Hyperbaric oxygenation in the comprehensive therapy of young and middle age patients in the acute period after mild craniocerebral trauma]

The results of treatment of 107 young and middle aged sufferers with mild craniocerebral trauma have been analysed. The regimen for use of hyperbaric oxygenation contributing to normalization of general cerebral, focal disorders in high nervous and psychic activity, prevention of certain posttraumatic complications has been developed.     

Alternative pathway complement activation induces proinflammatory activity in human proximal tubular epithelial cells

Background. Proximal tubular epithelial cells express a surface C3-convertase activity which induces C fixation and insertion of the C5b-9 membrane attack complex (MAC) into the cell plasma membrane. The physiopathological consequences of this phenomenon are unknown. Methods. The effect of C fixation on the production of inflammatory mediators by human proximal tubular epithelial cells in culture was explored. Results. Proximal tubular epithelial cells incubated with a sublytic amount of normal human serum as a source of C, but not with heat-inactivated human serum, showed a time-dependent calcium influx and a concomitant release of ¹⁴C-arachidonic acid (¹⁴C-AA). Eicosanoid synthesis following the arachidonic acid mobilization was studied as prostaglandin E2 release. Mg²⁺/EGTA, which did not prevent C activation by the C3-convertase, and p-bromodiphenacyl bromide, a phospholipase A2-inhibitor, inhibited mobilization of ¹⁴C-AA. These results suggest the activation of an extracellular Ca²⁺-dependent, phospholipase A2. Complement fixation was associated with the synthesis of proinflammaotry cytokines such as IL-6 and TNF-&agr;. Experiments with C6-deficient sera indicated that the release of ¹⁴C-AA and the production of cytokines were dependent on the insertion of the terminal components of complement in the plasma membrane. Indeed, the reconstitution of normal haemolytic activity of C6-deficient sera with purified C6 restored also the release of ¹⁴C-AA and the production of cytokines. Conclusion. In vitro complement activation on the proximal tubular cell surface triggers the generation of proinflammatory mediators, which may potentially contribute to the pathogenesis of tubulointerstitial injury.     

A comparative analysis of radiological and surgical placement of central venous catheters

Purpose To compare the differences in practice and outcome of all radiologically and surgically placed central venous catheters retrospectively over a 2-year period simultaneously, at a single institution. Methods A total of 253 Hickman catheters were inserted in 209 patients; 120 were placed radiologically in 102 patients and 133 were placed surgically in 107 patients. The indication was chemotherapy in 76% of radiological and in 47% of surgical cases; the remainder were for total parenteral nutrition and venous access. Results There were 6 (4.5%) primary surgical failures and a further 17 (13%) surgical cases requiring multiple placement attempts. Pneumothorax occurred once (0.8%) surgically and four times (3.3%) radiologically. There were no radiological primary misplacements but there were five (3.7%) surgical ones. Catheter or central vein thrombosis occurred in four (3.3%) radiological and five (3.7%) surgical cases. The rate of infection per 1000 catheter-days was 1.9 in radiologically placed catheters and 4.0 in surgically placed ones (p<0.001). Average catheter life-span was similar for the two placement methods (100±23 days). Conclusion Radiological placement is consistently more reliable than surgical placement. There are fewer placement complications and fewer catheter infections overall.     

Regulation of the water-electrolyte balance during neurosurgical operations with balanced anesthesia using sodium oxybutyrate]

Water-electrolyte homeostasis and its basic regulatory hormones have been studied in 36 patients with neurosurgical brain pathology during surgical interventions performed under balanced anesthesia (sodium hydroxybutyrate combined with NLA drugs). The study has revealed 3 types of reactions in hormones regulating water-electrolyte homeostasis: type I--a decrease in vasopressin (VP) concentration and renin-angiotensin-aldosterone system (RAAS) activity; type II--VP increase and RAAS activation; type III--an increase in VP content and RAAS disbalance. It has been shown that type I reaction is accompanied by marked osmotic disturbances. The impact of sodium hydroxybutyrate on RAAS is manifested in aldosterone secretion suppression.     

Trends in perinatal, neonatal and post-neonatal mortality in Austria and Tyrol, with special reference to 1979-1988]

Analysis of neonatal, perinatal and infant mortality rates is a useful basis to compare the quality of neonatal care in a country. During the last decades these parameters have been falling steadily in Austria as well as in other industrialized countries. Regarding the various provinces of Austria substantial regional differences occur. Apparently the decline in mortality rates is not only contributable to medical progress but as strongly influenced by social and economic changes. In the mid-seventies absolute and relative neonatal mortality rates in Austria definitely decreased, most probably attributable to the installation of neonatal intensive care units. During 1968-1978 the decrease in neonatal mortality was mainly due to reduced first-day-mortality, whereas during the following decade it was mainly due to reduced mortality of the 2nd until 7th day of life. Interestingly, the rate of preterm infants in Austria remained virtually constant during 1968-1988 despite improved pre- and perinatal care. Paralleling the development in full-term neonates the peri-/neo- and postneonatal mortality rates of preterm infants decreased. Predictably - as in other countries - the highest improvement was found in the low birth weight groups Nevertheless, premature births have accounted for the majority of neonatal and perinatal deaths.     

