Blood platelet function in patients with obliterative arteriosclerosis of the lower limbs

The specific markers of platelet activation, e.g. platelet aggregation induced with ADP, AA and PAF as well as the levels of Beta-TG, TXB2, 6-keto-PGF1 alpha and cyclic AMP in the patients suffering from obliterative arteriosclerosis of the lower limbs were measured. It was found that these patients revealed hyperfunction of blood platelets expressed in increased sensitivity of platelets to ADP and PAF, increased levels of Beta-TG and TXB2 as well as decreased levels of 6-keto-PGF1 alpha and cyclic AMP. Obtained results support the concept that atherosclerosis consists of a wide-spread functional alteration of various types of cells.     

糖尿病性下肢动脉硬化闭塞症的护理体会

目的:探讨糖尿病性下肢动脉硬化闭塞症的护理措施.方法:对糖尿病性下肢动脉闭塞症的52例患者,给予适当的心理疏导,合理调整饮食,加强患肢和创面护理,有效的时症处理,以及有针对性的出院指导等系列护理措施.结果:合理恰当的护理措施可以有效地促进糖尿病性下肢动脉硬化闭塞症患者的恢复.结论:糖尿病性下肢动脉硬化闭塞症患者除采用恰当的外科治疗手段,实施高质量的,有针对性的护理措施十分重要.     

Plasma lipoproteins affect platelet malondialdehyde and thromboxane B2 production

Platelet interaction with plasma lipoproteins was studied using gel-filtered platelets free of plasma constituents and purified lipoproteins. On incubation of gel-filtered platelets with plasma lipoproteins at 30 degrees C for 30 min, 100 micrograms of protein/ml of very-low as well as low-density lipoprotein caused 10% increment in platelet aggregation and [14C]serotonin release in parallel to elevation of around 15% of malondialdehyde and thromboxane B2 production. High-density lipoprotein showed the opposite effect and reduced platelet aggregation as well as thromboxane B2 synthesis by 17 and 32%, respectively. Lipoprotein-deficient plasma enhanced platelet function. Preincubation of the platelet suspension with prostacyclin did not prevent the effect of the lipoproteins on the in vitro platelet response as well as on the platelet prostaglandin pathway. Our results suggest that the formation of thromboxane B2 and malondialdehyde is influenced by plasma lipoproteins and that these, in turn, affect platelet aggregation and the release reaction. The possible significance of these results to platelet function in hyperlipidemic patients is discussed.     

Kallikrein in the treatment of patients with obliterative atherosclerosis of the lower limbs and its mechanism of action]

Kallikrein (Padutin-Depot) was administered to 20 patients with obliterative atherosclerosis of the lower limbs of the II degree (19 patients) and IV degree (1 patient). The drug was given in the daily dose of 40 U i.m. for 28 days. An effect of kallikrein on the distance in intermittent claudication, rate of pain relieve after walking the maximal distance, blood flow in the lower limbs, and on the index of circulating aggregates have been determined. Clinical improvement has been noted after a 4-week therapy with kallikrein. The drug in a single dose of 40 U activates plasma fibrinolytic system for 5 hours and decreases the number of circulating aggregates (2-5 h). The authors explain kallikrein action as the release of endogenous bradykinin, which subsequently releases two epithelial mediators, i.e. PFG1 and EDRF.     

Ozone therapy and viscosity of blood and plasma, distance of intermittent claudication and certain biochemical plasma components in patients with occlusive arteriosclerosis of the lower limbs]

Blood and plasma viscosity, total lipids, triglycerides, total cholesterol, free fatty acids, fibrinogen, lipid-gram, and hematocrit were determined in 53 patients with occlusive arteriosclerosis in the lower limbs prior to and after ozone therapy. At the same time the distance of the intermittent claudication was measured. A significant prolongation of the distance walked painlessly, reduction in blood and plasma viscosity as well as the decrease in total cholesterol after therapy with ozone correlated with a decrease of the blood viscosity.     

Plasma thromboxane B2 in haemodialysed patients

Plasma thromboxane B2 (TXB2) concentration was measured in 7 cases of terminal renal failure before and after haemodialysis. The TXB2 levels were higher in the investigated group than in the control group (p less than 0.05). Haemodialysis induced a further increase in the TXB2 concentration. Increased thromboxane production may play a part in the pathogenesis of accelerated atherosclerosis in uraemic patients treated with chronic haemodialysis.     

Prevention of Ca(2+)-induced or thromboxane B2-induced hepatocyte plasma membrane bleb formation by thromboxane receptor antagonists.

Isolated hepatocytes incubated in the presence of either Ca2+ ionophore A23187 or thromboxane B2 develop many plasma membrane blebs which are a characteristic feature of toxic or ischaemic cell injury. When hepatocytes are incubated in the presence of both Ca2+ ionophore A23187 and any one of three thromboxane receptor antagonists (SK and F 88046, B.M. 13505, B.M. 13177), bleb formation is strongly inhibited. Hepatocytes incubated in the presence of both thromboxane B2 and any one of the three thromboxane receptor antagonists are also well protected from the formation of blebs. Treatment of isolated hepatocytes with Ca2+ ionophore A23187 is known to stimulate the production of thromboxanes. The data presented are consistent with thromboxane B2 acting as an intermediary in a proposed mechanism of cell injury and death in which elevated cytosolic free Ca2+ levels activate phospholipase A2 and the arachidonate cascade.     

