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To prolong the preservation period of donor kidneys, we tried to evaluate the effect of human atrial natriuretic peptide (hANP), which has vasodilator, natriuretic, and GFR-increasing effects. Autotransplantations were successful in 6 of 8 hANP-treated cases, but only one of 7 untreated cases (P less than 0.05) was successful. When removed kidneys were perfused prior to preservation, the gravity perfusion time was shorter in hANP-treated kidneys, resulting in rapid cooling. Renal biopsy 1 hr after transplantation revealed normal histology in the hANP-treated kidneys while a remarkable capillary collapse occurred in controls. A hANP-like immunoreactivity contents of biopsied tissue in the hANP-treated kidneys showed a higher value than in the controls, and cyclic GMP contents were also higher in the hANP-treated kidneys. Microangiography showed complete clarity, down to the peripheral vessels, in the hANP-treated kidneys, but not in the controls. Thus, the present study suggests that hANP is useful for prolonging the preservation time of donor kidneys.
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PMID:Prolongation of the kidney preservation period by simple cold storage up to 72 hours by human atrial natriuretic peptide. 185 84

The relationship between inferior vena cava diameter (VCD), collapse-index (CI) determined by echography, and alpha-human atrial natriuretic peptide (alpha-h-ANP) concentrations were studied in 19 chronic haemodialysis patients. A significant correlation was found between VCD and alpha-h-ANP before dialysis (r = 0.78; P less than 0.0001). No such correlation was found between CI, left atrial diameter and left ventricular end-diastolic diameter, and alpha-h-ANP values. In nine patients who according to vena cava indices were hypervolaemic before dialysis (group I), alpha-h-ANP concentrations were significantly greater than in ten normo- or hypovolaemic patients (group II): 392.8 +/- 134.1 pg/ml and 168.0 +/- 62.5 pg/ml respectively. Although the same amount of fluid was ultrafiltrated in both groups, alpha-h-ANP decreased significantly in group I only, whereas in group II the decrease was not significant: 392.8 +/- 134.1 to 185.2 +/- 81.7 (P less than 0.001); 168.0 +/- 62.5 to 130.0 +/- 59 respectively. After achieving normovolaemia alpha-h-ANP concentrations in patients with a mitral valve insufficiency grade I was doubled compared to normovolaemic patients without mitral valve insufficiency, suggesting that alpha-h-ANP release will also occur from the left atrium. In the latter group alpha-h-ANP values were approximately doubled compared to healthy controls. The highly significant correlation between VCD before dialysis and changes in alpha-h-ANP during dialysis with fluid removal underlines the value of vena cava diameter in estimating volume status.
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PMID:Plasma alpha-human atrial natriuretic peptide and volume status in chronic haemodialysis patients. 252 86

A correct estimation of volume status and so-called dry weight in dialysis patients remains a difficult clinical problem. Clinical status and chest X-ray are not sensitive enough, while invasively measured central venous pressures are not routinely available. Recently, the sonographic determination of the diameter and collapse of the inferior vena cava (IVC) has been proposed as a noninvasive method for estimating intravascular volume. We tried to evaluate the clinical relevance of this method in dialysis patients by comparing it with central venous pressures (CVP) and atrial natriuretic peptide (ANP). To establish a normal range and to control for confounding variables, we examined a large number of healthy controls. Furthermore, the influence of tricuspid insufficiency was examined echocardiographically. Measurements of the IVC diameters were well reproducible, with a coefficient of variation for interobserver error of 2.2%, and a coefficient of variation of 1.4% for intraobserver error. The collapse index was less well reproducible and therefore not used for further analysis. In 86 normal controls (age 18 to 76 years), IVC diameters showed a wide variation, and they were not correlated to age, height, weight, or body surface area. However, there was a significant correlation of IVCex to heart rate (r = 0.63, P < 0.001). Therefore, we calculated percentiles of the heart rate-IVCex relation in normals, and compared the results in patients to these. In 10 overhydrated haemodialysis patients, CVP was closely correlated to IVCex (r = 0.72, P < 0.001), but there was a wide interindividual variation of the slope of this relation. An IVCex above the 95th percentile of normal was a good predictor of an elevated CVP (i.e. > 12 cmH2O). In another 39 stable, chronic haemodialysis patients, there was a significant correlation of the intradialytic decrease of ANP and IVCex (r = 0.69, P < 0.001). However, this correlation existed only in patients without tricuspid insufficiency. In summary, sonography of the inferior vena cava is a valuable tool for estimating dry weight in dialysis patients, provided that some caveats are kept in mind: (i) there is a wide variation of IVC diameters in normals, and single measurements are not helpful in individual patients; (ii) there is a significant, inverse correlation between IVC diameters and heart rate, and the precision of intravascular volume assessment is enhanced by interpreting heart rate corrected diameters; (iii) the presence of tricuspid insufficiency leads to unreliable results, as it influences IVC diameters per se. Intravascular volume changes are reflected by IVC measurements, as shown by the correlation to other indices of intravascular volume, such as CVP and alpha-hANP. IVC sonography is noninvasive and easily available; serial measurements allow an estimation of changes of intravascular volume in patients without cardiac filling impairment. However, unlike with body impedance, interstitial volume is not reflected by IVC diameters.
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PMID:Vena cava diameter measurement for estimation of dry weight in haemodialysis patients. 880 90

During cardiac remodelling, the heart generates higher levels of reactive species; yet an intermediate 'compensatory' stage of hypertrophy is associated with a greater ability to withstand oxidative stress. The mechanisms underlying this protected myocardial phenotype are poorly understood. We examined how a cellular model of hypertrophy deals with electrophilic insults, such as would occur upon ischaemia or in the failing heart. For this, we measured energetics in control and PE (phenylephrine)-treated NRCMs (neonatal rat cardiomyocytes) under basal conditions and when stressed with HNE (4-hydroxynonenal). PE treatment caused hypertrophy as indicated by augmented atrial natriuretic peptide and increased cellular protein content. Hypertrophied myocytes demonstrated a 2.5-fold increase in ATP-linked oxygen consumption and a robust augmentation of oligomycin-stimulated glycolytic flux and lactate production. Hypertrophied myocytes displayed a protected phenotype that was resistant to HNE-induced cell death and a unique bioenergetic response characterized by a delayed and abrogated rate of oxygen consumption and a 2-fold increase in glycolysis upon HNE exposure. This augmentation of glycolytic flux was not due to increased glucose uptake, suggesting that electrophile stress results in utilization of intracellular glycogen stores to support the increased energy demand. Hypertrophied myocytes also had an increased propensity to oxidize HNE to 4-hydroxynonenoic acid and sustained less protein damage due to acute HNE insults. Inhibition of aldehyde dehydrogenase resulted in bioenergetic collapse when myocytes were challenged with HNE. The integration of electrophile metabolism with glycolytic and mitochondrial energy production appears to be important for maintaining myocyte homoeostasis under conditions of increased oxidative stress.
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PMID:Responses of hypertrophied myocytes to reactive species: implications for glycolysis and electrophile metabolism. 2127 2