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The dynamic properties of membrane protein are closely correlated to the membrane functions in erythrocytes. The anion transport function of band 3 protein, the constituents and the translational diffusion of membrane protein was detected in 25% TBSA burn rats. The changes in membrane protein SH were investigated by using the spin label of 3-maleimide-proxyl. The results showed that, in delayed fluid resuscitation group after burn shock, membrane crosslinking protein appeared in erythrocytes, the function of band 3 protein was damaged, the recovery time after fluorescence photobleaching of membrane protein was obviously prolonged, and the ratio of peak heights of strong to weak immobilization was increased, especially in the six-hour delayed resuscitation group, suggesting that the ischemia-reperfusion injury was more serious during the early shock stage. The authors believe that the results may represent the mechanism of damage biological membrane after burns. The alterations of membrane properties caused by free radicals play an important role in erythrocyte injury.

Immunosuppression following injury influences infectious morbidity and mortality. Impaired T-cell activation conceding to inadequate antigen recognition contributes to this immunosuppression. Successful activation and proliferation of T-cells requires precisely specified levels of intracellular calcium thresholds and peak signals. The purpose of this study was to evaluate intracellular calcium signaling following injury. Hospitalized blunt and penetrating trauma patients in a Level 1 Trauma Center following injury and sepsis were tested for immune cell calcium signaling. Peripheral blood mononuclear cells (PBMC) were isolated and calcium signaling tested with Fura-2 AM. PBMC from trauma patients had significantly depressed values of baseline, peak and sustained levels of intracellular calcium prior to and following phytohemagglutinin stimulation when compared to normal controls. This deficit in intracellular calcium signaling is more severe in septic trauma patients (60% reduction). Suppression of calcium signaling appears to be mediated by at least, in part, circulating serum factors. Prostaglandin E2 seems to have a limited contribution to this effect as it is suppressive only when in direct contact with PBMC. Immune cell activation failure can in part be explained by the inadequacy of calcium signaling; restoration of immunocompetence following trauma will have to be addressed by strategies to restore calcium signaling, a vital step necessary for T-cell proliferation following antigen recognition.

Dynamic changes of contents of beta-endorphin, leu-enkephalin and oxytocin in plasma were determined in seventeen fracture patients with shock, fascial space syndromes, or infection postoperation. There was significant rise of contents in beta-endorphin and leu-enkephalin but not in oxytocin after trauma, Of those accompanied by infection postoperation, beta-endorphin and oxytocin remained high. The contents of beta-endorphin and enkephalin decreased gradually in non-infectious group, but were still higher than normal. The most obvious change was seen in beta-endorphin, suggesting that beta-endorphin plays a more important role in trauma. This was also confirmed in rat injury model.

The anion transport property is the one of the most important functions of the erythrocyte. In this paper a new method is used to measure the NO2- and Cl- ions transport across the erythrocyte membrane in burned rats. It was found that the NO2- and Cl- transport rate across erythrocyte membrane became slower during shock stage in burned rats, being contrary to the results found in heat-treated erythrocytes in vitro. By using a specific inhibitor of anion transport, DIDS, it was shown that the abnormality of NO2- transport across the erythrocyte membrane in burned rats is due probably to a damage of extracellular domain of band 3 protein. The authors consider that the influence of membranotoxic factors and the disturbance of energy metabolism during burn shock stage are accounted for all the noticed alterations.

Sixty seven burn patients (TBSA > 30%) were entered in a prospective study. Among them, twenty seven experienced delayed fluid resuscitation (DFR group) and the rest had early resuscitation (non-DFR group). Oxygen free radical (OFR) content in the blood was measured with ESR technic, and levels of blood SOD, blood GSHpx, serum MDA were also determined. The results showed: 1 The morbidity and mortality of burn shock and MSOF were higher in DFR group as compared with non-DFR group. 2 There was a significant increase of blood OFR content subsequent to resuscitation in DFR group as compared with that in non-DFR group. 3 The level of MDA in the serum of patients with burn shock was higher in DFR group than that in non-DFR group. 4 In DFR group, the level of serum MDA is higher in patients who developed MSOF as compared with that in patients who did not develop MSOF. The data indicated that DFR augmented the morbidity and mortality of burn shock and MSOF, in which OFR might play a role.

