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Biomedical subjects

A Leaf

Publications and source records attributed to A Leaf.

At least 127 records · Page 7Linked to original sources

Effects of verapamil in models of ischemic acute renal failure in the rat.

This study was designed to determine whether verapamil protects renal function in experimental ischemia in the rat and, if so, whether the protection is mediated by verapamil's vasodilatory action or by an effect on renal cells independent of vascular perfusion. Inulin clearance (CIn) was examined for 3 h subsequent to 40 min of unilateral intrarenal infusion of norepinephrine (0.75 microgram X kg-1 X min-1) and 3 and 48 h subsequent to 40 min of unilateral renal pedicle clamp. In norepinephrine-induced ischemia CIn fell to 0.8 +/- 0.4% of preischemic values in saline-treated kidneys and 0.5 +/- 0.3% in verapamil post-treated kidneys. By contrast, CIn fell only to 52.3 +/- 6.5% of preischemic values in verapamil-pretreated kidneys. Verapamil pretreatment significantly counteracted the intrarenal vasoconstriction produced by norepinephrine, sustaining renal blood flow during the norepinephrine infusion. In pedicle clamp-induced ischemia verapamil pre- and posttreatment had no beneficial effect on preservation of glomerular filtration rate, whereas mannitol pretreatment was beneficial. Parallel studies in the isolated perfused rat kidney confirmed the in vivo observations. In conclusion, verapamil exerts no protective effect on renal function at 3 or 48 h when ischemia is induced by renal pedicle clamp. Likewise, verapamil administration subsequent to norepinephrine-induced ischemia is ineffective in preserving renal function. Verapamil pretreatment in norepinephrine-induced ischemia preserves renal function probably by attenuating the vasoconstrictive ischemic insult due to norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗

From toad bladder to kidney.

Studies using the urinary bladder of the toad to elucidate the mechanism of transepithelial ion transport are reviewed. Sodium ions are reabsorbed from bladder urine across the granular cells, accounting for all the electrical activity of this epithelium. Sodium ions enter the granular cells passively through selective sodium channels down an electrochemical gradient, mix in the intracellular "active transport pool," and are pumped actively out of the cell across the basolateral plasma membrane. The concentration of sodium within the active transport pool is normally low, 10-14 mM, with Ringer solution bathing both surfaces. The apical plasma membrane is the major resistance barrier; both vasopressin and aldosterone stimulate sodium transport across the tissue by increasing the permeability of this barrier. The apical plasma membrane is impermeable to chloride ions and they are reabsorbed passively, in response to the transepithelial electrical potential established by active sodium transport, through paracellular channels. The bladder reabsorbs 18 sodium ions per molecule of suprabasal oxygen consumed. The relatively high apical membrane resistance buffers the basolateral active transport system from changes in osmotic work in pumping sodium out of the cell over the physiologic range of transepithelial potentials.

Aldosterone↗

Effect of endogenous angiotensin on the efferent glomerular arteriole of rat kidney.

The local, direct effect of endogenous angiotensin II (AII) in the isolated, perfused rat kidney was studied in an "open-circuit," single-pass preparation perfused at a constant pressure with an artificial solution containing 6.5% bovine albumin in Krebs-Ringer solution. After the addition of purified renin substrate (tetradecapeptide, 3 to 5 X 10(-8) M), renal plasma flow fell from 25.3 +/- 1.6 to 14.4 +/- 1.0 ml x min-1 (N = 6, P < 0.001) and GFR rose from 0.3 +/- 0.03 to 0.63 +/- 0.06 ml.min-1 (P < 0.001). Filtration fraction rose accordingly from 0.015 +/- 0.001 to 0.044 +/- 0.002 (P < 0.001). The effects of the renin substrate were promptly reversed by the addition of an angiotensin antagonist, Sar1-Al8-AII (3 X 10(-6) M). Measurements of distribution of perfusate flow between outer and inner cortex were made with radioactive microspheres. Outer cortical flow was 75.3 +/- 3.5% of the total cortical flow during the control periods and 73.7 +/- 2.3% during the maximal renin substrate effect. We conclude that endogenous AII is active locally, independent of systemic recirculation. Its major site of action in this preparation is on the efferent glomerular arteriole.

Angiotensin II↗

Protection of cultured renal tubular epithelial cells from anoxic cell swelling and cell death.

In order to study the relationship between cell swelling and cell death due to ischemia, we have developed an in vitro model by using primary cultures of renal tubular epithelial cells. With this model, we have studied two components of ischemia--namely, anoxia along with substrate deprivation. After 2 hr of anoxia in the absence of substrate, the cultured cells swelled and blebbed. Cells similarly treated in the presence of 8% polyethylene glycol, an oncotic agent, did not swell and bleb, and when cells were counted 18 hr later, similar numbers of cells were seen as in the untreated cultures. However, tubule cells exposed to anoxia without 8% polyethylene glycol had 50% fewer cells 18 hr later. Therefore, if cell swelling is prevented during 2 hr of anoxia, cell viability is improved.

Animals↗

Nuclear power.

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Environmental Exposure↗

Inpatient performance of primary care residents: impact of reduction in time on the ward.

The inpatient (ward/intensive-care-unit) performance of primary care medical residents was compared with that of their peers in the standard internal medicine residency program. The primary care residents spent half as much time on inpatient rotations as did their peers in the first two years of training. History-taking, physical examination, case presentation, record-keeping, patient management, and overall performance were assessed and scored by the attending physicians using the American Board of Internal Medicine's Clinical Performance Evaluation Form. The performances of the two groups were nearly identical, suggesting that substantial time in the first two years of residency can be devoted to ambulatory training without markedly compromising development of acute care skills.

Clinical Competence↗

Electron microprobe analysis of the different epithelial cells of toad urinary bladder. Electrolyte concentrations at different functional states of transepithelial sodium transport.

The electrolyte composition of toad urinary bladder epithelial cells has been measured using the technique of electron microprobe analysis. Portions of hemibladders, which had been mounted in chambers and bathed with a variety of media, were layered with albumin solution on their mucosal surfaces and immediately shock-frozen in liquid propane at -180 degrees C. From the frozen material 1--2 micrometer thick cryosections were cut and promptly freeze-dried for 12 hr at-80 degrees C and 10(-6) Torr. Electron microprobe analysis using a scanning electron microscope, an energy dispersive X-ray detector, and a computer programme, to distinguish between characteristic and uncharacteristic radiations, allowed quantification of cellular ionic concentrations per kg tissue wet wt by comparison of the intensities of the emitted radiations from the cells and from the albumin layer. Granular, mitochondrial-rich, and basal cells, and the basal portions of goblet cells, showed a similar composition, being high in K (about 110 mM/kg wet wt) and low in Na (about 13 mM/kg wet wt). The apical portions of goblet cells were higher in Ca and S and lower in P and K, presumably reflecting the composition of the mucus within them. With Na-Ringer's as the mucosal medium, cells gained Na and lost K, when their serosal surfaces were exposed to ouabain, 10(-2) M. Replacement of mucosal Na by choline virtually prevented these ouabain-induced changes. Cellular ion contents were unchanged when Na in the serosal medium was replaced by choline. No differences in Na and K concentrations were detected between nuclei and cytoplasm. These results provide independent support for the hypothesis the the cellular Na transport pool in toad bladder epithelial cells derives exclusively from the mucosal medium and that no important recycling of Na occurs from the serosal medium to the cells.

Animals↗