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The authors show a new method to study erythrocyte aggregation; the results of in vitro study, obtained by modification of several parameters (hematocrit, immunoglobulins, fibrinogen concentrations), are exposed. The authors did not find in vivo correlations between MAE and hemorheological parameters in different diseases; they found low MAE values only in myelomatous subjects. Adding erythrocytes from healthy donors to myelomatous plasma and vice versa, they found low MAE values only in samples containing erythrocytes and plasma from myeloma. These results suggest that many factors, not only erythrocyte aggregability, contribute to determine MAE (Mean Aggregation Entity).

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A new method to measure erythrocyte ATP levels is used. The authors have incubated 6 whole blood samples and 7 samples containing washed red blood cells for 6 h. They measured ATP levels and confirmed an important decrease of the values during the time. If the same samples were incubated with pentoxifylline (1.4 X 10(-4) M), the ATP decrease was less relevant.

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The aim of this study was to evaluate the possible action in vitro of the platelets on the rheological behavior of red blood cells in healthy subjects and in patients with peripheral obliterative arterial disease before and after an isotonic exercise. Red blood cells and platelets from control subjects and from patients were tested in several ratios before and after the exercise studying the erythrocyte filterability. beta-thromboglobulin, a platelet-specific protein, was determined in vivo in all subjects before and after the exercise and in vitro as percent of increase between PPP and PRP activated, to monitor the platelet release. The results showed the interrelationship between platelet activation and rheological behavior of red blood cells.

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This study has been performed to evaluate the in vivo effect of acetylsalicylic acid (ASA) i.v. infusion at two different dosages: 500 and 2,000 mg on the main hemorheological parameters (blood viscosity and filtrability, hematocrit) and on beta-thromboglobulin (a platelet-specific protein) in patients with peripheral obliterative arterial disease, before and after an ischemic exercise. The results obtained before and 3 and 24 h after the drug administration induced us to think that platelet-specific substances released during the ischemic exercise can affect the hemorheological parameters and that ASA may be able to interfere with these reactions by inhibiting the platelet release.

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Ischemic cardiopathy in its various clinical manifestations, whether acute (angina pectoris or myocardial infarction) or chronic (chronic coronary insufficiency), has shown in recent years particular hemorheological characteristics of its own. The observation of patients with such diseases has allowed us to record the existence of modifications in the parameters indicative of rheological damage. Numerous studies have been made, many of which are still in progress, with the aim of clarifying the relationships between these data and the disease. In our experience an increase in blood and plasma viscosity and a decrease in red cell deformability are often present in a manner which is statistically significant, if these patients are compared with normal subjects. Hemorheological change is more evident in the acute forms of myocardial ischemia. In fact, in angina pectoris the occurrence of pain is always accompanied by an increase in blood viscosity and by a worsening of red cell deformability both during spontaneous crises and during provocative tests. The hemorheological damage tends to diminish fairly rapidly when the crisis is over, even if the level of stabilization proves to be still higher than normal. In myocardial infarction higher levels of viscosity appear for a brief period after the onset with a slight tendency to diminish up until the 30th day. With the aim of ascertaining whether the alteration is more evident precisely at the point where the ischemia occurs, we chose a necessarily limited number of subjects, undergoing coronarography and atrial pacing for diagnostic purposes, and decided to control the hemorheological data not only in the systemic venous blood but also in the blood taken from the coronary sinus. Our data has shown that the level of viscosity and of red cell filtrability, in the blood taken from the coronary sinus, is worse than those of the systemic venous blood and that, after atrial pacing, in negative pacing subjects the variations are of slight significance whilst in positive pacing subjects we observe a rapid increase in viscosity and a decrease in red cell filtrability. This seems to confirm what we have already observed in the limbs affected by peripheral ischemia, and to demonstrate the existence of a local hyperviscosity syndrome which, even in the myocardium, appears to be dependent on the tissue ischemia.

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We have demonstrated how temperature affects whole blood filterability. The filtration index appears to be dependent on temperature; the higher temperature is, the higher it rises. At body temperature of 37 degrees C the method resulted more reliable.

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We have demonstrated how conservation time affects whole blood filterability. The filtration index decay appears just after withdrawal and is present, with different characteristics, both at room temperature and at 37 or 4 degrees C. It is absolutely necessary to take measurements immediately after blood withdrawal.

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We have counted the different types of blood cells before and immediately after filtration. During filtration, an almost equal quantity of each type of cells remained in the filter, with a slightly higher percentage of leucocytes. The problem regarding occlusion of filter pores should be considered in the light of these findings.

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