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Results for “Shock, Traumatic”

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At least 127 records · Page 7Linked to original sources

PubMed1998

L-arginine attenuates endothelial dysfunction and prolongs survival in rats subjected to traumatic shock.

We investigated the effects of L-arginine administration in a rat model of traumatic shock. Pentobarbital-anesthetized rats subjected to drum trauma developed a severe shock condition characterized by marked hypotension to 55-70 mmHg, a survival time of only 90 +/- 21 min, and significant increases in ileal myeloperoxidase (MPO) activity (P < 0.01). In addition, superior mesenteric artery (SMA) rings isolated from rats subjected to traumatic shock relaxed to the endothelium-dependent vasodilator acetylcholine significantly less than rings isolated from control rats (p < 0.01). Administration of L-arginine (30 mg/kg bolus + 10 mg/kg/hr, i.v.) 10 min following trauma prolonged survival time to 213 +/- 33 min (p < 0.05) and attenuated ileal MPO activity (p < 0.01) indicative of reduced neutrophil infiltration. Furthermore, SMA endothelial function was significantly (p < 0.01) preserved in L-arginine treated traumatic shock rats. These results indicate that L-arginine plays a key role in the endothelial dysfunction associated with traumatic shock and affords significant protective effects which may be manifested by an inhibition of leukocyte-endothelial cell interactions.

Animals↗

PubMed1988

Protective effects of CG-4203, a novel stable prostacyclin analog, in traumatic shock.

We studied the effects of CG-4203, a novel stable prostacyclin analog, in a severe model of traumatic shock in rats. Traumatic shock was produced by Noble Collip drum trauma and was characterized by marked hypotension, a 4- to 5-fold increase in plasma cathepsin D and myocardial depressant factor activities, and survival time of 95 +/- 15 minutes. Treatment with CG-4203 (100 ng/kg/min) significantly prolonged survival time to 194 +/- 20 min (p less than 0.002). Traumatized rats treated with CG-4203 exhibited significantly lower plasma activities of the lysosomal hydrolase cathepsin D (p less than 0.05). Furthermore, the plasma accumulation of myocardial depressant factor (MDF) activity was also significantly blunted in traumatized CG-4203 treated rats when compared with traumatized rats receiving only the vehicle (p less than 0.01). Our results suggest that a combination of membrane stabilizing and anti-proteolytic effects and inhibition of platelet aggregation may mediate the protective effects of CG-4203 in traumatic shock.

Animals↗

PubMed1995

Beneficial effects of LEX032, a novel recombinant serine protease inhibitor, in murine traumatic shock.

The effects of LEX032, a novel recombinant serine protease inhibitor (i.e., serpin), were investigated in an experimental model of Noble-Collip drum shock. Pentobarbital-anesthetized rats subjected to drum trauma and receiving only the vehicle, developed severe traumatic shock with hypotension. These traumatized rats exhibited a survival time of 135 +/- 29 min, endothelial dysfunction, and a significant increase in intestinal myeloperoxidase activity. In contrast, LEX032 given intravenously (15 mg/kg bolus) resulted in a significant prolongation of survival time to 264 +/- 25 min (p < .01), a significant and sustained increase in mean arterial blood pressure, and a significant attenuation of intestinal myeloperoxidase activity (p < .05). Moreover, administration of LEX032 significantly preserved superior mesenteric artery (SMA) endothelial function as measured by the relaxation response of isolated (SMA) rings to acetylcholine, an endothelium-dependent vasodilator (64 +/- 10% vs. 25 +/- 6%, p < .01 compared with untreated trauma rats). Vasorelaxation responses to an endothelium-independent vasodilator, NaNO2, were unchanged in trauma. Our results indicate a significant protective role of LEX032 in traumatic shock, based on the preservation of endothelial function, reduced neutrophil accumulation in injured tissues, and increased survival time. These findings suggest that inhibition of serine proteases, some of which are from neutrophils, can be beneficial in traumatic shock in rats.

Animals↗

PubMed1981

[Functional state of the cerebral cortex and midbrain reticular formation during traumatic shock].

Acute experiments on cats were carried out during traumatic shock to study evoked potentials in the sensorimotor cortex and reticular formation (RF) of the midbrain in response to electrodermal irritation of the contralateral paw. The cortical function was judged by thresholds of convulsant reaction while function of RF by thresholds of activation reaction in the cortex of the course of high-frequency electrical stimulation of the structures under study. It was shown that in traumatic shock, initial and pronounced depression of the cortical function paralleled long enough stability of RF functional activity.

