Glaucoma in a patient with subclavian steal syndrome

Vascular disease may be an underlying factor in certain patients with normal tension glaucoma. Normal tension glaucoma patients with specific vascular and neurological symptoms, in correlation with results of clinical tests (i.e. intraocular pressure, ophthalmodynamometry, blood pressure), will benefit from a further work-up for systemic vascular disease. Subclavian steal syndrome is one such vascular disease which can produce symptoms and clinical signs which alert the clinician to evaluate the patient further. Subclavian steal syndrome can potentially decrease perfusion to the optic nerve head, making it more susceptible to glaucomatous cupping in the presence of normal intraocular pressures. The following case report illustrates a patient who developed subclavian steal syndrome and contralateral optic nerve head hypoperfusion.     

Effects of crush syndrome on insulin receptor interactions in cells

Comparative study of binding insulin receptor mononuclears, erythrocytes and hepatocytes of crush-syndrome revealed great difference in these parameters. In the early period of crush-syndrome (stress period insulin insufficiency hyperglycemia, insulin resistance, decrease in the activity of insulin binding in the mononuclears and increase in the activity of erythrocytes. By the 6 hour crush-syndrome (toxemic period) hyperinsulinemia, hyperglycemia, are observed as well as prolongation of the decrease in the activity of insulin binding of mononuclears.     

Possible experimental model of Korsakoff's syndrome

Study of the effects of chronic alcohol intoxication on conditioned behaviour in rats revealed spatial desorientation, the lack of a stable level of alertness, "negative attitude" to novelty, automatism of motor habit and periodical impairment of temporary connection reproduction. The authors conclude that the observed changes are comparable to a certain degree with the clinical pattern of Korsakov syndrome.     

On the subclavian steal syndrome in vitro studies.

An elastic model of the arterial system has been used in which a specially designed pumping unit simulated the heart action. Physiological pressures and normal geometry, size, and flow distribution together with the normal cardiac output and use of prosthetic heart valves are the features of the system. Atherosclerosis was simulated by introducing blockages of known cross-section at specific sites of predilection. It has been shown that, for some specific occlusion magnitude in the left or right subclavian, or in the brachycephalic arteries, the stagnant no blood flow condition will appear in the left vertebral, or the right vertebral, or right common carotid, or the right internal carotid arteries. For larger occlusions the blood flow in these arteries reverses its direction, i.e., the "steal syndrome" appears. It is shown that besides the known single steal syndrome there exists also a double steal syndrome, i.e., blood reverses its flow direction simultaneously in two arteries, both on the right side of the arterial system. This blood is taken from the circle of Willis, which at the same time is significantly supplemented by the increased blood flow through the other arteries leading into the circle of Willis.     

Activity of antioxidants in serum of animals with experimental crush syndrome]

Ischemia of soft tissues in crush syndrome results in activation of free radical oxidation processes, which negatively effect the functions of many biological systems. The presence of antioxidant system in the body can inhibit the action of free radicals. Antiradical effect of this system is seen in vitamin K, ubiquinone and ascorbic acid. The results of the experiment showed that the quantity of vitamin K, ubiquinone and ascorbic acid increases in the serum of blood after decompression of soft tissues in 14 hours, three and seven days. This fact supports an active participation of antioxidant system in the pathogenesis of crush syndrome.     

Possible hyperendorphinergic pathophysiology of the Rett syndrome

The Rett syndrome is a postnatal developmental and neurological disorder seen only in girls. Many of the symptoms of this disorder, such as microcephaly, stereotypy, respiratory disturbances and seizures, are analogous to the effects of the administration of beta-endorphin or other opioids in animals. Preliminary reports of elevated beta-endorphin-like immunoreactivity in the cerebrospinal fluid of girls with the Rett syndrome, as well as improvement in some of their symptoms during the administration of the opioid antagonist naltrexone, are suggestive of endorphinergic hyperactivity. Thus, the pathophysiology of the Rett syndrome might involve excessive stimulation of opioid receptors in the central nervous system by beta-endorphin or other endogenous opioids.     

Energy potential of the liver in the early period of the crush syndrome

Experiments on rats with a severe compression trauma were made to study the liver content of ATP, ADP, AMP and inorganic phosphate. It was established that in the early period of the crush syndrome, the rats manifested pronounced changes in the energy potential of the liver, attesting to the disturbances of the processes of energy production in that vitally important organ. It is assumed that liver ischemia and direct action on the liver of toxic factors of the protein nature circulating in the blood may be one of the reasons for the disturbances under discussion.     