Objective: To examine plasma atrial natriuretic factor activity during hypovolemia and after vascular volume replacement., Design: Prospective, descriptive study., Settings: Scene of emergency, Emergency Department, and the ICU of a university hospital., Patients: A total of 47 trauma patients with evidence of hypovolemia were grouped according to their major injury into a thoracic injury group (15 patients; mean Injury Severity Score = 38.5 +/- 3.1 [SEM], Hospital Trauma Index = 14.1 +/- 0.7), an abdominal injury group (14 patients; Injury Severity Score = 36 +/- 3.3, Hospital Trauma Index = 14 +/- 0.9), and a severe head injury group (18 patients; Injury Severity Score = 23 +/- 1.5, Hospital Trauma Index = 10 +/- 0.6)., Measurements and Main Results: Measurements were taken at the scene of emergency; after volume replacement in the Emergency Department; and after 3, 7, 12, 24, 36 hrs and on day 5 in the ICU. In all groups, the average plasma atrial natriuretic factor levels were increased at the scene of emergency and declined significantly to normal values with volume replacement. In the thoracic injury group, plasma atrial natriuretic factor activity decreased from 253 +/- 73 to 115 +/- 83 pg/mL (p less than .0017); in the abdominal injury group, plasma atrial natriuretic factor activity decreased from 194 +/- 42 to 91 +/- 24 pg/mL (p less than .006); in the severe head injury group, plasma atrial natriuretic factor activity decreased from 167 +/- 28 to 70 +/- 13 pg/mL (p less than .02) with volume replacement. Plasma atrial natriuretic factor levels at the scene of emergency were significantly (252 +/- 73 vs. 167 +/- 28 pg/mL; p less than .05) higher in the thoracic injury group and in the abdominal injury group (194 +/- 42 vs. 167 +/- 28 pg/mL; p less than .05), as compared with the severe head injury group., Conclusions: In trauma patients, plasma atrial natriuretic factor concentrations were markedly increased in patients with untreated hypovolemia and were decreased to normal values with vascular volume replacement. Thus, atrial natriuretic factor seems to play an important physiologic role during hypovolemia.

Hyaluronan (HYA) is an ubiquitous polysaccharide in connective tissue interstitium; its normal plasma concentration is in the nanogram/ml range. Following major burn injury in sheep, plasma HYA can increase to levels tenfold greater than normal. The present study aimed to determine the effects of major cutaneous burns on plasma HYA concentration in rat, since in this species, the HYA elimination kinetics may better resemble those in man. Thermal injury did not alter the weight-average molecular weight of HYA in skin. HYA concentration in plasma was 46 +/- 4 ng/ml (mean +/- SEM) in controls. Three hours after scald burns to 40% of the body surface area, plasma HYA was 61 +/- 10 ng/ml in unresuscitated animals (P less than 0.1 vs. controls). After fluid replacement by lactated Ringer's plasma HYA was 75 +/- 8 ng/ml (P less than 0.01 vs. control), whereas plasma infusion prevented the elevation of plasma HYA. HYA also increased significantly after lactated Ringer's infusion in noninjured animals. The increased plasma concentration of HYA after major burns is probably a consequence of increased lymph flow, increasing its transport from skin interstitium. Possibly, plasma concentrations of connective tissue components may be used as indicators of the severity and extent of burn injuries.

The influence of thyroid hormones and vasopressin on lipid peroxidation (LP) in the rat kidneys in the posttraumatic period has been investigated. The rats with more pronounced disturbances of renal concentration mechanisms had a more increased LP, especially in the renal cortex. It is typical, that in some cases vasopressin levels did not correlate with the values of concentration index. A decrease in the affinity of the collecting duct cells to vasopressin may be a disturbance of renal concentration mechanisms in the posttraumatic period. It is found, that the character of thyroid hormones action on LP in renal tissue can be determined by tri- and tetraiodthyronine ratio.