Prevention of thromboxane B2-induced hepatocyte plasma membrane bleb formation by certain prostaglandins and a proteinase inhibitor

Isolated hepatocytes incubated in the presence of thromboxane B2 developed many plasma membrane blebs which are a characteristic feature of toxic or ischaemic cell injury. When hepatocytes were incubated in the presence of both thromboxane B2 and the non-lysosomal proteinase inhibitor, leupeptin, were also well protected from the formation of blebs. This implies that thromboxane B2 is able to activate non-lysosomal proteinases which appear to attack certain cytoskeletal proteins. The data presented are consistent with thromboxane B2 acting as an intermediary in a proposed mechanism of cell injury and death in which elevated cytosolic free Ca2+ levels activate phospholipase A2 and the arachidonic acid cascade.     

Plasma thromboxane B2 levels and thromboxane B2 production by platelets are increased in patients during spinal and epidural anesthesia

Concentrations of thromboxane (Tx) B2 in plasma and its production by platelets were measured in 20 spinal and 10 epidural anesthesia patients scheduled for small operations in the lower extremities. The main metabolite of prostacyclin, 6-keto-PGF1 alpha and prostaglandin (PG) E2 in plasma were also determined. Plasma TxB2 and TxB2 production by platelets increased during both spinal and epidural anesthesia. Plasma TxB2 levels also remained elevated 1 h after anesthesia. The plasma concentrations of 6-keto-PGF1 alpha and PGE2 did not change during spinal or epidural anesthesia. In in vitro studies, only low concentrations of lidocaine (0.5-1.0 micrograms/ml) and bupivacaine (0.5-3.0 micrograms/ml) increased platelet TxB2 production. In platelet rich plasma, neither lidocaine nor bupivacaine in concentrations of 0.5-3.0 micrograms/ml caused constant changes in ADP-induced platelet aggregation, but they inhibited it in toxic concentrations (12 micrograms/ml). The results suggest that the increased TxB2 plasma levels and platelet TxB2 production during regional anesthesia are not caused by local anesthetics itself but by other factors, e.g. tissue trauma. In clinically found concentrations, local anesthetics do not cause any constant changes in platelet aggregation.     

Use of nitrendipine in treating patients with obliterative atherosclerosis of arteries in the lower extremities]

Twenty patients with obliterative atherosclerosis in the lower extremities arteries (Fontaine's stage II) were treated with nitrendipine (Bayotensin) given in the dose of 20 mg daily for 6 weeks. This therapy with nitrendipine produced improvement manifested by the prolongation of the distance of intermittent claudication, shortening of pain duration, increase in blood flow in the ischemic extremity, and increase in pressure index. At the same time, nitrendipine decreased ADP-produced platelet aggregation and activated fibrinolytic system. Clinical trials have shown that nitrendipine is effective in the obliterative atherosclerosis in the lower extremities.     

Platelet endoperoxide/thromboxane A2 ( ) receptors in patients with myeloproliferative disorders

In patients with myeloproliferative disorders (MPD) an altered sensitivity of platelets to antiaggregatory prostaglandins and to the endoperoxide analogue U 46619 has been found. In this study we examined U 46619-induced platelet aggregation and binding of the endoperoxide/thromboxane A2 (TXA2) receptor antagonist SQ 29548 in 11 patients with MPD and 11 healthy controls. Although platelet responsiveness to U 46619 was significantly enhanced (p less than 0.05) in MPD, binding affinity and binding capacity of the corresponding endoperoxide/TXA2 receptor were not altered (Bmax 0.67 +/- 0.20 vs. 0.58 +/- 0.14 pmol/10(9) platelets, Kd 0.41 +/- 0.11 vs. 0.55 +/- 0.09 nM). These data exclude the possibility that changes in the presentation of endoperoxide/TXA2 receptors are responsible for the enhanced platelet sensitivity to endoperoxides found in MPD.     

Abnormalities in mutual influences of upper and lower limbs in patients with stroke

Previously, in healthy subjects the common pattern of muscle activation and specifics of interlimb neuron connections during performance of rhythmic separate and simultaneous movements of arms and legs in the lying position, which reflect functional meaningful of interlimb interactions, were shown. The aim of this research was to investigate such mutual influences of upper and lower limbs during the execution of similar motor tasks by patients with stroke. In sixteen poststroke patients with different stage of hemiparesis arms movements together with or without legs movements were performed, while lying supine. It was demonstrated that the common pattern of muscle activity distribution under the execution of voluntary cyclic movements by both arms was disordered. Passive rhythmic movements of each arm caused the phased EMG activity in shoulder muscles in patients with mild hemiparesis, but no activation was observed in patients with severe paresis. The loading of nonparetic arm resulted in an increasing of activity in shoulder flexor muscles of paretic arm in patients with weak paresis (which was typical for healthy subjects), while it not exerted essential influences in patients with severe paresis. Under connecting the cyclic movements of arms with stepping movements of legs in diagonal synergy the activity in proximal muscles of both arms was decreased irrespective of the paresis degree, as it was seeing in healthy subjects. Simultaneous arms and legs movements did not change the muscle activity in non-paretic leg in both groups of patients, but in some muscles of paretic leg the activity even decreased. The results obtained revealed important features of poststroke motor disturbances, which caused the changes of interlimb interaction and in great degree depended on the level of paresis. The data of investigation can be of a great importance for developing the new methods for rehabilitative procedure in patients with stroke.