Course of pain sensitivity in aging: pathogenetical aspects of silent cardiopathy.

Aging is often considered a risk factor for silent ischemic cardiopathy. Using endermic electric stimuli, we assessed the course of pain threshold and pain tolerance in 23 male subjects affected by silent myocardial ischaemia, and in 20 male subjects with symptomatic cardiopathy; we also attempted to define the role played by age. Values of pain threshold were assessed using the same method in a group of 40 healthy subjects, five for each age decade, between 10 and 90 years. Our data show a significant difference in pain threshold and tolerance between subjects with silent and symptomatic cardiopathies (34.7 +/- 12.6 mA versus 25.2 +/- 12.5 mA: P < 0.001 for the threshold and 68.5 +/- 21.2 mA versus 46.0 +/- 22.3: P < 0.001 for tolerance). The fact that the significance of our results is superior to that of other studies may be due to the particular method of stimulation used and to the uniformity of the sample studied (sex, age, exclusion of subjects with anxiety-depressive symptoms). No difference was found in pain threshold as regards age. It seems probable that the difference found between subjects with silent and symptomatic cardiopathies is due to the different modulation of the perception of pain at a central level, independently of the age factor.

[Silent cardiopathy and aging. Assessment of pain threshold and tolerance]. / Cardiopatia silente ed invecchiamento. Valutazione della soglia e tolleranza dolorifica.

The increase in pain threshold is one of the most significant hypothesis regarding the origin of silent ischaemic cardiopathy. The relations between silent ischaemia and aging aren't clear, although age is considered a risk factor in this pathology, in relation to a supposed peripheral neuropathy. In our study we evaluated the trend of pain threshold and of pain tolerance in subjects affected by silent ischaemic cardiopathy; we especially considered the role of aging. We studied 15 subjects with silent ischaemic cardiopathy and 15 with symptomatic cardiopathy; we evaluated the pain threshold and tolerance in three points using short and low frequency transcutaneous electrical impulses. All subjects were male; the exclusion criterion was a high level of anxiety and depression. Pain threshold values were measured with the same method in 40 healthy subjects, 5 per each decade and ranged from 10 to 90 years. Our data show a significant difference in pain threshold and tolerance between subjects affected by silent and non silent cardiopathy (33.9 +/- 12.9 mA vs 25.0 +/- 12.6 mA: p = 0.001 in the comparison of thresholds, and 66.8 +/- 20.9 mA vs 45.0 +/- 21.8: p = 0.000 in the comparison of tolerances). Regarding the higher significance of our data, compared with other studies, we considered the importance of our particular stimulation method and of the uniformity of the studied group. We didn't note any correlation between pain threshold and age. These data suggest that the differences evident between subjects with silent and symptomatic cardiopathy are linked to a different modulation of central pain perception uncorrelated with age.

[Effects of insular hormones on the secretion of atrial natriuretic factor]. / Effetti degli ormoni insulari sulla secrezione del fattore natriuretico atriale.

Aim of this study was to verify the existence of a correlation between the insular hormones and the atrial natriuretic factor (ANF). We studied 70 subjects (20 control, 20 obese, 20 non insulin-dependent diabetic obese, 10 insulin-dependent diabetic subjects) submitted to a glucagon test (1 mg i.v.). Blood samples were collected at -15, 0, 3, 6, 12, 15, 30, 60, 120, 150 minutes to assay insulin, C-peptide, serum electrolytes and ANF levels. The results to point out are: the ANF basal values are significantly higher (p < 0.01) in non insulin-dependent obese patients than in controls; the obese subjects also present a significant difference (p < 0.05). After glucagon injection no variations have been found in the ANF values until the 15th minute; then the controls, the obese and, above all, the non insulin-dependent diabetic obese subjects showed a significant increase of the ANF values between 60' and 90' (basal values 38 +/- 4 ng/ml; 90' values 85 +/- 7 ng ml). As these high values appear only after the induction of hyperinsulinism in our experiment and are not present in the type-1 diabetic subjects, it's probable that insulin, rather than glucagon, stimulates, directly or indirectly, the ANF secretion. If this hypothesis is confirmed, the correlation between insulin and ANF should deserve attention from a therapeutic point of view in subjects with glycometabolic imbalance.