The interrelations of changes in plasma fibronectin (FN) level, hemostatic parameters and RES function were studied in the time course of traumatic or burn disease. A combination of interdependent disorders in the systems studied reflecting features of varying periods of extreme states was established in rat experiments. The analysis of the data obtained has suggested that FN is involved in the pathologic process and participates in the pathogenesis of shock and its complications by interacting with hemostasis and RES as a mediator thus playing an important role in maintaining the level of nonspecific body resistance.

An analysis of serum free amino acid profiles in 8 patients dying from major burns revealed that free amino acid began to decrease in shock period, decrease 31.12% in infection period and 41.3% before death in comparison with the control group. The amount of BCAA-also decrease 36.27% in infection period and 56.83% before death. If the serum free amino acid in major burn drops steadily, the prognosis will be worse.

We evaluated the potential side effects of rapidly infusing 250 mL of either 7.5% sodium chloride or 7.5% sodium chloride per 6% dextran 70, using lactated Ringer's as the control, to 106 critically injured patients in two prospective double-blinded emergency department trials. Eight patients had a significant hyperchloremic acidemia in association with infusion of the hypertonic solutions, but all eight were moribund before infusion and many factors other than hyperchloremia could have contributed to their acidemia. Other blood chemistry changes that might have been associated with the hypertonic solutions, such as hyperosmolality or hypernatremia, were made insignificant by other factors, such as high blood alcohol levels or concomitant administration of sodium bicarbonate. There were no cases of central pontine myelinolysis; bleeding was not potentiated. There was no difficulty with crossmatching of blood. No anaphylactoid reactions occurred. In a setting of limited volume resuscitation, the solutions are likely to have a favorable risk-to-benefit ratio.

It was established that the activity of trypsin and the content of its inhibitors--alpha 1-inhibitor of proteinases and alpha 2-macroglobulin--undergo phase changes of different meaning and direction with the gradual development of traumatic shock. The character of these changes indicates that trypsinemia is an important pathogenetic link of traumatic shock and corresponds to its severity. The compensatory activation of the trypsin inhibitors is directed to increasing the resistance of the body to trypsinemia. Deficiency of the inhibition system leads to activation of organic proteolysis and growth of the content of middle-molecular peptides in the blood. Such a character of homeostasis disorders substantiates the need for the search for effective measures of correction of the trypsin-antitrypsin system and freeing the organism of the excess of middle-molecular molecules.

Eighteen infants with compression syndrome (CS) were managed with simultaneous evaluation of changes in the blood colloid osmotic status. The examination findings showed that plasma osmolality is an integral index of endogenous intoxication which objectively reflects the gravity of the general condition of patients and requires adequate correction. The osmolality gap was measured by the difference between the measured and calculated osmolalities; its stable two- or threefold increase was found to be the most unfavourable factor in the disease course and prognosis. It was found that control of osmotic homeostasis in infants with CS is essential to decide that extracorporeal blood clearance techniques be used and to elaborate effective infusion therapy programmes.

A hemorrhagic-traumatic shock model in 20 domestic pigs (Sus scrofa) was used to evaluate the pharmacologic effect of methylprednisolone in preventing disseminated intravascular coagulation (DIC). Pairs of animals were anesthetized with thiopental and both femoral arteries cannulated. Four ml/kg-1 of blood were withdrawn, frozen, thawed, and returned to the animal. One femoral artery cannula was connected to a blood pressure monitor for arterial systolic, diastolic, and mean pressures along with heart rate and ECG. The other catheter was used to bleed the animal down to and maintain a mean arterial pressure of 50 mm Hg for 2 hours. Blood samples were taken during the control period before bleeding, and at the end of the 2-hour shock period. Blood samples were analyzed for prothrombin time, partial thromboplastin time, fibrinogen level, and platelet count. The combination of hemorrhagic shock and hemolysis produced DIC and a fatal shock. Pharmacologic doses (30 mg/kg-1) of methylprednisolone significantly prevent the DIC.

