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PubMed1995

Beneficial effects of oligotide, a novel oligodeoxyribonucleotide, in murine traumatic shock.

The effects of oligotide, an oligodeoxyribonucleotide analog, were investigated in an experimental model of traumatic shock. Pentobarbital-anesthetized rats subjected to Noble-Collip drum trauma and receiving only the vehicle (i.e., Krebs-Henseleit solution) developed a severe form of traumatic shock characterized by marked hypotension (61 +/- 6 mmHg), a survival time of 115 +/- 21 min, endothelial dysfunction, significant increases in plasma free amino-nitrogen concentration (p < .001) as well as elevated intestinal myeloperoxidase activity. In contrast, oligotide given intravenously (15 mg/kg bolus + 10 mg/kg/h infusion for 5 h) resulted in a significant prolongation of survival time to 209 +/- 31 min (p < .01), a significant and sustained increase in mean arterial blood pressure, a significant attenuation of plasma free amino-nitrogen concentration (p < .01), and intestinal myeloperoxidase activity (p < .05). Furthermore, oligotide significantly preserved superior mesenteric artery (SMA) endothelial function as seen by the relaxation response of isolated SMA rings to acetylcholine (71 +/- 5% vs. 36 +/- 5%, p < .01 compared to untreated trauma rats). Moreover, oligotide in a concentration-dependent manner attenuated unstimulated human neutrophil adherence to either thrombin or trauma-activated SMA endothelium in vitro (p < .001). Thus, our data suggest that the mechanism of the protective effect of oligotide in traumatic shock is improving endothelial function and diminishing neutrophil accumulation leading to reduced tissue injury.

Animals↗
PubMed2003

[Therapeutic efficiency of nitric oxide synthase inhibitor on traumatic shock in rats].

OBJECTIVE: To evaluate the effects of aminoguanidine (AG) used as a selective inhibitor of the inducible form of nitric oxide synthase (iNOS) and N-nitro-L-arginine methyl ester (L-NAME) used as a non-selective inhibitor of nitric oxide synthase (NOS) on traumatic shock. METHODS: Thirty SD (Sprague-Dawley) rats were used to create a animal model of traumatic shock. Both shaft of femurs were crashed and bled to mean arterial pressure of 35-45 mm Hg (1 mmHg=0.133 kPa) via femoral artery. Hypotension was maintained 30 minutes, the shed blood was then returned, followed by an infusion with Ringer's solutions. Animals were randomly divided into three groups: traumatic shock group (n=10), AG group (AG 8 mg/kg was infused at resuscitation, n=10), L-NAME group (L-NAME 8 mg/kg was infused at resuscitation, n=10). Plasma levels of nitric oxide (NO) were determined before and after shock, immediately after resuscitation and 0.5, 2 and 4 hours after resuscitation. The 24 hours survival rates were recorded. Lung, liver and kidney, intestine tissues were obtained 24 hours after shock for microscopic examination. RESULTS: The plasma level of NO markedly increased after shock. The plasma level of NO markedly decreased and less tissue damages with highly survival rates in AG group. Lower plasma level of NO and survival rates and highly tissue damages were seen in L-NAME group. CONCLUSION: NO plays an important role in development of pathologically traumatic shock. AG is beneficial of treatment in traumatic shock, but L-NAME can only decrease the plasma level of NO and can not improve the outcome of shock.

Animals↗
PubMed2004

[Influence of inhibitors of nitric oxide synthase and L-arginine on the survival rate in a rat model of traumatic shock].

