[Blood viscosity disorders as an etiopathological factor in sudden deafness]. / Trastornos en la viscosidad sanguínea como factor etiopatogénico en la sordera brusca.

Because idiopathic sudden deafness is regarded as the result of a cochlear microcirculation disorder, its treatment has been based mainly on vasoactive therapy with little regard for the blood-flow conditions produced by these circumstances. In a group of 16 patients with sudden-onset deafness, we determined blood viscosity at different shear rates, as well as erythrocyte aggregability, deformability, and filterability, and other potentially influential parameters, such as hematobrit, fibrinogen, and leukocyte and platelet count. These values correlated with hearing loss and average recovery after conventional treatment. Our results showed a trend to high blood viscosity in patients in relation to a control group of persons with normal hearing, with a notorious increase in aggregability, which correlated significantly with recovery of hearing capacity, and a decrease in blood filterability, which correlated with average hearing loss. This suggests a potential etiopathogenic mechanism of the disease and an alternative treatment complementary to current treatment.

[An experimental analysis of the development of local capillary stasis]. / Eksperimental'nyi analiz razvitiia mestnogo kapilliarnogo staza.

Micro-application of NaCl induced a local slowdown to full stoppage of the blood flow in the lamina of individual capillaries in the Wistar rats mesenterium. The blood stasis resulted from local disturbances of the blood rheological properties. The erythrocyte aggregates obstructed the capillaries leaving no space for the parietal plasma layer. The findings suggest the intravascular erythrocyte aggregation to be the immediate cause of the blood flow disturbances and the blood stasis in the microvascular lumina.

Role of leukocytes in the activation of intravascular coagulation in patients with septicemia.

To elucidate the role of leukocytes in intravascular coagulation in patients with septicemia, plasma levels of thrombin-antithrombin III complex (TAT), soluble fibrin monomer complex (SFMC) and fibrinogen (Fbg) were determined in 33 patients with septicemia. Twenty of 33 patients revealed marked leukopenia caused by suppression of hematopoiesis by the administration of chemotherapeutic agents for the treatment of hematological malignancies; the total leukocyte count of these patients was less than 1,000/microliters. Thirteen of 33 patients showed normal or increased leukocyte counts. Plasma levels of TAT and SFMC in septicemic patients without leukopenia were significantly higher than in patients with leukopenia. Although plasma TAT and SFMC levels correlated well with the number of leukocytes, a more significant positive correlation was found between the number of monocytes and the levels of TAT and SFMC. Plasma levels of Fbg were significantly lower in patients without leukopenia than in patients with leukopenia. No significant correlation was found between the number of leukocytes and the levels of Fbg. However, a significant negative correlation was found between the number of monocytes and the levels of Fbg. TAT levels did not correlate with the number of platelets. The fibrinolytic system was activated only in septicemic patients without leukopenia, which may be explained by secondary fibrinolysis following leukocyte-activated coagulation. These findings suggest that leukocytes, in particular monocytes, may play a critical role in the pathogenesis of intravascular coagulation in septicemia.

[Thrombosis of the middle abdominal aorta during pregnancy. 21-year follow-up]. / Trombose van de mid-abdominale aorta tijdens de zwangerschap. 21 jaar follow-up.

The unusual case of a 31-year old female, pregnant for the second time and in the sixth week of pregnancy, who developed a very localised low mid-aortic thrombosis with typical claudication and associated clinical findings, is presented 21 years after corrective surgery for this condition. The authors wish to emphasize the fact that this case shows no similarity with the middle aortic syndrome, classically described by Debakey, in which major visceral branches of the lower abdominal aorta are involved. After ruling out, every possible classical cause of this condition, such as described in the discussion of this paper, the authors have to conclude that this situation was caused by increased red cell aggregation of the blood during pregnancy in a woman with moderate degree of hypoplasia of the abdominal aorta. After corrective surgery, the patient is still free of symptoms and of peripheral atherosclerotic disease.

Increased red blood cell aggregation in retinal vein occlusion.

Reversible aggregation of red blood cells (RBC) plays an important role in determining the flow properties of blood, and is the cause of the increase in blood viscosity at low shear rates. Retinal venous circulation is characterized by the combination of a low flow state and a high vascular resistance which might severely limit its capacity to adjust to high blood viscosity. These characteristics make the venous circulation in the retina particularly dependent on haemorheological factors. To test the possibility that high RBC aggregation could predispose to the onset and development of retinal vein occlusion (RVO), RBC aggregation and disaggregation (SEFAM erythroaggregameter, France) were measured in 64 patients with RVO. Results were compared to those of a group of 64 controls, similar in age, sex, smoking habit and associated pathologies. Increased RBC aggregation was observed in 52% of the patients, and the mean values showed a highly significant elevation of RBC aggregation parameters in RVO patients (+14%) when compared with controls (P less than 0.001). Subgroups were compared to study the influence of site (central versus branch), form (ischaemic versus non-ischaemic), duration and severity of the occlusion on the aggregation parameters. No significant differences were found between these various subgroups. An increase in RBC aggregability and in the shear resistance of RBC aggregates, by predisposing to circulatory stasis, is likely to contribute to the onset of RVO.

Rheology of paraproteinaemias and the plasma hyperviscosity syndrome.

The proper understanding of the causes, pathophysiology, diagnosis and management of the plasma hyperviscosity syndrome is based on good knowledge of malignant paraproteinaemias, properties of immunoglobulins, rheology of blood in the microcirculation, and modern plasma separation techniques. This multifaceted syndrome complicates less than ten per cent of IgA and IgG myelomas, and up to one-third of Waldenström's macroglobulinaemias. A few cases of HVS have also been reported in association with polyclonal hypergammaglobulinaemias. Excessive paraproteinaemia may cause the plasma HVS, especially when paraproteins are extraordinarily large, asymmetrical or cryosensitive, or if they aggregate into hyperviscous macroaggregates. The resultant severe microcirculatory impairment is mainly due to the combined effects of plasma hyperviscosity, significant plasma volume expansion and intense red cell aggregation. The individually variable general symptoms, bleeding tendency, ocular, neurological, cardiovascular, and renal manifestations and laboratory parameters of the HVS are summarized briefly. The majority of patients present hyperviscosity manifestations when the plasma viscosity exceeds 5-6 mPa.s. Plasmapheresis or plasma exchange have established themselves as efficient and safe modes of therapy of hyperviscosity and hypervolaemia. The therapeutic guidelines for the plasma HVS are briefly discussed with regard to recent experience with developing plasma separation techniques. Diagnostic and therapeutic advances combined with increasing haemorheological knowledge have greatly improved the proper management of this potentially lethal complication of paraproteinaemias.

[Pathogenesis of acute osteomyelitis]. / O patogeneze ostrogo osteomielita.

Pathogenesis of acute osteomyelitis is analyzed from the standpoint of disorders in the bone microcirculation. It is stated that in acute osteomyelitis there occur some disorders in microcirculation due to extravascular compression and intravascular occlusion of the bone vessels. The analysis of pathogenesis of acute osteomyelitis from the standpoint of disorders in the microcirculation of the osseous tissue is believed to be expedient for the correct understanding of pathological processes occurring in the bone, and for purposeful pathogenetic therapy.