Animals↗

PubMed1998

Cellular mechanisms of heparinase III protection in rat traumatic shock.

Pentobarbital-anesthetized rats subjected to traumatic shock developed a shock state characterized by marked hypotension to 65-70 mmHg, a survival time of 88 +/- 13 min, significant increases in ileal myeloperoxidase activity (P < 0.01), and severe endothelial dysfunction as evidenced by a significant (P < 0.01) decrease in vasorelaxation to endothelium-dependent dilators. Treatment with heparinase III (45 microg . kg-1 . min-1) 10 min posttrauma prolonged survival time to 223 +/- 19 min (P < 0.001), significantly attenuated ileal myeloperoxidase activity (P < 0.01), and significantly preserved endothelial function (P < 0.05). Intravital microscopy of the rat mesentery showed that infusion of heparinase III (45-67 microg . kg-1 . min-1) significantly (P < 0.01) attenuated both leukocyte rolling and adherence in the rat mesenteric microvasculature in response to NG-nitro-L-arginine methyl ester stimulation. Immunohistochemical localization of surface-expressed P-selectin on mesenteric venules showed that heparinase III infusion at 45-67 microg . kg-1 . min-1 significantly (P < 0.05) attenuated the increase in surface P-selectin expression. The beneficial effects of heparinase III are mediated at least in part by attenuating leukocyte-endothelial cell interactions via a P-selectin-dependent mechanism.

Anesthesia, General↗

PubMed1992

[Functional state of the endogenous opioid peptide system in traumatic shock in rats].

The experiments have been performed on 120 Wistar rats and 546 CBWH mice. Met-enkephalin (ME) and beta-endorphin (BE) levels were determined to increase in blood and mid-brain 3 hours later after soft tissue compression of pelvic extremities. 48 hours later after six-hour compression BE and ME level in blood was increased, BE concentration in blood was also increased, and enkephalins' content in brain and blood was decreased as against the control. Opioid peptides influence on the host compression period has been studied. D-agonists were established to decrease, but mu-agonists were established to increase mice survival in shock. Opioid peptides' significance in traumatic shock pathogenesis is being discussed.

Animals↗

PubMed1987

Beneficial effects of prostaglandin E1 infusion in experimental traumatic shock.

The effects of prostaglandin E1 (PGE1) were studied in a standardized model of traumatic shock in rats. Pentobarbital anesthetized rats were subjected to standardized drum trauma of 525 revolutions in a Noble-Collip drum. These traumatized rats were characterized by a survival time of 108 +/- 19 min, a 12-fold increase in plasma cathepsin D activity, and a three-fold increase in plasma myocardial depressant factor (MDF) activity. PGE1 (1.2 micrograms/kg X min) significantly improved survival time during traumatic shock (191 +/- 29 vs. 108 +/- 19 min), drug vs. vehicle, respectively (p less than .03). In addition, PGE1 significantly attenuated plasma MDF activity during traumatic shock (58 +/- 10 vs. 27 +/- 7 U/ml), vehicle vs. drug, respectively (p less than .02). Plasma cathepsin D activity was also significantly retarded (12.1 +/- 1.8 vs. 1.70 +/- 1.50 U/ml), vehicle vs. drug, respectively (p less than .01). PGE1 appears to exert a membrane stabilizing effect, decreasing plasma cathepsin D and attenuating MDF production. PGE1 thus appears to have significant antishock activity.

Alprostadil↗

PubMed1984

Studies of hemorrhagic and traumatic shock influence on liver oxygen tension: effects of a single large dose of dexamethasone.

