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Results for “SHOCK, TRAUMATIC”

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At least 19 recordsLinked to original sources
PubMedDate not supplied

Effect of recombinant soluble P-selectin glycoprotein ligand-1 on leukocyte-endothelium interaction in vivo. Role in rat traumatic shock.

-Traumatic shock induces profound pathophysiological alterations and initiates inflammatory reactions in many tissues, thus resulting in acute multiple organ damage (eg, intestine, pancreas, and liver). In the rat, Noble-Collip drum trauma increases P-selectin expression on the vascular endothelium as a result of loss of endothelium-derived NO. Here we postulated that blockade of the earliest steps in leukocyte adhesion (ie, leukocyte rolling) via administration of a recombinant soluble form of P-selectin glycoprotein ligand-1 (PSGL-1; the recombinant soluble form is rsPSGL.Ig) would attenuate selectin-mediated events observed in the rat during traumatic shock. Using intravital microscopy of the rat mesenteric microvasculature, we found that intravenous infusion of rsPSGL.Ig significantly inhibited leukocyte-endothelium interaction (ie, leukocyte rolling, adherence, and transmigration) induced by traumatic shock as well as by activation of the microvascular endothelium with 50 micromol/L NG-nitro-L-arginine methyl ester. Immunohistochemical detection of P-selectin on the mesenteric venular endothelial surface demonstrated that rsPSGL.Ig functionally neutralizes effects of P-selectin on the endothelial cell surface rather than attenuating P-selectin expression. Systemic administration of rsPSGL.Ig to traumatized rats prolonged survival time and survival rate, significantly attenuating ileal myeloperoxidase activity and significantly preserving mesenteric endothelial function. Furthermore, PSGL-1 mRNA levels were significantly increased in the blood of traumatized rats and were reduced after systemic administration of rsPSGL.Ig. Thus, soluble recombinant forms of PSGL-1 are able to ameliorate acute shock states by suppressing selectin-mediated leukocyte-endothelium interaction at both the functional and molecular levels.

Acetylcholine↗
PubMed1996

Time course of endothelial dysfunction and neutrophil adherence and infiltration during murine traumatic shock.

Traumatic shock in rats has been shown to induce endothelial dysfunction, and to increase intestinal myeloperoxidase activity (MPO) indicative of neutrophil infiltration. To examine the time course of endothelial dysfunction and neutrophil adherence and infiltration, pentobarbital anesthetized rats, subjected to Noble-Collip drum trauma, were studied prior to and 15, 30, 60, 90, 120, 150, and 180 min following drum trauma. Superior mesenteric artery rings obtained from traumatized rats were tested for responsiveness to acetylcholine (ACh), a receptor-mediated endothelium-dependent vasodilator, and to NaNO2 an endothelium-independent vasodilator. ACh-induced relaxation was not impaired immediately after the induction of trauma (time 0). However, 15-30 min after trauma, responses to ACh were significantly depressed (p < .05) and were further reduced (p < .01) 90-180 min after trauma. No significant changes occurred in response to the direct vasodilator NaNO2 at any of the times studied, indicating no vascular smooth muscle injury. Moreover, the adherence of polymorphonuclear leukocytes (PMNs) to the post-traumatic mesenteric vascular endothelium also showed an increase that peaked 30 min post-trauma. Intestinal MPO activity, indicative of neutrophil infiltration, was characterized by a continuous and sustained increase from 30-180 min. Our findings suggest that endothelial dysfunction resulting in reduced NO release occurs in the early phase of murine traumatic shock, and that this phenomenon is followed by a time-dependent increase in adhesivity of neutrophils to the vascular endothelium leading to a progressive accumulation of PMNs in injured tissues (e.g., intestine).

Animals↗
PubMed1984

Beneficial effect of a thromboxane synthetase inhibitor in traumatic shock.

Traumatic shock was induced in anesthetized rats using the Noble-Collip method. This resulted in an abrupt decline in mean arterial blood pressure (MABP) and heart rate. Plasma cathepsin D activity increased sixfold, plasma thromboxane B2 (TxB2) concentration increased 2.5-fold, plasma myocardial depressant factor (MDF) activity increased 3.5 fold, and the mean survival time was 1.4 +/- 0.2 hours. Administration of the selective thromboxane synthetase inhibitor 5-(3-pyridinylmethyl) benzofuran-2-carboxylate (U-63,557A) (4 mg/kg) resulted in a significant improvement in survival time, 3.3 +/- 0.5, p less than 0.01. Plasma cathepsin D activity was not affected by U-63,557A (7.4 +/- 0.8 vs. 8.5 +/- 1.1 U/ml). However, both plasma and peritoneal fluid TxB2 concentration were significantly reduced and accumulation of the toxic peptide, MDF, was significantly blunted (69 +/- 6 vs. 40 +/- 5 U/ml, p less than 0.01). Our data indicate that blockade of thromboxane A2 (TxA2) production by selective synthetase inhibition is beneficial in trauma and support a role for TxA2 in the pathogenesis of circulatory shock.

Animals↗
PubMedDate not supplied

[Application of the principles of the systemic approach to interpretation of the pathogenesis of traumatic shock and traumatic disease].

