KFLC Index utility in multiple sclerosis diagnosis: Further confirmation.

The Multiple Sclerosis (MS) diagnosis is based on dissemination of focal lesions in time and space. The free light chains (FLCs) determination might be a sensitive alternative to oligoclonal bands assay. The study aim was to redefine sensitivity, specificity of the kFLC Index cut-off. We analyzed serum and cerebrospinal fluid of 176 patients, with different neurological disorders. We obtained a cut off of 12,3 for kFLC Index with a sensitivity and specificity of 93% and 100% respectively. Our data confirm that the kFLC Index is a valid tool in the diagnosis of MS.

Cardiovascular Diseases Risk Factors in oil and gas workers: a ten years observational retrospective cohort.

OBJECTIVES: The study aim was to examine the trend of major clinical biochemistry factors associated with cardiovascular diseases and dyslipidemia onset over a 10-year period (2000-2010) in Oil and Gas workers. METHODS: The information extracted from "Computerized management of individual medical services database" regarding 439 Italian workers of an oil and gas company were analysed. RESULTS: A constant and significant increase of the average Body Mass Index and serum cholesterol were found, and in particular in workers < 36 years: BMI was 24.4 (2000) and 25.8 (2010) with p < 0.001, and cholesterol was 188.3 mg/dL (2000) and 206.5 mg/dL (2010) with p < 0.001. CONCLUSION: Analysed variables are the most important risk factor for cardiovascular, neurological and neoplastic diseases, as well as they reduce life expectancy. Occupational medicine in particular in extreme working environmental conditions, such as for workers in oil and gas companies, monitoring health status and promoting healthy life style, has a strategic role to perform cost-effective strategies to reduce health risks, thus improving the workers lifestyle.

Angiotensin II directly stimulates release of atrial natriuretic factor in isolated rabbit hearts.

BACKGROUND: Previous studies have shown that infusion of angiotensin II (Ang II) increases plasma concentrations of atrial natriuretic factor (ANF) in vivo. This phenomenon has been considered secondary to the effects of Ang II on cardiac and systemic hemodynamics. The present study was designed to assess whether Ang II may exert a direct stimulatory effect on ANF release from the heart independent of changes in hemodynamics. METHODS AND RESULTS: Isolated rabbit hearts were perfused in the Langendorff mode. Heart rate, coronary flow, and atrial and left ventricular (LV) volumes were kept constant. After stabilization, Ang II was infused intracoronary at increasing doses (10(-11) to 10(-8) M) in nine hearts and at a single dose of 10(-10) M in 10 hearts. Each infusion lasted for 5 minutes and was followed by a 10-minute washout period. Four hearts received vehicle alone for 80 minutes. Ang II induced a dose-dependent increase in coronary perfusion pressure and in LV developed pressure. ANF release, measured by radioimmunoassay on the extracts of the cardiac effluent, also increased during Ang II infusion and returned to the basal values during the 10-minute washout period. In the control group, coronary perfusion pressure, LV developed pressure, and LV end-diastolic pressure did not change appreciably over the observation period, whereas ANF release progressively decreased during perfusion. CONCLUSIONS: Ang II can directly stimulate cardiac release of ANF in isolated rabbit hearts independently of changes in hemodynamics.

Effect of complete cardiac denervation on atrial natriuretic factor release in baboons.

We investigated the influence of cardiac innervation on atrial natriuretic factor (ANF) release in baboons. For this purpose, plasma ANF levels were measured in control conditions and in response to head-down (-45 degrees) and head-up tilt (+45 degrees) in six anesthetized baboons before and after complete cardiac denervation obtained by orthotopic autotransplantation of the heart. Cardiac denervation did not modify baseline plasma ANF levels (60.4 +/- 17 pg/ml before and 63.1 +/- 16 pg/ml after heart autotransplantation). In contrast the significant ANF responses to changes in central venous pressure (CVP) induced by postural maneuvers (-45 degrees, + 16.2 +/- 4 pg/ml; +45 degrees, -18.5 +/- 4 pg/ml) were markedly altered after cardiac denervation (-45 degrees, +5.8 +/- 2 pg/ml; +45 degrees, -7.6 +/- 1 pg/ml). The changes in CVP and systemic blood pressure evoked by the postural challenges were comparable before and after cardiac denervation. These results demonstrate that cardiac nerves play a role in the control of ANF release.

Modulatory role of angiotensin-II in the secretion of atrial natriuretic factor in rabbits.

This study was designed to investigate whether the increase in circulating atrial natriuretic factor (ANF) levels produced by angiotensin II (Ang II) is a consequence of the hemodynamic changes or whether it occurs also in the absence of pressor changes. For this purpose in anesthetized and awake rabbits we evaluated the effects of Ang II (0.1 micrograms/kg.min) alone or during the simultaneous infusion of sodium nitroprusside (NP) at a dose titrated to abolish the pressor effects. Systemic blood pressure increased from 76 +/- 4 to 113 +/- 5 mm Hg (P less than 0.001) during Ang II and from 76 +/- 2 to 75 +/- 3 mm Hg (P = NS) during Ang II plus NP. The alpha-adrenergic agonist phenylephrine, used as a control, raised blood pressure from 65 +/- 2 to 101 +/- 8 mm Hg (P less than 0.001), and its pressor effect was abolished by the concomitant infusion of NP (64 +/- 2 to 61 +/- 1 mm Hg; P = NS). The increase in plasma ANF levels produced by Ang II alone (from 36.5 +/- 5 to 237 +/- 57 pg/ml; P less than 0.001) was not different from that observed during Ang II plus NP (from 46 +/- 10 to 207 +/- 88 pg/ml; P less than 0.001). In contrast, the stimulatory effect on ANF release of phenylephrine (from 56.1 +/- 9 to 202 +/- 40 pg/ml; P less than 0.001) was completely abolished when its pressor effects were prevented by the combined infusion of NP (from 58.5 +/- 15 to 42.3 +/- 10 pg/ml; P = NS). These results show that the stimulatory effect of Ang II on ANF release can be clearly dissociated from its pressor effect, whereas the increase in plasma ANF levels caused by phenylephrine is strictly related to its hemodynamic effect. Therefore, Ang II is capable of modulating ANF secretion in a manner that is independent of its pressor actions. In addition, our results suggest that ANF release is not solely linked to myocyte stretch.