OBJECTIVE: To investigate the influence of inhibitors of nitric oxide synthase (NOS) and L-arginine on the survival rate in a rat model of traumatic shock. METHODS: A rat model of traumatic shock was established by fracturing the posterior limb of the rat. Nomega-nitro-L-arginine-methyl ester (L-NAME, non-selective NOS inhibitor, 10 mg/kg), amino- guanidine (AG, selective inducible nitric oxide synthase (iNOS) inhibitor, 100 mg/kg) and L-arginine (L-Arg, the precursor of nitric oxide (NO) synthesis 100 mg/kg) were injected intravenously during resuscitation,survival time and survival rate were observed. RESULTS: There were no significant changes in survival time and 24-hour survival rate between L-NAME ((23.80+/-9.09) hours and 40 percent) and control group (18.78+/-4.64)hours and 10 percent, both P>0.05); the survival time of AG group (28.72+/-6.25) hours and L-Arg group (30.64+/-8.77) hours prolonged apparently (both P<0.01), and 24-hour survival rate was also increased (both 80 percent, both P<0.01). CONCLUSION: Selective iNOS inhibitor AG and L-Arg exert beneficial effects on after traumatic shock rats.

Animals↗
PubMed1994

Beneficial actions of S-nitroso-N-acetylpenicillamine, a nitric oxide donor, in murine traumatic shock.

We studied the effects of the nitric oxide donor, S-nitroso-N-acetylpenicillamine (SNAP), in rat traumatic shock characterized by hypotension, increases in plasma free amino-nitrogen (5.3 +/- 0.5 U/ml vs. 2.5 +/- 0.3 U/ml controls) and intestinal myeloperoxidase activities (2.7 +/- 1.0 U/100 mg vs. 0.2 +/- 0.1 U/100 mg controls), and a survival time of 143 +/- 20 min. Moreover, superior mesenteric artery rings isolated from rats in traumatic shock relaxed to the endothelium-dependent vasodilator acetylcholine only 21 +/- 6% of U-46619 induced contraction. Administration of 100 micrograms/kg SNAP 10 min post-trauma followed by 10 micrograms/kg/h infusion prolonged survival time to 273 +/- 18 min (p < .05), attenuated the increases in plasma free amino-nitrogen (3.1 +/- 0.4 U/ml, p < .05) and tissue myeloperoxidase activities (0.6 +/- 0.3 U/100 mg, p < .05). Moreover, SNAP significantly preserved superior mesenteric artery endothelial function; the vasorelaxation to acetylcholine was 54 +/- 4% (p < .01). Protective effects were not seen in traumatic shock rats treated with the non-NO-donating parent compound N-acetylpenicillamine. These results indicate that SNAP affords significant protection in murine traumatic shock which may be achieved through maintenance of systemic blood pressure, preservation of vascular endothelial integrity, and inhibition of neutrophil-endothelial interaction and the resultant reduced microvascular leakiness.

Acetylcholine↗
PubMedDate not supplied

[Mechanisms of the beneficial effect of indomethacin and nimodipine in the treatment of traumatic shock in rats].

Aiming to study the pathogenetic mechanisms of the disturbed function of the central nervous system in traumatic shock we have determined the dynamics of changes of eicosanoids (PGF2 alpha, TxB2, 6-keto-PGF1 alpha, peptidoleukotrienes) in the brain structures (medulla oblongata, hypothalamus) of the experimental animals subjected to bilateral trauma of the hind legs (tourniquet trauma, LD50). Considering that our previous data have shown the importance of eicosanoid mediatory system in the pathogenetic mechanisms of shock, we have studied possible use of prostaglandin synthesis inhibitors (indomethacin) and calcium channel antagonists (nimidipine) in traumatic shock. The authors have concluded that in the pathogenetic mechanism of the disturbed function of the CNS in traumatic shock the important role has peptidoleukotrienes as well as that the combined use of prostaglandin synthesis inhibitors and antagonists of voltage-dependent calcium channel would be useful in the therapy of the injured patients.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Quantitative assessment of leukostasis in experimental hypovolemic-traumatic shock.

