[Traumatic shock in the works of Soviet scientists].
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[Further studies on traumatic shock].
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[Experimental bases in complex therapy of traumatic shock and Pavlov's theory].
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[Present concept of traumatic shock].
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[Etiopathogenesis and rational therapy in surgery; traumatic shock and related conditions].
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Disturbances in energy metabolism during traumatic shock and their pharmacological correction.
In compression traumatic shock caused by mechanical crushing of the lower limbs and eventuating in death of 80% animals, hemodynamic disorders by the end of day 1 lead to the development of energy deficiency most pronounced in skeletal muscles and less pronounced in the liver and kidneys. Energy production in the brain and heart was not impaired. Inhibition of ATP synthesis correlated with decreased SOD activity in organs, but not always with activation of lipid peroxidation, which can occur without concomitant disorders in energy metabolism (in the heart and brain). Therapy with succinate-containing hydroxypyridine derivative decreased animal mortality to 10%; this treatment did not modify hemodynamic parameters, but normalized energy metabolism in organs and activity of the antioxidant and prooxidant systems. These findings suggest that tissue (bioenergetic) hypoxia plays an important role in the pathogenesis of compression traumatic shock and that antihypoxic drugs are essential components of therapy of this condition.
Adenosine Triphosphate↗
[Fluid resuscitation in traumatic shock].
OBJECTIVE: To investigate fluid resuscitation affecting the result of treatment of patients with traumatic shock. METHODS: Two hundred and fifty-six cases of patients with traumatic shock treated in our hospital between January 1989 and December 2002 were analysed retrospectively, and the volume-effect relationship between fluid resuscitation during the first hour and future of traumatic shock was summarised. RESULTS: The successful rate of resuscitation was 73.05 percent (187 cases), and traumatic mortality was 26.95 percent (69 cases). After 1-hour trauma, the survival rate was 52.27 percent in patients with 1 liter of resuscitation fluid, 75.90 percent in patients with 15-20 liter of resuscitation fluid, and 78.29 percent of more than 20 liter resuscitation fluid, 86.79 percent in mild shock, 80.34 percent in middle shock and 54.65 percent in severe shock. CONCLUSION: Severe trauma and shock, hypotension and incorrect resuscitation manipulation are the main factors affecting the result of resuscitation and treatment of traumatic shock. It is important to early and correctly expand, especially at the first hour. The aim of resuscitation of traumatic shock is to maintain the hemodynamics and correct O2 defect.
Adolescent↗
Intervention with nitric oxide synthase inhibitors for traumatic shock in rats.
OBJECTIVE: To evaluate the effects of a selective inhibitor of inducible nitric oxide synthase (iNOS) aminoguanidine (AG) and a non-selective inhibitor of nitric oxide synthase (NOS) N(G)-nitro-L-arginine methylester (L-NAME) on traumatic shock in rats. METHODS: Animal models of traumatic shock were established in 44 Sprague-Dawley rats following fractures in both femur shafts and subsequent depletion until the mean arterial pressure in the femoral artery dropped to 35 to 45 mmHg(4.67-6.00 kPa). Hypotension was maintained for 30 min before the collected blood was infused back into the rats supplemented with Ringer's solution of the same volume. The rat models were then randomly divided into 3 groups, namely traumatic shock group (n=10), AG group (which was subdivided into AGI, AGII, and AGIII groups, each consisting of 8 rats and receiving 2, 8, and 60 mg/kg x b.w AG infusion respectively during resuscitation), and L-NAME group (with 8 mg/kg x b.w L-NAME infusion during resuscitation, n=10). Plasma NO levels were determined before and after shock, immediately after resuscitation and 0.5, 2, 4 h after resuscitation, and the survival rates within 24 h were recorded with tissue samples of the lung, liver, kidney and intestine obtained 24 h after shock for microscopic examination. RESULTS: Plasma NO level was seen to increase markedly after traumatic shock in the rat models. In the 3 AG groups, the elevated NO levels following the shock were obviously reduced after resuscitation with less tissue damages and higher survival rates, as compared with the other 2 groups. The best protective effect against traumatic shock was observed in AGIII group. In spite of obvious plasma NO level-lowering effect after resuscitation, L-NAME exhibited little efficacy in alleviating the tissue damages in the organs and hence failed to improve the survival rate of the rats. CONCLUSIONS: NO plays an important role in the pathological process of traumatic shock, and the application of AG may improve the condition. L-NAME can decrease plasma NO level after resuscitation, but fail to improve the outcome of traumatic shock in rats.
