Showing papers by "Marco Valgimigli published in 2002"

Oxidative Stress EPR Measurement in Human Liver by Radical-probe Technique. Correlation with Etiology, Histology and Cell Proliferation

Abstract: The role of reactive oxygen species (ROS) in liver disease is controversial. This mostly reflects the difficulties to quantify ROS in vivo, particularly in humans. We aimed to measure the presence of ROS in diseased human liver and identify possible relations between ROS levels and etiology, histology and hepatocyte proliferation. Liver biopsy specimens from 102 individuals: 18 healthy controls and 84 patients (42 HCV chronic hepatitis (CHC), 19 HBV chronic hepatitis (CHB), 7 PBC, 4 PSC, 4 HCV relapsing hepatitis after liver transplantation, 3 autoimmune hepatitis, 3 hepatocellular carcinoma, 2 alcoholic hepatitis) underwent analysis by radical-probe electron paramagnetic resonance (EPR). ROS in patients (median=5 2 10 m 6 mmol/mg) were higher than in controls (median=3 2 10 m 11 mmol/mg) ( p <0.001). Progressively increasing levels of ROS were recorded passing from control values to CHB (median=4 2 10 m 7 mmol/mg), CHC (median=3 2 10 m 6 mmol/mg) and PBC (median=2 2 10 ...

Neurohormonal modulation in chronic heart failure

Abstract: During the past 50 years there have been vast improvements in the treatment of chronic heart failure (CHF). CHF was initially considered to be a cardio-renal problem - an acute disorder leading to volume expansion and oedema. Diuretics and digitalis were the only available treatments. Subsequently, CHF was considered to be the result of both myocardial dysfunction and increased tone in the pulmonary and peripheral circulations. The presence of peripheral vasoconstriction suggested that circulatory failure was an important component of the disease, and vasodilators were added to therapy. In the more recent past, experimental and clinical studies have demonstrated that CHF is also characterized by increased neurohormonal activation. This has led to the use of angiotensin-converting enzyme inhibitors, beta-blockers and spirouolactone in CHF. Increased neurohormonal activity is now recognized as one of the major pathophysiological factors that contribute to the progression of CHF. Activation of neurohormonal mechanisms is only compensatory in the short term; chronic activation produces detrimental changes in the myocardkma, kidneys and peripheral vasculature. This article provides an overview of the key neurohormonal systems that are activated in CHF.

Angiotensin II overproduction: enemy of the vessel wall

Abstract: Unfortunately, the vessel wall has several enemies and, regrettably, overproduction of angiotensin II seems to be one of the most aggressive, often causing several principal diseases such as arteriosclerosis, hypertension, coronary artery disease and heart failure. Obviously, it is unrealistic to consider angiotensin II as the only player but, certainly, it is one of the most important, as the reduction of its overproduction by drugs such as ACE inhibitors or angiotensin II receptor blockers is able to counteract the above mentioned pathological conditions. This review mainly deals with the importance of overproduction of angiotensin II in causing endothelial dysfunction and the mechanisms which are involved, such as the activation of angiotensin I and II which have opposite effects. It is clear that a precise picture of the molecular changes induced by angiotensin II at tissue level cannot yet be described although progress is continuously made at the additive role of oxidative stress and activation of the nuclear factor kB is addressed. The mechanism of action of ACE inhibitors and the angiotensin II receptor blockers is also highlighted in the attitude which is considering the biological effect of these drugs and rather than their pharmacological effects. (Eur Heart J Supplements 2002; 4 (Suppl A): A26‐A30)