Using a hypovolemic-traumatic shock model without reinfusion of shed blood, 111In-oxine-labeled granulocytes were injected to quantify pulmonary leukostasis in dogs. Labeling was facilitated by a non-traumatic and rapid technique for granulocyte processing and a commercially available 111In-oxine solution. Lung biopsy material taken before and after shock showed granulocyte-associated radioactivity to be significantly increased 90 min after the onset of shock. This observation established that pulmonary leukostasis in shock models is not caused solely by reinfusion of shed blood, but rather by humoral factors operative during shock, e.g. by complement activation. The described experimental design should also be useful for in vivo tests of drugs which act on granulocyte function and may have a potential place in the management of shock.

Animals↗
PubMed1980

[Clinical multifactorial evaluation of the severity of traumatic shock].

The analysis of data of 780 cases of patients with traumatic shock enabled the author to show the dependence of the duration of shock in hours (+T) and life-span in the same unit (-T) on the age of the patient (A), pulse rate (P) and level of the systolic arterial pressure (AP) and the sum number assessment of severity of the trauma (K), calculated according to a special table. The dependence is expressed by the formula: (Formula: see text) The clinical verification has shown 90% of coincidence of the real and prognostic severity of the traumatic shock by the outcome.

Factor Analysis, Statistical↗
PubMed1990

Beneficial actions of BN 50739, a new PAF receptor antagonist, in murine traumatic shock.

We studied the effects of BN 50739, a novel PAF antagonist, in a rat model of traumatic shock. Pentobarbital anesthetized rats subjected to Noble-Collip drum trauma developed a shock state characterized by marked hypotension, significant increases in plasma cathepsin D (4.2-fold), free amino-nitrogen (2.8-fold) and myocardial depressant factor (4.7-fold) activities and a survival time of 1.62 +/- 0.16 h. Treatment with BN 50739 (10 mg/kg, i.v.) 10 min post-trauma prolonged survival time to 3.14 +/- 0.44 h (p less than 0.01) and attenuated the accumulations of cathepsin D (5.8 vs. 12.5 U/ml, p less than 0.01), free amino-nitrogen (4.6 vs. 12.5 U/ml, p less than 0.001) and myocardial depressant factor (19.4 vs. 65.1 U/ml, p less than 0.001). Moreover, in washed rabbit platelets, BN 50739 inhibited PAF (1.85 nM)-induced aggregation (IC50: 50 nM) without affecting ADP (5 microM)-induced aggregation. In anesthetized rats, BN 50739 (10 mg/kg, i.v.) attenuated PAF (10-30 ng/kg, i.v.)-induced hypotension for longer than 5 h, without influencing acetylcholine (10 micrograms/kg, i.v.)-induced hypotension. These findings indicate that BN 50739 is a specific PAF receptor antagonist with a long duration of action in vivo. The beneficial effects of PAF antagonism on traumatic shock are significant in the present study, and are consistent with the concept that PAF is involved in the pathogenesis of traumatic shock.

Animals↗
PubMed2006

Disturbances in hormonal regulation of vascular tone during traumatic shock.

Changes in hormonal regulation of the vascular tone in Wistar rats were studied on Cannon model of traumatic shock. The pressor response to angiotensin II decreased by 30-40% 3 h after the incidence of trauma. The reaction to vasopressin remained unchanged. However, phenylephrine in medium and high doses produced a more pronounced pressor response under these conditions. One day after trauma we revealed a decrease in vascular sensitivity not only to angiotensin II, but also to vasopressin and alpha1-adrenoceptor agonist phenylephrine. The vascular response was observed only after treatment with phenylephrine in maximum doses. Traumatic shock was accompanied by inverse response to serotonin: hypertensive effect instead of blood pressure drop. Our results show that traumatic shock is accompanied by specific changes in vascular reactivity.

Angiotensin II↗
PubMed2006

Androstenetriol improves survival in a rodent model of traumatic shock.

