Showing papers by "Marco Valgimigli published in 2000"

Measurement of oxidative stress in human liver by EPR spin-probe technique.

Abstract: A method for the measurement of reactive oxygen species (ROS) in human hepatic tissue has been developed. The method is based on the EPR detection of the nitroxide radical produced by reaction of the hydroxylamine spin-probe bis(1-hydroxy-2,2,6,6-tetramethyl-4-piperidinyl)decandioate with ROS generated under pseudo-physiologic conditions in fine needle biopsies of healthy (10 controls) and diseased (22 patients) human liver. Measures of malonaldehyde in 9 liver biopsies (3 controls and 6 patients) have also been obtained by high pressure liquid chromatography and values parallel those obtained by the spin-probe technique. The amount of ROS found in healthy human liver (median = 1.8 × 10-11 mol/mg) was significantly lower than values found in liver affected by hepatitis B (median = 5.8 × 10-10 mol/mg; p < 0.02) or by hepatitis C (median = 2.7 × 10-9 mol/mg; p < 0.003) as well as compared to some other non-viral liver diseases (NVLD): autoimmune hepatitis, primary biliary cirrhosis, primary schlerosing chol...

Doppler Ultrasound in Portal Hypertension

Abstract: Doppler ultrasound (US) evaluation of splanchnic hemodynamics has proved to be of enormous value in the diagnostic approach to portal hypertensive patients. No less important, its use seems to offer indirect parameters able to gradate the severity of portal hypertension itself, providing prognostic and therapeutic implications.

Cardioprotection with ACE inhibitors : non-angiotensin II-related mechanisms

Abstract: Angiotensin-converting enzyme (ACE) is primarily localized (>90%) in various tissues and organs, most notably within the endothelium. This localized ACE, known as tissue ACE, is now recognized as a key factor in cardiovascular and renal disease. ACE activation, in response to a number of risk factors or injury, such as hypertension, diabetes mellitus, hypercholesterolaemia, cigarette smoking, acute ischaemia and heart failure, has deleterious effects on the heart, vasculature and the kidneys. Furthermore, local ACE activation contributes to endothelial dysfunction, a condition in which the balance between vasodilation and vasoconstriction, vascular smooth muscle cell growth, and the inflammatory and oxidative state of the vessel wall is disrupted. These effects are mediated through increased local formation of angiotensin II and decreased bradykinin (BK) formation. Thus, the selective inhibition of tissue ACE favourably modifies the underlying pathophysiology of cardiovascular disease. The enhanced BK availability consequent on ACE inhibition seems to be particularly relevant for the improvement in endothelial dysfunction which, in turn, is pivotal for the anti-ischaemic profile of ACE inhibition. BK exerts several effects on the endothelium, including physiological stimulation of endothelial constitutive nitric oxide (NO) synthetase (ecNOS), the key enzyme for NO production. In addition, it exerts potent anti-growth action as well as a pre-conditioning effect on the heart. Recent evidence suggests that ACE inhibitors may be differentiated from one another according to their binding affinity for tissue ACE and their capacity for improving BK formation. This distinction is important: whereas all ACE inhibitors effectively reduce high blood pressure, the greatest biological and structural cardio- and renoprotective effects of ACE inhibition may be attributed to those agents with the highest affinity for tissue ACE and for reversing BK breakdown.