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Biomedical subjects

W F Finn

Publications and source records attributed to W F Finn.

At least 37 records · Page 2Linked to original sources
PubMed1985

Mechanisms of lysine-induced acute renal failure in rats.

We have previously found that lysine produces acute renal failure in rats. To define the acute effects of lysine, rats given lysine at 8.9 mg/kg/min, i.v. for 4.5 hr were compared with control rats receiving equiosmolar dextrose. Systemic blood pressure was stable in both groups. Mean intratubular pressure, inulin clearance (CIn), and renal blood flow were determined at 45-min intervals. Intratubular pressures measured with a servonulling micropressure device were elevated by 90 min in lysine-treated animals, with tubular heterogeneity, while pressures in dextrose-treated rats were normal and homogeneous. By 135 min CIn in lysine-treated rats was 45% of CIn in dextrose rats. Urine output fell in lysine-treated rats. Renal blood flow determined by flow probe remained normal in lysine-treated rats through 135 min and did not decline significantly until 180 min. Significant dilatation of surface tubules was documented by intravital microscopy beginning at 90 min in lysine-treated rats. The sequence of elevated intratubular pressure and tubular dilatation, followed by decreased CIn, and then by decreased renal blood flow suggests that lysine produces acute renal failure primarily through tubular obstruction. The tubular obstruction is followed later by an increase in renal vascular resistance.

Acute Kidney Injury↗
PubMed1985

Renal counterbalance.

Unilateral renal injury, whether caused by ureteral obstruction or ischemia, is followed by an increase in RVR, a decrease in RBF, and eventual tubular atrophy. Each of these abnormalities can be modified by a reduction in the function of the contralateral kidney. Whether this occurs as a result of increases in vasodilatory substances or decreases in vasoconstrictor compounds is unknown. Equally uncertain is the possibility that the response is mediated by the accumulation of naturally occurring cytoprotective agents. In either case, a stimulus for growth of the previously damaged kidney seems to be necessary for full recovery to occur. It appears that this response primarily involves the regeneration of tubular epithelial cells and differs from that associated with compensatory hypertrophy. This may require adjustments in the action of other growth factors or inhibitors. Hinman believed that counterbalance described a relationship between a hypertrophic kidney and an injured kidney and required the presence of both. However, it is quite possible that a similar relationship may exist in instances of bilateral disease when the injury does not involve all nephrons to the same extent. If so, a vicious circle may be established in which the least-damaged nephrons, which are first to recover, later hypertrophy. This internal redistribution of function may not only suppress the recovery of the most severely injured nephrons but also promote their eventual atrophy. Ultimately, the continued hypertrophy and hyperfusion of the functioning nephrons may lead to sclerotic changes within their glomeruli.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1984

Maternal Welfare--Nassau County, New York, 1957-1981.

The Maternal Welfare Committee of the County of Nassau reports on the past 25 years of its activity. Its activities rapidly changed from a retrospective analysis of maternal deaths to a much broader concern of all subjects pertaining to maternal welfare. The function of the committee has never been punitive, but has always been educational. This was appropriate because the incidence of maternal deaths decreased to such a degree that it is no longer a major health problem in the United States. The identification of high risk factors in patient, physician, hospital, and society in general are outlined. Current major problems are: general anesthesia, pulmonary embolism, and ectopic pregnancy.

Adolescent↗
PubMed1984

Attenuation of injury due to unilateral renal ischemia: delayed effects of contralateral nephrectomy.

The functional abnormalities associated with unilateral postischemic acute renal failure in the rat, as produced by 60 min of complete renal artery occlusion, are influenced by the presence or absence of the contralateral kidney. When the contralateral kidney is removed prior to the ischemia, reflow of blood to the postischemic kidney is more complete. To determine whether this maneuver influenced the ultimate severity of the injury and, if so, to investigate the mechanism by which this occurred, studies were performed conjointly at Tel-Hashomer, Israel, and Chapel Hill, N.C., in uninephrectomized (UNx) and sham-operated (Sh) rats. At Tel-Hashomer, V from UNx rats was nearly double that found in Sh rats at 1 to 3, 3 to 5, and 24 hr after ischemia. By 24 hr, CCr was substantially greater in UNx rats and was similar to that from the nonischemic kidney of Sh rats. Differences in tubular function were also noted. In UNx rats, FENa at 24 hr was significantly less and TCH2O was significantly greater than the corresponding values determined in Sh rats. At Chapel Hill, by 24 hr, RBF and PGCe in UNx rats were significantly greater than the corresponding values in Sh rats, although both were less than values obtained in nonischemic kidneys. In UNx rats, RT and RPG were considerably less than the corresponding values in Sh rats and similar to the values obtained in nonischemic kidneys. Microscopic examination at 24 hr revealed widespread tubular epithelial cell necrosis in Sh rats. In contrast, tubular epithelial cell structures were preserved in UNx rats. These data indicate that substantive differences exist in the response to temporary unilateral renal ischemia, which depend in part on the absence of the contralateral kidney and which result in less severe reduction in RBF and CCr and the preservation of tubular epithelial structure and function.