Possible genetic heterogeneity in the Saethre-Chotzen syndrome

Saethre-Chotzen syndrome is an autosomal dominant acrocephalosyndactyly syndrome whose gene has been assigned to chromosome 7p. Cytogenetic and linkage analyses have enabled the interval encompassing the disease gene to be delimited to a short region of chromosome 7p15.3–p21.2. Based on the genetic analysis of three unreported families, we confirm the location of the disease gene(s) in the interval defined by loci D7S664 and D7S493 (Z_max = 4.78 at * = 0 at the D7S488 locus) but fail to decide whether one or more disease-causing genes map in this genetic interval. Received: 2 January 1996 / Revised: 21 March 1996     

Ocular complications of the acquired immunodeficiency syndrome

The acquired immunodeficiency syndrome (AIDS) affects the ocular structures in several ways. Kaposi's sarcoma has been observed on the bulbar conjunctiva of the globe. Retinal complications, however, are of major concern. Cotton-wool spots are commonly seen in AIDS patients and are usually of no consequence, except that they must be distinguished from the early stages of cytomegalovirus (CMV) retinitis, seen in 20-40% of these patients. CMV causes a necrotic-type retinitis potentially leading to blindness. 9-[2-Hydroxy-1-(hydroxymethyl)ethoxymethyl]guanine (DHPG) has been found effective in the short-term treatment of this disorder. It is planned to use AS101 in the regimen to see if a long-term cure from this disease can be affected. Care must be taken in handling ocular tissue of AIDS patients or the re-use of ophthalmic instruments touching the eye of AIDS patients since the human immunodeficiency virus has been found in these structures.     

Pulmonary complications of the acquired immunodeficiency syndrome

Cardiac transplantation has evolved from an experiment to an accepted therapy for severe heart failure. Increasing competition for donor organs mandates a greater emphasis on selection and timing for transplantation and paradoxically forces more reliance on aggressive medical therapy for all patients after evaluation. The growth of recipient and donor pools may enhance the opportunity for assessing histocompatibility, for which distinguishing between autoantibodies and human leukocyte antigen-determined reactivity is important, and some general nonresponders may be detected. Therapy with cyclosporine has improved the outcome after transplantation, but further refinement is needed, perhaps with pharmacologic synergy, to minimize nephrotoxicity and maximize specific immunosuppression. Survival is more than 80% at 1 year, after which the incidence of acute rejection and infection declines and accelerated atherosclerosis becomes prominent. Although resuming employment is not always possible, the overall quality of life is excellent after cardiac transplantation.     

Morphological bases of liver insufficiency in the early stages of the prolonged crush syndrome

Light and electron microscopies were employed to examine liver of 45 rats and 20 dogs under 6- and 9-hour compression of soft tissues of the thigh and 2 to 7 hours after pressure was taken off. Morphology of liver microcirculatory disorders is presented, the incremental derangement of the cells of the reticuloendothelial system (RES) with the appearance of the signs of its function depletion after decompression is described. Alterations in the liver RES correlated with destructive changes in hepatocytes and their necrosis. The morphological alterations in the liver RES in the crush syndrome reflect the impairment of its barrier function. They may play a role in the impairment of liver regeneration processes and immunological homeostasis of the host.     

Disorder of electromechanical coupling in the cells of the myocardium in protracted crush syndrome

Experiments on papillary muscles of normal (control) rabbits and of those with the compression syndrome (CS) were made to explore the action of the control and "syndromic" blood plasma on electric and contractile activity of the myocardium. Isometric contractions of myocardial preparations were recorded at varying stimulation frequencies (0.1-2 Hz). Intracellular rest potentials (RP) and action potentials (AP) were led away with the aid of glass microelectrodes filled with 2.5 M KCl. The replacement of Tyrode solution by the control plasma raised the amplitude of papillary muscle contractions, that being greater as regards the muscles from rabbits with the CS. The "syndromic" plasma (diluted by Tyrode solution in a 1:1 ratio) markedly inhibited the amplitude of contractions of papillary muscles from both the control rabbits and animals with the CS. Reduction of the contractions induced by the "syndromic" plasma seen in all the preparations was followed by two patterns of changes in electrical activity of myocardial fibers. In one pattern, the RP, the amplitude and duration of the AP declined. In the other, on the contrary, the changes were reduced to a greater AP duration. The conclusion is made about the absence of a direct relationship between the decrease in myocardial contractility and changes in intracellular potentials induced by the "syndromic" plasma. It is suggested that the "syndromic" plasma deranges the process of stimulation and contraction coupling in heart papillary muscles.