Successful Treatment of Kasabach-Merritt Syndrome with Prednisone and Epsilon-Aminocaproic Acid

The Kasabach-Merritt syndrome is characterized by thrombocytopenia and localized coagulopathy associated with a hemangioma. Most techniques applied to eradicate the tumor or accelerate its involution (surgery, radiation therapy, embolization) are invasive and require transfusion of large amounts of blood products. In some cases, medical treatment is the only alternative. Efficacy of steroids and antifibronolytic agents has already been described, but even this approach is associated with the administration of blood products. We report two cases of infants with Kasabach-Merritt syndrome associated with cardiac and hepatic hemangiomas. At admission, both had signs of cardiac failure. They were successfully treated with prednisone and epsilon-aminocaproic acid (EACA). Blood products were not required once the diagnosis was made. These observations have important implications for the management of patients with Kasabach-Merritt syndrome because they show that even in severe cases blood transfusions can be avoided by the use of prednisone and EACA.     

Evaluating risk adjustment by partitioning variation in hospital mortality rates

The variation in mortality rates among hospitals has often been described informally as having three major components: patient severity, quality of care and random variation. These informal concepts are characterized formally by partitioning sums of squares and finding their expected values. The partition relates to commonly used tests for whether individual hospitals have unusual mortality rates. Application of the partition to the hospital mortality reports by the Health Care Financing Administration shows that their models for patient risk account for about one-half the variation among hospital mortality rates. An example using clinical measures of severity accounts for about two-thirds of mortality variation among hospitals.     

Chronic Administration of Glucocorticoids Directly Upregulates Prepro-Neuropeptide Y and Y1-Receptor mRNA Levels in the Arcuate Nucleus of the Rat

The complete sequence of the cDNA encoding the neuropeptide Y (NPY) Y₁-receptor has recently been deduced from a rat brain library, and the presence of messenger ribonucleic acid (mRNA) encoding Y₁-receptor protein has been demonstrated within the brain. Using quantitative in situ hybridization histochemistry, the content and distribution of Y₁receptor and preproNPY mRNAs have been investigated in the hypothalamic arcuate nucleus of adrenalectomized rats receiving glucocorticoid replacement therapy for 12 days by means of either high doses of dexamethasone in their drinking water or by subcutaneous corticosterone pellets. Basal metabolic parameters such as weight gain or loss, blood glucose and plasma insulin were monitored: Dexamethasone treatment induced weight loss and a state of hyperinsulinemia with normoglycemia, while corticosterone treated animals displayed metabolic parameters identical to sham ADX animals. Within the arcuate nucleus of glucocorticoid treated animals, levels of Y₁receptor and preproNPY mRNAs were increased. In contrast, adrenalectomy itself had no effect upon Y₁-receptor mRNA levels or preproNPY mRNA levels in the arcuate nucleus. These studies demonstrate that glucocorticoids exert a stimulatory action on levels of Y₁-receptor mRNA and preproNPY mRNA levels in the hypothalamic arcuate nucleus. This is the first evidence to suggest that the expression of a neuropeptide-receptor gene in the central nervous system may be directly sensitive to peripheral hormonal signals.     

Generation of nitric oxide from organic nitrovasodilators during passage through the coronary vascular bed and its role in coronary vasodilation and nitrate tolerance

This study investigated the release of nitric oxide (NO) from glyceryl trinitrate (GTN) and SIN-1 in Langendorff rabbit hearts. Infusion of either GTN (10-40 microM) or SIN-1 (0.45-4.5 microM) into the coronary inflow tract resulted in a decrease in coronary perfusion pressure and NO release (oxyhemoglobin technique) into the coronary effluent. NO release from SIN-1 occurred spontaneously whereas passage through the coronary circulation, i.e. active metabolism, was required for NO release from GTN. Removal of the coronary endothelium and blockade of endothelial NO formation did not affect NO release from GTN and SIN-1. In GTN-tolerant hearts, there was a considerable inhibition of GTN- but not SIN-1-induced NO formation and coronary vasodilation. These data suggest (1) that metabolic NO release from GTN occurs during passage of the coronary circulation and is independent of the presence of endothelium, and (2) reduced NO release is a major cause of nitrate tolerance.