell membrane (due to activity of Na+-K+-dependent adenosine triphosphatase) is not the only driving force for uptake of organic cations into intact renal tubule cells.
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PMID:Procainamide uptake by rabbit proximal tubules. 682 56