Acute Kidney Injury↗
PubMed1983

Compensatory hypertrophy of single nephrons following ischemic injury in the rat.

In Sprague-Dawley rats, the increase in single nephron glomerular filtration rate (SNGFR) following uninephrectomy is due to an increase in glomerular plasma flow (GPF) along with an increase in the glomerular capillary ultrafiltration coefficient (Kf). Hypertrophy of individual nephrons also occurs when renal mass is reduced by disease or ischemic injury. To characterize the factors determining SNGFR in the minority of nephrons that recover from a severe ischemic insult, rats were studied 4 weeks after 1 hour of complete unilateral renal artery occlusion and the results compared to those obtained in normal rats. Indirect determination of the dynamics of glomerular ultrafiltration along with microangiographic studies indicated that despite a reduction in total renal blood flow in the postischemic kidney, a minority of nephrons were hyperperfused. The increase of GPF in these nephrons along with a significant increase in Kf was responsible for the observed increase in SNGFR.

Animals↗
PubMed1982

Compensatory renal hypertrophy in Sprague-Dawley rats: glomerular ultrafiltration dynamics.

The factors responsible for the increase in glomerular filtration rate associated with compensatory hypertrophy in Sprague-Dawley rats were studied 2 weeks following uninephrectomy. In sham-operated rats, the single nephron glomerular filtration rate (SNGFR) was 40 nl/min and the calculated glomerular plasma flow (GPF) was 138 nl/min. Proximal intratubular free-flow (PT) and stop-flow (PSF) hydrostatic pressures were 12 and 34 mm/Hg, respectively. The estimated glomerular capillary hydrostatic pressure (PGC) was 49 mm Hg and the estimated efferent effective ultrafiltration pressure (PUFEA) was 12 mm Hg, indicatng filtration pressure disequilibrium. The specific ultrafiltration coefficient was calculated to be 0.039 nl/s . mm Hg per glomerulus. In uninephrectomized rats, SNGFR increased to 61 nl/min and the calculated GPF increased to 266 nl/min. PT was 12 mm Hg; PGCe was 49 mm Hg and PUFEA was 15 mm Hg. Kf was calculated to be 0.053 nl/s . mm Hg per glomerulus. These data indicate that in Sprague-Dawley rats under conditions of filtration pressure disequilibrium, the increase in GFR associated with compensatory hypertrophy is in part related to a significant change in Kf.

Adaptation, Physiological↗
PubMed1982

Personal characteristics of house staff candidates: a quantitative analysis of relative weights.

We surveyed the faculty, fellows, and residents of a department of medicine to determine the relative importance of each of eight personal characteristics evaluated during the interview of house staff candidates. A booklet containing all possible pairings of the eight characteristics was distributed to 219 participants who were asked which member of each pair should have greater weight for assigning an overall interview grade. Usable data were returned by 172 persons (79%) and analyzed by the psychometric scaling method of paired comparisons. The four characteristics with the greatest relative weights were professional attitude, maturity, enthusiasm and energy, and knowledge. The faculty, fellows, and residents were highly consistent in their judgments. However, three of the characteristics (motivation for clinical practice, knowledge, and verbal skill) significantly distinguished the three departmental groups. These results show that utility of the paired comparison method for identifying a department's weighting of variables for selection of house staff.

Attitude of Health Personnel↗
PubMed1980

Effects of propranolol on post-ischemic acute renal failure.

The effects of constant intravenous infusion of propranolol, 1 mg/kg/h, on acute renal failure produced by 1 h occlusion of the left renal artery in the rat were investigated by clearance and micropuncture techniques. Propranolol infusion resulted in a significantly smaller rise in proximal intratubular pressure than that observed following renal ischemia in the saline-infused group. When compared with saline-infused animals, this effectwas accompanied by a significant improvement in inulin clearance without commensurate increase in renal blood flow or stop flow pressure and suggests attenuation of intratubular obstruction by the drug. A complex metabolic effect may be involved.

