Diabetes mellitus (DM) causes multiple dysfunctions including circulatory disorders such as cardiomyopathy, angiopathy, atherosclerosis and arterial hypertension. Moreover, DM can strongly affect pulmonary circulation, enhancing the wall thickness of the pulmonary arteries, changing their tone and contractility, and gas exchange in the lungs. It can lead to marked loss of lung function and respiratory efficiency. It is also known that protein kinase C (PKC) activity increases in DM and that PKC is involved in the mechanisms of DM-associated vascular complications. However, the effect of DM on pulmonary artery tone has been poorly investigated and the role of PKC in this remains unknown. The aim of this study was to investigate changes in contractility of pulmonary arteries in rats with DM and to determine the possible role of PKC in this process. Experimental type 1 DM was elicited in male Wistar rats by single streptozotocin (STZ, 65 mg/kg) injection. DM was verified by the presence of hyperglycaemia. The investigation was performed on the isolated rings of the main pulmonary arteries using the method of vascular tone registration. Phenylephrine (PhE, 0.1 nM – 1 mM) caused dose-dependent constriction of the pulmonary arteries. The pD2 (negative logarithm of the agonist concentration required for half-maximum response) of this constriction increased in rats with DM, however significant changes in amplitude of PhE-induced constriction were not observed. PKC inhibition with chelerythrine and staurosporine (1 µM) significantly shifted PhE the concentration-response curve to the right in intact diabetic vessels but had no effect on sensitivity to PhE in deendothelised diabetic vessels. Our data suggest that type 1 DM leads to enhancement in pulmonary artery α1-adrenoceptor-mediated contractility and PKC activity in the endothelium rather than in vascular SMCs is involved in this process.

Objective: We determined the plasma protein C and coagulation factor X activities, prothrombin, fibrinogen and soluble fibrin monomer complex (SFMC) content and performed the haemostatic screening coagulation time tests under acute ischemic stroke patients with or without type 2 diabetes mellitus, as well as evaluated the significance of biochemical haemostatic markers as predictors of mortality in stroke regardless of diabetes presence. Methods: The baseline data were collected from 87 patients during the admission. Neurological disturbances were assessed using the NIH stroke scale. The functional outcome was estimated using Barthel index. All patients underwent fibrinogen and SFMC (gravimetric methods), prothrombin level (ELISA), plasma protein C and coagulation factor X activity assessment, haemostatic screening coagulation time tests with coagulation analyzer, glucose and glycosylated hemoglobin content and BMI (body mass index) measurements. Results: The conducted research had established the changes of fibrinogen and SFMC levels in both investigated patient groups comparing to the control. The protein C activity was found to be significantly decreased in blood of patients with ischemic stroke with and without diabetes. There were differences in factor X activity change in patients with stroke only comparing with patients with diabetes and stroke and high level of this parameter as well as the increase in SFMC can be regarded as death predictors of stroke independently of diabetes mellitus presence. Conclusion: Among ischemic stroke patients with type 2 diabetes mellitus the differences were more significant for all Time tests of the coagulation cascade, but deviations of haemostatic biochemical markers were more pronounced in ischemic stroke patients without diabetes mellitus.

Diabetes mellitus (DM) is acompaining by vascular tone desorders development. Regulatory enzyme protein kinase C (PKC) is involved in mechanisms of these desorders development. Numerous studies have demonstrated that contractile responces of vascular smooth muscle are enchansed in DM and endothelium-independent PKC-mediated mechanisms are involved in this process. Such mechanisms are PKC-mediated inhibition of Ca2+ activated K+ channels (BKCa) in vascular smooth muscle cells (SMCs) and SMCs myophilaments Ca2+ sensitization. PKC is a potential therapeutic target for treating vascular diabetic complications. A few compounds among PKC inhibitors already exist, such as ruboxistaurin, indolylmaleimide and its derivatives. Recently discovered method of RNA-interference (RNAi) is an essential gene-silencing tool and can also be used for PKC inhibition and DMassociated vascular complicaions elimination.

Abstract-Introduction:The estіmated number of people with diabetes worldwide in 2015 is 415 million persons, up to 91% of adults hadtype 2 diabetes and the crude incidence of stroke among patients with diabetes of the 2 nd type can be more than 3 times that in the general population. It is known platelet activation and aggregation are critical in the pathogenesis of acute ischemic cerebrovascular diseases. Thus to examine the evidence of platelet functioning such as platelet count,aggregation in response to ADP, coagulation von Willebrand factor and serotonin content, monoamine oxidase (MAO) activity in the blood of patients with ischemic stroke and with ischemic stroke complicated with the 2 nd type diabetes are the aim of the present study. Methods: The platelet aggregation was assayed for photo-optical aggregometer, von Willebrand factor was determined by Elisa, serotonin determination included ion-exchange chromatography and fluorescence spectrophotometry. Determination of monoamine-oxidase serum activity was spectophotometry. Results: The investigation has shown an increase of serotonin and Von Willebrand factor blood content in both groups of patients with ischemic stroke andtype 2 diabetes and stroke alone compared with the values of the control group. The monoamine oxidase activity and platelet count were reduced in blood of patients with diabetes of the 2 nd type with ischemic stroke against to the values from the group of healthy donors. Platelet aggregation in response to ADP increased under the investigated pathologies. Conclusions: These obtained data suggested a significant imbalance in vascular platelet element of hemostasis under the ischemic stroke and amplification of negative changes under the stroke with the 2 nd type diabetes.