Experimental and clinical studies for many years led the authors to the conclusion that systemic approach seems most adequate for current interpretation of pathogenesis of traumatic disease (TD) and its component--traumatic shock (TS). It seems valid to assess TD and TS severity and dynamics by the proportion of pathological and adaptive reactions. Drugs should be used for maintenance and stimulation of adaptive reactions. Strong correlations of dynamics and severity of TD and TS enable prediction of TD course and outcome in acute period by time criterion (+)-T and distinguish three degrees of TD severity as well as evaluation of probability of favorable or unfavorable (lethal) outcome.

Adaptation, Physiological↗
PubMed1990

Physiologic response to traumatic shock.

Traumatic injury results in major physiologic alterations that begin at the time of injury and persist until recovery is complete. The response of the body is divided into two phases--the acute phase and the flow phase. The acute phase is characterized by shock with changes in hormone concentration. These hormones, either alone or in combination, result in lipolysis, amino acid release, gluconeogenesis,, and glycolysis. The flow phase of injury is a catabolic process that is characterized by an increased protein metabolism. Hypermetabolism and increased nitrogen losses are seen. The magnitude of these alterations is directly related to the severity of injury. Tissues with the highest oxygen consumption are more susceptible to injury and death. Cellular function does not depend on oxygen alone but also on the ability of the cells to use available oxygen. If the body is unable to compensate through biochemical, hormonal, and metabolic activities, an irreversible state results unless appropriate interventions are instituted promptly.

Humans↗
PubMed1997

P-selectin is up-regulated in vital organs during murine traumatic shock.

Murine traumatic shock is associated with increased adherence of neutrophils to the vascular endothelium resulting in neutrophil infiltration and tissue damage. We examined the effects of trauma on the expression of the adhesion molecule P-selectin in several vital organs (i.e., heart, lungs, liver, kidneys, and small intestine) 2 h after induction of Noble-Collip drum trauma in anesthetized rats. Total RNA was extracted from these organs and P-selectin mRNA was quantified by RNase protection assays. P-selectin mRNA was significantly increased over control nontraumatized, anesthetized rats in all vital organs (P<0.05 or less), with the largest increase occurring in the lung (P<0.01). Immunohistochemical analysis showed increased expression of P-selectin protein in postcapillary venules of all vital organs after trauma. To further investigate the possible mechanisms of increased P-selectin mRNA transcription promoter activity during trauma, we quantified binding of proteins from nuclear extracts to the kappaB site (-218GGGGGTGACCC[-207]) of the P-selectin gene by electrophoretic mobility shift assay. We confirmed the results of NF-kappaB binding by demonstrating increases in p50 and p52, as well as decreases in IkappaB in cytoplasmic and nuclear extracts from the lungs of trauma rats by Western blotting. Increased activity of the transcription factor, nuclear factor kappaB (NF-kappaB), occurred in all vital organs of the trauma rats compared to sham-operated controls. Our findings suggest that severe trauma results in up-regulation of P-selectin at the transcriptional level, which is partly controlled by an NF-kappaB-responsive element in the region of the P-selectin promoter. This increased activation of NF-kappB binding may contribute to the widespread increases in P-selectin expression observed in several vital organs 2 h after trauma, which in turn may play a key role in the pathogenesis of traumatic shock.

Animals↗
PubMedDate not supplied

Comparison of bacterial translocation during traumatic shock and hemorrhagic shock in rats.

UNLABELLED: Traumatic shock has been classified as a kind of hypovolemic shock similar to hemorrhagic shock. Since bacterial translocation has been observed in shock, this study investigated the difference in bacterial translocation during traumatic shock and hemorrhagic shock, and considered this effect on lung injury during sepsis. METHODS: Forty-eight male or female Sprague-Dawley rats were divided into 2 groups, hemorrhagic shock and traumatic shock. Bacterial translocation, endotoxin, and blood gas were evaluated. Alterations of the lungs morphologically and functionally were observed. RESULTS: Traumatic shock induced more bacterial translocation and endotoxemia from the gut. Blood gas analysis shows a more severe disorder in traumatic shock than in hemorrhagic shock. Pathological morphologic changes of lungs were more severe in traumatic shock than in hemorrhagic shock. CONCLUSIONS: Traumatic shock cause more bacterial translocation and endotoxemia which subsequently caused serial pathological alterations in lung morphologically and functionally than pure hemorrhagic shock does. These results suggest that this trauma activates more severe mechanism to damage lungs.

Animals↗
PubMed2006

Traumatic shock.

The association of shock with trauma has long been recognized. There are three types of shock, i.e., (1) hypovolemic or hemorrhagic shock, (2) traumatic shock, and (3) septic shock. The conditions and their treatments are described.

Humans↗
PubMed1977

[Changes in several indices of gas exchange in dogs during the initial stage of Cannon's traumatic shock].

In experiments reproducing traumatic shock according to Cannon on 35 dogs it was shown that metabolic acidosis developed in shock against the background of sharply elevated oxgen consumption at the very beginning of injury, when the arterial pressure exceeds considerably the inital level. In traumatic shock the brain is under the most favourable conditions of gas exchange and the skeletal musculature of the extremities--under the worst ones. It was concluded that in severe trauma, despite the strain of respiratory and cardiovascular system function the tissues of the brain and the skeletal muscles failed to obtain an adequate O2 quantity because of their sharply increases needs in oxygen, as well as of hemodynamic disturbances.

Acid-Base Equilibrium↗