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Biomedical subjects

A Mezzetti

Publications and source records attributed to A Mezzetti.

126 records · Page 7Linked to original sources
PubMed1979

Study of the metabolic effects of bunitrolol (Koe 1366) in angina induced by catecholamine infusion.

In ten angina patients responding with a myocardial anaerobic metabolic pattern to isoproterenol infusion, a new beta-blocking agent, bunitrolol, was effective in normalizing the myocardial lactate extraction ratio. The correlation with lipid metabolism was also interesting because beta-blocker action reduced significantly arterial non-esterified fatty acids (NEFA) level as well as myocardial NEFA extraction. The metabolic behavior suggests the effectiveness of bunitrolol in the treatment of ischemic heart disease.

Angina Pectoris↗
PubMed1977

[Changes in myocardial metabolism during atrial pacing and catecholamine stimulation in normal subjects and patients with angina].

5 patients with angina had their threshold for angina evaluated by atrial pacing and by stimulation with catecholamine (dopamine). The authors then studied the metabolic changes induced by the two types of anginogenic load (AP and D-test) applied successively, and compared them with the post-ergometry ECG changes (lowering of the ST segment by at least 2 mm) and the findings on coronary arteriography (complete obstruction of at least 75% stenosis of a major branch vessel). The metabolic measurements were controlled against those of 5 normal subjects after standard ergometry. In the patients with angina, the AP test led to a constantly negative value for %. L. By contrast, the values of D(a-v)c and % O2 which were reduced in the normals, as indirect evidence of an increased coronary flow, remained practically static. During the dopamine infusion, although the % L was reduced, it remained essentially positive, while the D(a-v)c and % O2 were consistantly lowered.

Adult↗
PubMedDate not supplied

Relationship between reduced BCL-2 expression in circulating mononuclear cells and early nephropathy in type 1 diabetes.

Microalbuminuria is the earliest clinical evidence of diabetic nephropathy, but the mechanisms linking hyperglycemia and kidney complications are not clear. The aim of this study was to evaluate whether enhanced oxidative stress in patients with microalbuminuria can contribute to diabetic nephropathy development through downregulation of the antiapoptotic gene Bcl-2 that promotes in turn a pro-inflammatory status. We studied 30 patients with type 1 diabetes (15 with and 15 without microalbuminuria) compared to 15 matched healthy controls. Plasma oxidant status, and expression of Bcl-2, activated NF-kB, inducible Nitric Oxide synthase (iNOS), and monocyte chemoattractant protein (MCP)-1 in circulating monocytes were evaluated at baseline and after 8-week oral vitamin E treatment (600 mg b.i.d.). Bcl-2 expression was significantly reduced in microalbuminuric diabetic patients as a consequence of increased oxidant burden secondary to persistent hyperglycemia. Bcl-2 down-regulation was associated with enhanced expression of NF-kB, iNOS and MCP-1, and showed a strong correlation with the albumin excretion rate. Low Bcl-2 expression and high inflammatory status were normalized by vitamin E both in vivo and in vitro. Our study showed that Bcl-2 down-regulation in diabetic patients with poor glycemic control results in the activation of the NF-kB pathway leading to the development of nephropathy. Vitamin E might provide a novel form of therapy for prevention of nephropathy in diabetic patients in which an acceptable glycemic control is difficult to achieve despite insulin therapy.

Adolescent↗
PubMedDate not supplied

Factors associated with apoptosis in symptomatic and asymptomatic carotid atherosclerotic plaques.

The aim of this study was to investigate the differences that are present between apoptosis in symptomatic (with symptoms of cerebral ischemic attack) and asymptomatic carotid atherosclerotic plaques. The apoptotic process in macrophages and smooth muscle cells was evaluated. Cellular markers and products of immune cells in symptomatic and asymptomatic atherosclerotic plaque and endoarterectomy specimen were analyzed by immunohistochemistry. No statistically significant differences were present regarding the mean SMC actin-positive area. Using double staining of alpha-smooth muscle actin and TUNEL techniques, the number of smooth muscle cells in apoptosis was statistically higher in symptomatic plaque as compared with asymptomatic plaque. Statistically significant differences (p=0.009) were also found in the CD45-positive cells in the inflammatory infiltrate. The CD68-positive macrophages showed statistically significant differences (p=0.0001). Similarly, the double staining with CD68 and TUNEL revealed that apoptotic macrophages were mainly present in asymptomatic plaques rather than symptomatic plaques. Statistically significant differences (p<0.001) were found in the Bcl-2 expression, with higher values in asymptomatic plaques. Our data showed that the increase of the inflammatory cells contributes to plaque instability and that death due to apoptosis of smooth muscle cells in symptomatic plaques could contribute to their destabilization and explains their tendency to fracture.

Aged↗