Arteriosclerotic changes

Vascular arteriosclerotic changes may be a unifying mechanism for the toxic effects caused not only on the cardiovascular system but also in the liver and kidney (Beauchamp et al. 1983). 

Thrombosis is a condition occurring in the cardiovascular system related to the normal, physiological function of haemostasis. Clinically, thrombosis is thought of as those situations where formation of thrombi has proceeded to the point where, by interfering with the circulation to an organ or part, there is interference with function and therefore symptoms result. The thrombus may produce these effects in situ or as an embolus produces such effects elsewhere. Arteriosclerotic changes in the arterial wall are the most common cause of thrombi forming in the heart and arteries. 

Interferon-y can induce arteriosclerotic changes in the absence of immunocytes by potentiating VSMC mitogenesis (190). In Apo E -/-mice, interferon-y deficiency decreased atherosclerosis, in males only, by decreasing T-lymphocyte presence and cell activation without influencing serum cholesterol concentration (191). 

Antithrombotic therapy for acute peripheral occlusive disease is largely empirical. Thrombolytic therapy typically is reserved for patients in whom the occlusion is not amenable to surgery and for those in whom a possible delay between the initiation of therapy and thrombolysis would not jeopardize the viability of the limb. Evidence that antithrombotic therapy changes the natural course of the peripheral disease is sparse, but these patients are at an increased risk of cardiovascular mortality and should receive long-term aspirin therapy. Initial trials suggest that ticlopidine may improve the symptoms of chronic arteriosclerotic arterial insufficiency and also reduce fatal and nonfatal cardiovascular events, but further studies are needed. 

In arteriosclerotic processes, the mucopolysaccharide spectrum changes Buddecke (B17) has demonstrated that the amounts of sulfated mucopolysaccharides are increased by 50, whereas the amounts of hyaluronic acid and chondroitin fall to 40% and 15% of their original values, respectively. The increase of sulfated mucopolysaccharides in arteriosclerotic aortae is related to the increased deposition of calcium. 

It has been postulated that carbon disulfide cardiotoxicity may be mediated by disruption of the energy supply in the heart (Klapperstiick et al 1991). The mechanism for carbon disulfide acceleration of arteriosclerotic plaque formation involves direct injury to the vessel epithelium and changes in lipid metabolism. 

Parkinsonism is usually idiopathic but can arise from ischaemic changes in the brains as in arteriosclerotic and postencephatic parkinsonism. 

The underlying causes of the nervous changes that can occur in patients with diabetes mellitus present a challenge that is still with us. Symptoms of diabetic neuropathy may develop in mild, severe and controlled states of the disease, and with or without accompanying arteriosclerotic lesions. 

Trauma and vascular processes are the most common causes of neurological symptoms. Needle punctures and catheters may injure the spinal cord, nerve roots, bone, ligaments, or the blood vessels in the area. Vascular pathology includes thrombosis and embolization of the spinal arteries, arterial spasm without intraluminar clotting, and severance of the intercostal and lumbar arteries, and the risk of vascular complications if there is compression of the vessels due to tumours or vertebral processes, or by the presence of arteriosclerotic and thrombotic changes in the aorta. Other causes of neurologicjd sequelae are infections, chemicals, and previous neurological disease. 

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