UNLABELLED: Trauma results in activation of the hypothalamic-pituitary-adrenal axis to mediate a cascade of neurohormonal changes as a defensive mechanism. Its prolongation, however, leads to a hypermetabolic, hypoperfused, and immunosuppressed state, setting the stage for subsequent sepsis and organ failure. Androstenetriol (5-androstene-3beta, 7beta, 17betatriol - AET), a metabolite of dehydroepiandrosterone, up-regulates the host immune response markedly, prevents immune suppression and controls inflammation, leading to improved survival after lethal infections by several diverse pathogens and lethal radiation. Such actions may be useful in improving survival from traumatic shock. HYPOTHESIS: The neurosteroid AET will increase survival following traumatic shock. METHODS: A combat relevant model of traumatic shock was used. Male Sprague-Dawley rats were anesthetized, catheterized and subjected to soft tissue injury (laparotomy). Animals were allowed to regain consciousness over the next 0.5 h and then bled 40% of their blood volume over 15 min. Forty-five minutes after the onset of hemorrhage animals were randomized to receive either a single subcutaneous dose of AET (40 mg/kg, sc) or vehicle (methylcellulose). Volume resuscitation consisted of l-lactated Ringer's (three times the shed blood volume), followed by packed red blood cells (one-third shed red cell volume). Animals were observed for three days. RESULTS: A total of 24 animals were studied. Of the 12 animals randomized to receive AET, all (100%) survived compared to 9 of 12 animals (75%) randomized to receive the vehicle (p < 0.05). CONCLUSION: AET significantly improved survival when administered subcutaneously in a single dose in this rodent model of traumatic shock. Further survival and mechanism studies are warranted.

Androstenols↗
PubMed2006

[The time for beginning of enteral nutrition in traumatic shock].

OBJECTIVE: To explore the value of monitoring CO(2) partial pressure of gastric mucosa (PiCO(2)) in patients with traumatic shock under enteral nutrition (EN) support. METHODS: Ninety-six patients who were clinically diagnosed as having traumatic shock were randomly divided into two groups: the test group and the control group. In the test group, EN was given after tissue oxygenation, indicated by the value of PiCO(2), approached normal and the clinical symptoms ameliorated. In control group EN was given at the early stage of recovery from shock. The course of convalescence of the primary disease, gastro-intestinal symptoms, the monitoring indexes, and the complications etc. were compared between the two groups. RESULTS: Acute physiology and chronic health evaluation II (APACHE II) scores were both gradually lowered in both groups. It was more significant in the control group than that in the test group 5 days later (both P<0.01). Compared with the control group, the cure rate in the test group was increased obviously (91.3% vs. 75.0%, P<0.01), and the hospital stay days were significantly less [(6.0+/-1.8) days vs. (7.5+/-2.3) days, P<0.01]. CONCLUSION: It is very important to choose the suitable time to give EN support in patients with traumatic shock, for it can protect and promote the recovery of the function of their intestinal tract, raise the survival rate.

APACHE↗
PubMed1989

Protective effects of a combination thromboxane synthesis inhibitor-receptor antagonist, R-68070, during murine traumatic shock.

The effects of R-68070 were studied in a well-characterized model of drum-induced traumatic shock in rats. R-68070 is a combination thromboxane A2 (TxA2) synthetase inhibitor-TxA2 receptor antagonist. Pentobarbital-anesthetized (50 mg/kg) rats subjected to Noble-Collip drum trauma developed a lethal circulatory shock state characterized by a marked decrease in mean arterial blood pressure (MABP) to about 75 mmHg, resulting in a survival time of 1.58 +/- 0.18 h. This compares with MABP of 120 +/- 4 mmHg 5 h after anesthetization in rats subjected to a sham traumatic shock protocol. Administration of R-68070 (1.5 mg/kg) significantly attenuated the plasma accumulation of the lysosomal protease, cathepsin D (p less than 0.05), as well as free amino-nitrogen concentration (p less than 0.05) and myocardial depressant factor activity (p less than 0.02). Additionally, R-68070 significantly prolonged survival time to 2.85 +/- 0.48 h (p less than 0.015) compared with traumatized rats given only the vehicle. These results suggest that TxA2 may be an important mediator in traumatic shock, and that R-68070 may prove to be a useful therapeutic agent in this situation if given early in the course of the shock state.

Animals↗