Acute Kidney Injury↗
PubMed1979

Recovery from postischemic acute renal failure in the rat.

To define the pattern of recovery from postischemic acute renal failure (ARF), we performed clearance and micropuncture studies at intervals of 1, 2, 4, and 8 weeks following 60 min of complete unilateral renal artery occlusion in the rat. At 1 week, the inulin clearance (CIn) of the postischemic kidney was less than 2% of normal. The presence of marked preglomerular vasoconstriction was indicated by the reductions in renal blood flow (RBF), and stop-flow (SFP) and estimated glomerular capillary hydrostatic pressures (GCPe). In additon, there was evidence of tubular obstruction. Proximal intratubular pressures (PITP) were elevated, and intratubular casts could be seen in vivo and on histologic sections. At 2 weeks CIn had increased more than tenfold. This change occurred in the absence of any significant elevation in RBF, SFP, or GCPe. PITP had fallen, however, to normal values, and histologic sections revealed a marked reduction in the extent of intratubular casts. Ipsilateral urinary recovery of 3H-inulin microinjected into proximal convolutions was complete. At 4 and 8 weeks, there were further but more gradual rises in CIn, which were associated with progressive increases in RBF, SFP, and GCPe. These observations indicate that recovery from postischemic ARF occurred in a biphasic pattern. The initial rise in CIn was associated with the relief of intratubular obstruction, whereas subsequent rises in CIn occurred in association with progressive renal vasodilation.

Acute Kidney Injury↗
PubMed1977

Renal hemodynamics in the rat before and during inhibition of angiotensin II.

Renal blood flow (RBF) was measured with a noncannulating electromagnetic flow transducer in anesthetized rats which had been maintained for 3-5 wk on low, normal, or high salt plus deoxycorticosterone diets. After base-line observations, one of two dissimilar inhibitors of the renin-angiotensin system, angiotensin I converting enzyme inhibitor SQ 20881 or the structural analogue [Sar1,Ala8]angiotensin II was administered intravenously. The employed doses of SQ 20881 and [Sar1,Ala8]angiotensin II effectively inhibited the pressor and renal vasoconstrictor responses induced by exogenous angiotensin I and II, respectively, in each dietary group. Both inhibitors vasodilated kidneys in salt-restricted rats; however, neither affected base-line renal hemodynamics in salt-loaded rats. Pressure-flow relationships were evaluated by clamping the aorta to reduce renal perfusion pressure. Renal blood flow was autoregulated between 100 and 140 mmHg with the same efficiency before and during inhibition of angiotensin II in each dietary group. These data indicate that angiotensin II modifies base-line RBF and renal vascular resistance and are consistent with the view that the renin-angiotensin system is not an essential mechanism responsible for autoregulation of RBF in the rat.

Angiotensin II↗
PubMed1977

Renal response to environmental toxins.

Several characteristics of normal renal function increase the risk to the kidney of damage by environmental toxins. Due to the magnitude of renal blood flow the total amount of noxious substance delivered may be disproportionately high. Furthermore, the capacity to concentrate substances within the kidney by processes of filtration, reabsorption and secretion has the potential to increase the toxicity of agents which would otherwise not lead to tissue injury. Unfortunately, there are few tests of renal function which are able to detect early functional abnormalities and which, at the same time, are suited for screening purposes by virtue of their simplicity, cost and safety. Furthermore, interpretation of the tests is complicated by adaptive changes in renal function which occur with aging and in response to other disease processes. Environmental agents produce a wide spectrum of renal dysfunction. Acute renal damage follows exposure to glycols, organic solvents, heavy metals, diagnostic and therapeutic agents and a variety of miscellaneous substances. Chronic renal disease may take the form of isolated tubular defects as seen with cadmium, interstitial nephritis due to the ingestion of lead, or vascular damage induced by external radiation. Some forms of glomerulonephritis may also be related to environmental toxins as are certain tumors of the urinary tract. In a somewhat different fashion, patients whose renal function is limited by the presence of pre-existing disease may manifest toxicity from substances ordinarily excreted in the urine. Particular problems exist with the patients on dialysis, as they are at considerable risk to alterations in the environment.

Aging↗