Liver surface oxygen tension in response to hemorrhagic shock (hs) and to combined hemorrhagic-traumatic shock (hts) as well as to hemorrhagic-traumatic shock with glucocorticoid application ( htsc ) has been studied using male rats (Wistar strain, 250-300 g b.w.). The animals were anaesthetized by i.p. injection of ketamine/xylazine. All animals were bled through a catheter inserted into the vena jugularis until a hypotension of 40 mm Hg mean arterial blood pressure (MAP) was attained. The hts rats were traumatized by fracturing the left tibia and crushing the adjacent muscle tissue with 45 N/2.25 cm2 for 5 minutes. The htsc animals were traumatized and treated with a single injection of a large pharmacological dose of dexamethasone (6-8 mg/kg b.w.). Initial surface Po2 of the liver was higher than published by others (29 +/- 7 mm Hg) probably due to the narcotic agents. Maximal blood withdrawal was 24.4 +/- 2.2 ml/kg b.w. for hs, 17.9 +/- 3.8 ml/kg b.w. for hts and 20.6 +/- 4.5 ml/kg b.w. for htsc rats. Liver surface Po2 decreased to zero mm Hg in response to hypovolemic hypotension in all rats. Retransfusion of the shed blood caused a MAP and surface Po2 increase to only about half of the initial levels in hts and htsc rats while in hs animals the initial values were approximated. The hts and htsc rats showed signs of progressive hypotension to about 45 mm Hg MAP within 90 minutes post retransfusion. Dexamethasone improved the arterial pH to 7.15 compared with 7.05 of the control. Pao2 was elevated to 60 mm Hg vs. 49 mm Hg of the control animals. The beneficial influence of glucocorticoids on liver surface Po2 has not been substantiated as would have been desirable for the patient. Nevertheless, from a physiological standpoint a positive trend in the liver O2 supply has been evaluated as a small right shift of the surface Po2 histogram as well as the blood gas and pH data.

Animals↗

PubMed1988

Protective effects of a platelet activating factor (PAF) antagonist and its combined treatment with prostaglandin (PG) E1 in traumatic shock.

We have investigated the role of platelet activating factor (PAF) in the pathogenesis of a murine model of traumatic shock using CV-6209, a specific antagonist of PAF. CV-6209, at a dose of 1 mg/kg (i.v.) given after trauma, significantly improved survival rate at 150 min and overall survival time. Furthermore, the plasma accumulation of the lysosomal hydrolase, cathepsin D, and a cardiotoxic peptide, myocardial depressant factor (MDF), were also attenuated by CV-6209 in traumatic shock. Combined treatment employing low doses of CV-6209 [0.2 mg/kg, i.v. and prostaglandin (PG) E1, 0.8 microgram/kg/min] in this shock model was also examined. CV-6209 (0.2 mg/kg) or PGE1 (0.8 microgram/kg/min) alone at these doses showed only minimal effects on survival, or plasma cathepsin D or MDF activities. However, combined treatment with CV-6209 (0.2 mg/kg, i.v.) and PGE1 (0.8 microgram/kg/min) significantly improved survival rate at 150 min, overall survival time, and decreased the accumulation of plasma MDF. These results suggest that PAF may play an important pathophysiologic role in traumatic shock in rats. Moreover, combination therapy using a PAF antagonist and PGE1 may be useful for the treatment of traumatic shock.

Alprostadil↗

PubMed1986

Significance of production of peptide leukotrienes in murine traumatic shock.

We studied the formation of a leukotriene metabolite in plasma and bile during traumatic shock. Anesthetized rats subjected to Noble-Collip drum trauma developed a lethal shock state characterized by a survival time of 1.9 +/- 0.3 h, a 4.5-fold increase in plasma cathepsin D activity, and a reduction in mean arterial blood pressure to 45 +/- 2 mmHg compared with 108 +/- 5 mmHg in sham-shock controls. Plasma and bile samples were analyzed by reverse-phase high-pressure liquid chromatography (HPLC) for peptide leukotrienes (e.g., LTC4, LTD4, and LTE4), and their retention times were confirmed by co-elution with radioactive standards, radioimmunoassay (RIA), and UV spectrophotometry. No leukotrienes or metabolites were found in plasma. The major peptide leukotriene from bile was eluted between LTC4 and LTD4 and corresponds to a metabolite of LTE4, N-acetyl-LTE4, which is also produced during endotoxin shock. The metabolite increased nearly sevenfold in traumatic shock compared with sham trauma. The identity of the metabolite was confirmed by UV scan, which revealed a spectrum consistent with a peptide leukotriene and similar to that of previously reported spectra for N-acetyl-LTE4. In conclusion, peptide leukotrienes are rapidly cleared from the blood and appear in the bile as N-acetyl-LTE4, a metabolite of the peptide leukotrienes. These findings support a role of the peptide leukotrienes in the pathogenesis of traumatic shock.

Animals↗

PubMed1959