In stress-resistant animals exposed to 5-minute immobilization, the metabolic reaction of leukocytes was marked by an increase in the activity of G-6-PDH, hexokinase (HK), cytochrome oxidase (CCO) accompanied by a decrease in the activity of succinate dehydrogenase (SDH). In stress-labile animals, there was a decrease in the activity of G-6-PDH, HK, CCO with an increase in the activity of SDH. The orientation of enzymatic processes in leukocytes of stress-labile animals after immobilization and of stress-resistant animals following intravenous injection of propranolol was discovered to be similar. After propranolol injection leukocytes did not show any glucose, while the activity of G-6-PDH, HK and CCO descended. Injection of propranolol decreased the animal's resistance to traumatic shock. In stress-resistant animals exposed to trauma after the blockade of beta-adrenoreactive structures, the metabolic reaction was marked by low mobility restitution of energy processes as was the case in stress-labile animals during the development of a severe shock.

The blood of healthy men and patients with methemoglobinemia of different genesis was incubated with chromosmon, ascorbic acid, riboflavin and glutathione, the percentage of erythrocytes with thorn-shaped protuberances-echinocytes being subsequently determined in the blood smears. The absorbtion spectra at the range 400-650 nm were investigated both in the smooth erythrocytes and in echinocytes. A correlation was found between the percentage of echinocytes and the methemoglobin content in the blood. The methemoglobin amount in the echinocytes was determined to be higher than in the smooth erythrocytes. It is discovered that effects of chromosmon, glutathione and riboflavin on production of methemoglobin depend on the dose, individual peculiarities of erythrocytes and on the illness that caused methemoglobinemia. The calculation of echinocyte percentage may be used as an express-diagnostics of methemoglobinemia and for purposes of studying the effect of methemoglobin-producing substances and drugs.

Plasma adrenaline and noradrenaline concentrations and dopamine-beta-hydroxylase activities were measured in patients with septicaemic, traumatic or haemorrhagic shock. Irrespective of the type of shock plasma adrenaline and noradrenaline concentrations were increased above the normal range. This is in keeping with the clinical features of increased sympathetic nervous system and adrenal medullary activity present in these patients. Plasma dopamine-beta-hydroxylase activities were within the normal limits in all forms of shock indicating the poor relationship of this measurement to sympathetic nervous system activity. In patients who died plasma noradrenaline concentrations remained persistently elevated above normal while in those who survived there was a rapid decline towards the normal range.

On the basis of experimental and clinical studies the authors recommend to use mebikar with promedol in complex with other drugs for the treatment of traumatic shock in the prehospital and hospital periods. It was found to substantially improve results of the antishock therapy.

The effect of alcohol upon admission serum insulin levels was studied in 114 injured patients with mean blood alcohol levels of 130 +/- 71 milligrams per deciliter, ranging from 10 to 350. These data were compared with those of 133 similar patients with no measurable blood alcohol levels and with those of 47 healthy volunteers. Whereas marked hyperglycemia caused by trauma or shock was unaffected by alcohol ingestion, insulin levels were more depressed in patients with blood alcohol levels 29.5 +/- 15.3 microunits per milliliter versus 37.8 +/- 36.7 microunits per milliliter, p less than 0.025. In fatally injured patients with measurable alcohol concentrations, insulin and glucose levels were markedly different from those for the corresponding surviving patients, p less than 0.001 and less than 0.01, respectively, with particularly large differences in the insulin-glucose ratio, p less than 0.001. The spontaneous reappearance of the insulin response to hyperglycemia was dependent upon the elapsed time and the severity of injury. Regardless of the blood alcohol concentrations, in patients admitted within two hours, there was no correlation between the levels of insulin and glucose. In patients admitted within two to eight hours, a significant correlation was found only in those with no detectable alcohol blood levels, p less than 0.001. In addition, a remarkable similarity of mean different admission times. These findings suggest that, in alcohol intoxication, recovery of insulin secretions suppressed by acute trauma is delayed; metabolism of alcohol in acute trauma is probably reduced.

A relationship has been established between varying metabolic response of leukocytes to immobilization stress and severity of the shock progress. Initiation of the shock is accompanied by different response of animal leukocytes that correlates with the severity of the subsequent process. Formation of the resistance to shock is associated with an active glucose involvement into energy and plastic metabolic reactions, activation of the substrate-enzymic systems of glycolysis, pentose shunt, terminal stage of the respiratory chain, decreased rate of succinte dehydrogenation.

