SEARCH · PubMed Health
Results for “Shock, Traumatic”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
A summary of recent findings in intravascular treatment of post-traumatic shock and the relative value of isotonic sodium chloride and 5% glucose solutions in such conditions.
Explore the source record for details and available documents.
[Prophylactic principle and therapy of traumatic shock in peace time].
Explore the source record for details and available documents.
[Clinical problems of traumatic shock].
Explore the source record for details and available documents.
[On current questions on the problem of traumatic shock].
Explore the source record for details and available documents.
[Some problems in the therapy of traumatic shock. (Experimental study)].
Explore the source record for details and available documents.
[Prophylaxis and therapy of post-traumatic shock].
Explore the source record for details and available documents.
Intravascular agglutination of erythrocytes (sludged blood) and traumatic shock.
Explore the source record for details and available documents.
Protective actions of aprotinin in acute traumatic shock.
The effect of the protease inhibitor, aprotinin, was examined in rats during traumatic shock. In sham-operated control rats, intravenous administration of aprotinin (20,000 or 40,000 KIU/kg) showed no immediate changes in the mean arterial blood pressure and heart rate. In rats subjected to Noble-Collip drum trauma, aprotinin at a dose of 20,000 KIU/kg prolonged survival time to 2.1 +/- 0.3 hr (p less than 0.05) and 40,000 KIU/kg prolonged the survival time of rats to a greater extent (3.1 +/- 0.4 hr, p less than 0.001) compared to rats given only its vehicle (1.1 +/- 0.2 hr, mean +/- SE). The improved survival was accompanied by inhibition of the plasma accumulation of the cardiotoxic peptide, myocardial depressant factor (MDF). However, aprotinin showed no inhibitory effect on the plasma accumulation of the lysosomal enzyme, cathepsin D. Aprotinin has a beneficial effect on traumatic shock in rats possibly by its potent inhibitory action on MDF formation.
A new treatment for traumatic shock and ARDS.
Trauma causes more years of lost life than any other cause of death. Traumatic shock and sepsis are the most common late causes of death following trauma. Traumatic shock and sepsis cause multiple organ failure. The most common organ to fail is the lung, which develops Adult Respiratory Distress Syndrome (ARDS). ARDS can be caused by Disseminated Intravascular Coagulation (DIC) with microscopic clots in the lungs. Trauma causes hemolysis and the red cell stroma may initiate DIC. Plasminogen activators, which causes lysis of blood clot, can lyse pulmonary microthrombi and prevent the onset of ARDS even when given several hours after the trauma.
[Behavior of the vascular system and of cerebral nerve tissue in experimental traumatic shock; protective action of anesthesia].
Explore the source record for details and available documents.
[Acute renal insufficiency after traumatic shock and circumscribed bilateral necrosis of the renal cortex; relation between acute nephrosis and acute thrombotic necrotic angiopathy].
Explore the source record for details and available documents.
[Traumatic shock in relation to tissue pathology].
Explore the source record for details and available documents.
[Problem of traumatic shock and possibilities of its prevention behind the front line].
Explore the source record for details and available documents.
Efficacy of two leukotriene antagonists in rat traumatic shock.
The effects of CGP 33304 and CGP 35949 were studied in standardized model of traumatic shock. Both drugs are dual leukotriene receptor antagonists and phospholipase A2 inhibiting agents. Pentobarbital anesthetized rats (35 kg/mg) subjected to Noble-Collip drum trauma were characterized by a 128 +/- 16 min survival time and a 4-fold increase in plasma myocardial depressant factor (MDF) activity. CGP 33304 and CGP 35949 both significantly (p less than 0.01) attenuated the accumulation of MDF activity in the plasma (24 +/- 3 and 29 +/- 3 U/ml, respectively, vs. 57 +/- 5 U/ml in the trauma and vehicle group). A significant improval in survival time (p less than 0.05) was observed in the CGP 33304 treated group (182 +/- 23 min) and the CGP 35949 treated group (204 +/- 33 min). Both drugs exhibited significant anti-proteolytic activity in pancreatic homogenates. CGP 33304 and CGP 35949 appear to attenuate MDF production, probably secondary to their anti-proteolytic effect and the improved state of the splanchnic circulation. Both drugs also may prevent hypoxia secondary to leukotriene induced bronchoconstriction in shock states. CGP 33304 and CGP 35949 may, therefore, prove to be useful therapeutic agents in acute ischemic disorders including traumatic shock.
Efficacy of a combination thromboxane receptor antagonist and lipoxygenase inhibitor in traumatic shock.
The effects of a thromboxane receptor antagonist having lipoxygenase inhibitory activity, L-655,240 (3-[1-(4-chlorobenzyl)-5-fluoro-3-methyl-indol-2-yl]2,2-dimethylpropa noic acid) (1 mg/kg per h) were studied in a standardized model of traumatic shock. Pentobarbital (35 mg/kg) anesthetized rats subjected to Noble-Collip drum trauma were characterized by a 82 +/- 12 min survival time, a 20-fold increase in plasma cathepsin D activity, and a 6-fold increase in plasma myocardial depressant factor (MDF) activity. L-655,240 significantly attenuated the accumulation of MDF activity in the plasma (74 +/- 3 vs. 46 +/- 4 units/ml), vehicle vs. drug, respectively, and significantly (P less than 0.01) prolonged survival time to 206 +/- 26 min. However, plasma cathepsin D was not significantly altered with L-655,240 administration during traumatic shock. L-655,240 at 20 micrograms/ml markedly attenuated minced rat lung fragments from producing LTC4 and LTD4.L-655,240 exhibited significant anti-proteolytic activity in pancreatic homogenates. Therefore, L-655,2340 does not stabilize lysosomal membranes directly, but exerts an anti-proteolytic action which appears to curtail the production of a myocardial depressant factor by the ischemic pancreas, thus protecting during traumatic shock. A combination anti-eicosanoid drug such as L-655,240 may therefore prove to be an important therapeutic agent in acute ischemic disorders including traumatic shock.