Influence of volume expansion on hemodynamic effects of atrial natriuretic factor in rabbits.

We investigated the influence of acute volume expansion on the hemodynamic and renal responses to the constant infusion of atrial natriuretic factor (ANF) (alpha-human ANP, 2 micrograms/kg bolus, 0.2 microgram.kg-1.min-1) in rabbits anesthetized with ketamine and acepromazine. The effects of the peptide were evaluated in 12 euvolemic rabbits and in 15 rabbits during the steady-state phase of volume expansion (0.9% NaCl 4.5 ml/min for 60 min). In the euvolemic animals, ANF caused an increase in natriuresis and a reduction in blood pressure (BP), which was associated with a decrease in cardiac output (CO), stroke volume (SV), and no significant changes in central venous pressure (CVP), peripheral hematocrit (Hct), and heart rate (HR). When the peptide was infused in the volume-expanded animals, the effects of ANF on BP and HR were comparable with those observed in the euvolemic animals. However, in these animals the ANF-induced changes in CO, SV, CVP, and Hct were significantly greater than those observed in the euvolemic group. In addition, the percent increases in diuresis and natriuresis were significantly smaller than those obtained in the euvolemic animals. In conclusion, volume expansion with saline potentiates the effects of ANF on systemic hemodynamics and blood volume.

Hemodynamic responses to atrial natriuretic factor in nephrectomized rabbits: attenuation of the circulatory consequences of acute volume expansion.

We investigated the hemodynamic responses to three doses of atrial natriuretic factor [human atrial natriuretic factor-(99-126)] (ANF) in nephrectomized rabbits anesthetized with ketamine and acepromazine. The influence of the different doses of the peptide on the hemodynamic consequences produced by acute volume expansion (0.9% NaCl, 1.4 ml/kg/min for 60 minutes) was also studied. All three dosages of ANF (0.001, 0.01, and 0.2 micrograms/kg/min for 20 minutes) significantly reduced blood pressure. With the lowest dose, the hypotensive effect was associated with reduction in systemic vascular resistance and no significant change in heart rate, stroke volume, central venous pressure, and hematocrit. In contrast, the intermediate and high doses, which resulted in markedly higher plasma levels, caused a significant decrease in heart rate, central venous pressure, and stroke volume; a slight rise in hematocrit; and no change in systemic vascular resistance. Volume expansion produced by saline infusion in an additional group of nephrectomized rabbits increased central venous pressure and decreased hematocrit. When ANF infusion was associated to volume expansion, each dosage of ANF was able to reduce the rise in central venous pressure, while only the higher dosage attenuated the progressive fall in hematocrit caused by volume expansion. Plasma volume, measured at the end of volume expansion was lower in the group treated with the highest dose of ANF than in the control animals (28.2 +/- 9 vs. 35.1 +/- 3 ml/kg, p less than 0.05). We conclude that 1) ANF induces significant hemodynamic effects independently from its renal action.(ABSTRACT TRUNCATED AT 250 WORDS)

Reproducibility of the new diagnostic criteria for impaired glucose tolerance.

Sixty-seven subjects with impaired glucose tolerance and 136 normoglycemic individuals defined according to the diagnostic criteria of the European Association for the Study of Diabetes were selected from among persons aged 40-59 years who participated in a health examination survey in Naples in 1980. A second oral glucose tolerance test was given under identical conditions between two and four months later with the participants having no knowledge of the results of the first test. Venous whole blood was utilized for blood glucose determination. At the second test, 93% of the control group were confirmed to be normoglycemic, but only 56% of the impaired glucose tolerance group were still intolerant. Reproducibility was poorest among subjects with blood glucose two hours after load of less than 140 mg/dl. Among these subjects, 47% reverted to normoglycemia at the second test. In contrast, 15% of those with blood glucose greater than or equal to 140 mg/dl two hours after load reverted to normoglycemia (chi 2 = 6.29, p less than 0.05). Subjects with impairment of glucose tolerance at the second test were reclassified according to the diagnostic criteria of the National Diabetes Data Group and the World Health Organization (WHO). Only 22 (46%) of the 48 individuals classified in the impaired glucose tolerance group according to the criteria of the European Association for the Study of Diabetes were so classified by the criteria of both the National Diabetes Data Group and WHO. The disagreement between the three diagnostic criteria was maximal in the lowest blood glucose range. It is concluded that the diagnosis of impaired glucose tolerance, despite the new diagnostic criteria, still has little reproducibility and uniformity.