The article analyzes changes in the protein metabolism of the organism of patients with associated trauma followed by shock. It was found that during shock and postshock period (as long as 14 days after trauma) of the traumatic disease hypoproteinemia was developing with the degree proportional to the severity of shock. To normalize protein metabolism it is necessary, in addition to a wide use of transfusions of blood and protein hydrolysates, to use protein mixtures (food concentrates) for oral feeding of critical patients in the complex of simultaneous measures directed to valuable correction of systemic and organic hemodynamics during this period.

The blood fibronectin concentration in rats was measured by the ELISA during burn shock. Fifteen minutes after burn the fibronectin level was found to drop by 30% of the initial level on the average. Deep hypofibronectinemis lasted up to 24 h after burn. At the same time the clinical and pathomorphological picture of the shock was fairly pronounced. The survived animals demonstrated a progressive normalization of the fibronectin level. The fibronectin level completely returned to normal by the outcome of the second day after burn and then progressed to reactive hyperfibronectinemia by 70-72 h. The data obtained point to the involvement of fibronectin into the pathogenesis of burn shock, which is likely to be connected with the mechanism of reticuloendothelial system dysfunction.

Inconsiderable hyponatremia and pronounced hypopotassemia were found to accompany the shock. In a mild course of the traumatic disease the concentration of natrium in blood plasma was restored within 3--6 days, potassium within 7--10 days after trauma, and in a grave course hypopotassemia retained for about 14 days. More continuous use of the infusion therapy including potassium and natrium was found to be expedient.

A major controversy in the treatment of the Adult Respiratory Distress Syndrome (ARDS) is the role of steroids, which may attenuate permeability as well as pulmonary vascular resistance (PVR). Empirically methylprednisolone (MP) in high doses (30 mg/kg) has been "the steroid of choice" in clinical practice. By autoradiography MP has been shown to penetrate more easily into lung tissue than other steroids tested. MP prevented the late phase increase in lung vascular permeability to endotoxin in sheep, whereas the inhibition of the pulmonary hypertensive response was far less pronounced. In human septic ARDS MP reduced both PVR and the increased vascular permeability. However, a few patients characterized by more severe ARDS did not respond to MP. There is some evidence that steroids may modulate both pre- and postcapillary vasomotion in the lungs. MP was found to inhibit pulmonary venoconstriction as well as pulmonary erythrocyte sludging in canine hemorrhagic shock. Oleic acid induced edema also appears to be attenuated by MP. This effect is partly due to a lowering of hydrostatic pressure in the lung capillaries, because MP blocks the downstream resistance increase. Hypoxic pulmonary vasoconstriction has predominantly a precapillary localisation. MP inhibits hypoxic vasoconstriction in a dose-dependent fashion in isolated rat lungs, but does not cause a general dampening of vascular reactivity, as the pulmonary constrictor response to angiotensin II is unchanged. However, MP inhibits histamine-induced vasoconstriction in isolated canine lung lobes. The increased vascular resistance in atelectatic lungs is also inhibited by MP. Corticosteroids may alter the reaction of the pulmonary vasculature to various stimuli or agents by influencing the release of mediators, for instance, the cyclooxygenase and lipoxygenase products of arachidonic acid, modulate the action of mediators, reducing the activation of leukocytes and/or platelets, or changing the state of the pulmonary vascular muscle cells. Which mechanisms are active in the various situations are at present objects of pure speculation. However, in most situations with ARDS a reduction in pulmonary arterial pressure and PVR may be regarded as beneficial.

In the experimental dogs and healthy humans it was shown that calcium ions promote activation of the adrenal glucocorticoids function, which duration is dependent on the day time. In patients the influence of calcium ions on the blood 11-hydroxycorticosteroid concentration is dependent on the initial steroid level and concentration of injected calcium chloride solution. The infusion of 1% calcium chloride solution exerted a stable effect. Possible mechanisms of the changes observed are discussed.