Effect of Diatrizoate on Renal Extraction of Pah in Man

The effect of diatrizoate on the renal extraction of para-amino hippurate (EPAH) was studied in 8 healthy male volunteers. The contrast medium was injected into an antecubital vein and into a renal vein in each individual. A single-injection technique for the determination of EPAH was used and EPAH was measured before and over a period of 30 min after each contrast medium injection. In addition, the renal extraction of diatrizoate was measured simultaneously. Small but significant and similar decreases in EPAH were observed after both antecubital and renal venous administrations of the contrast medium, with a duration of less than 30 min after the injection. The renal extraction ratio for the diatrizoate was 0.20. It is concluded that diatrizoate should not be used before the determination of EPAH, at least not until 30 min after the administration of the contrast medium. The decrease in EPAH caused by diatrizoate seems to be due to a direct tubular depressant effect. </jats:p

Vasoactive Agents and Blood Pressure Regulation in Sequential Ultrafiltration and Hemodialysis

Hypotension is a common and sometimes dangerous side effect of hemodialysis. Its etiology is multifactorial and largely unknown. Earlier studies on the role of endogenous blood pressure regulating agents such as catecholamines and renin have rendered conflicting results. We studied the influence of ultrafiltration and isovolemic hemodialysis separately on the plasma concentrations of the following blood pressure regulating agents: adrenaline, noradrenaline, dopamine, neuropeptide Y, calcitonin gene-related peptide (CGRP), renin (PRA), angiotensin II, vasopressin, aldosterone and Cortisol. During isolated ultrafiltration, plasma levels of two strong vasoconstrictors (noradrenaline and angiotensin II) and one strong vasodilator (calcitonin gene-related peptide, CGRP) increased significantly (noradrenaline 3.24 ± 0.60 nM to 4.31 ± 0.55 nM; p = 0.032, angiotensin II 19.74 ± 3.46 pmol/l to 28.49 ± 7.24 pmol/l; p= 0.047) No symptomatic hypotension occurred. At the end of isovolemic hemodialysis, plasma levels of all the vasoconstricting agents had decreased to pretreatment values, but those of CGRP had continued to rise (from 85.3 ± 17.6 pmol/l to 114.5 ± 25.3 pmol/l, p=0.031). During isovolemic hemodialysis, blood pressure fell to symptomatic levels, but was restored at the end of treatment. The study shows that hemodialysis patients respond to fluid removal by ultrafiltration with an increase in plasma levels of CGRP, noradrenaline and angiotensin II. The net effect is an appropriate vasoconstriction and adequate blood pressure is maintained during isolated ultrafiltration. During hemodialysis, the patients’ blood volumes remained unchanged as evident by a stable hematocrit, the vasoconstrictor hormones returned to normal levels, but in several patients there was a continuous release of vasodilating CGRP. Hypotension, then occurred in these patients due to the imbalance between vasoconstricting and vasodilating factors. </jats:p

Neurohormonal activation in heart failure after acute myocardial infarction treated with beta-receptor antagonists

Background: Few studies have described how neurohormonal activation is influenced by treatment with beta-receptor antagonists in patients with heart failure after acute myocardial infarction. The aims were to describe neurohormonal activity in relation to other variables and to investigate treatment effects of a beta, receptor-antagonist compared to a partial beta, receptor-agonist. Methods: Double-blind, randomized comparison of metoprolol 50-100 mg b.i.d. (n = 74), and xamoterol 100-200 mg b.i.d (n = 67). Catecholamines, neuropeptide Y-like immunoreactivity (NPY-LI), renin activity, and N-terminal pro-atrial natriuretic factor (N-ANF) were measured in venous plasma before discharge and after 3 months. Clinical and echocardiographic variables were assessed. Results: N-ANF showed the closest correlations to clinical and echo cardiographic measures of heart failure severity, e.g. NYHA functional class, furosemide dose, exercise tolerance, systolic and diastolic function. Plasma norepinephrine, dopamine and renin activity decreased after 3 months on both treatments, in contrast to a small increase in NPY-LI which was greater (by 3.9 pmol/l, 95% CI 1.2-6.6) in the metoprolol group. N-ANF increased on metoprolol, and decreased on xamoterol (difference: 408 pmol/l, 95% CI 209-607). Increase above median of NPY-LI (> 25.2 pmol/l, odds ratio 2.8, P = 0.0050) and N-ANF (> 1043 pmol/l, odds ratio 2.8, P = 0.0055) were related to long term (mean follow-up 6.8 years) cardiovascular mortality. Conclusions: Decreased neurohormonal activity, reflecting both the sympathetic nervous system and the renin-angiotensin system, was found 3 months after an acute myocardial infarction with heart failure treated with beta-receptor antagonists. The small increase in NPY-LI may suggest increased sympathetic activity or reduced clearance from plasma. The observed changes of N-ANF may be explained by changes in cardiac preload, renal function, and differences in beta-receptor mediated inhibition of atrial release of N-ANF. NPY-LI, and N-ANF at discharge were related to long term cardiovascular mortality. (C) 2002 European Society of Cardiology. All rights reserved