Animals↗
Dynamic changes in serum level of nitric oxide and its mechanisms in rats with traumatic shock.
OBJECTIVE: To investigate the dynamic changes of serum nitric oxide (NO) level and its mechanisms in rats in traumatic shock. METHODS: Rat models of traumatic shock were established by fracturing the posterior limb of the rats. Serum levels of nitrate/nitrite were measured with the method described by Griess. RESULTS: No significant changes in serum NO level took place during traumatic shock. One hour after resuscitation, however, serum NO level first underwent marked decline and then increased to the peak level at 6 h after resuscitation, retaining a high level till 24 h after resuscitation. No obvious changes of serum NO levels were observed in rats without resuscitation. CONCLUSION: Serum NO level does not significantly alter during traumatic shock, while after resuscitation, NO level increases after transient decrease, possibly due to reperfusion injury.
Animals↗
Inhibitors of lipoxygenase products improve survival in traumatic shock.
We have used three selective inhibitors of arachidonic acid metabolism in order to investigate the role of lipoxygenase metabolites in the pathogenesis of traumatic shock (LD90). The following inhibitors were used: CGS-5391B (2.5 mg/kg), a cyclooxygenase and lipoxygenase inhibitor, CGS-5677 (2.0 mg/kg), a selective lipoxygenase inhibitor, and U-60,257 (0.3 mg/kg), a putative inhibitor of glutathione-s-transferase. These inhibitors did not alter arterial blood pressure or heart rate when given to sham shock rats. The traumatic shock model was characterized by a 4.5-fold increase in plasma cathepsin D activity, a 4-fold increase in plasma myocardial depressant factor (MDF) activity, and a mean survival time of 1.5 +/- 0.2 h. Only the dual inhibitor significantly blunted the accumulation of cathepsin D in the plasma (7.5 +/- 0.8 vs 11.3 +/- 0.8 U/ml, p less than 0.01). However, all three inhibitors significantly suppressed plasma MDF accumulation by 50-60%: CGS-5391B, CGS-5677, and U-60,257 (p less than 0.01). Moreover, these three agents significantly improved survival time in traumatic shock. The increased survival time and reduced MDF activity afforded by these inhibitors suggest a significant role for lipoxygenase metabolites, particularly LTC4 and LTD4, in the pathogenesis of traumatic shock.
Animals↗
[L-arginine decreases P-selectin expression in traumatic shock].
OBJECTIVE: To investigate the changes of P-selectin distribution in the vital organs and plasma during traumatic shock and explore the significance of these changes. METHODS: Twenty-four normal SD rats were randomly assigned into 3 groups (n=8), namely traumatic shock group, L-arginine (L-Arg) treatment and control group. The rats in the former 2 groups were subjected to traumatic shock with L-Arg treatment group given 100 mg/kg L-Arg during resuscitation while the other receiving no medication. The control group received only intubation without trauma or phlebotomy. P-selectin expression in the vital organs including the heart, lungs, spleen, liver and small intestine was determined by means of streptavidin-biotin (SABC) immunocytochemical staining technique and serum P-selectin level assayed by enzyme-linked immunosorbent assay. RESULTS: Before traumatic shock, P-selectin was scarcely detected in the vital organs except the lungs, and the serum was positive for P-selectin expression. Four hours after shock, intense P-selectin expression was observed in almost all the vital organs and the serum P-selectin level was significantly higher than that of the control group. In L-Arg treatment group, P-selectin levels were significantly lowered than those of shock group. CONCLUSIONS: P-selectin expression in the vital organs and serum is up-regulated during traumatic shock in rats, possibly due to severe microcirculatory disorder and endothelial dysfunction in this condition. L-Arg may decrease the expression of P-selectin very likely through promoting endothelial NO synthesis.
Animals↗
[Effect of methylene blue on traumatic shock in rabbits].
OBJECTIVE: To observe the effect of methylene blue (MB) on the changes in plasma nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and visceral pathologic changes in rabbits with traumatic shock. METHODS: Eighteen rabbits were randomly assigned into 3 groups (n=6): sham operation group, traumatic shock with normal saline (NS) resuscitation group (NS group), and traumatic shock with MB resuscitation group (MB group). In NS group and MB group, hemodynamics was monitored, and plasma contents of NO, TNF-alpha and IL-6 were determined before shock, after shock, after resuscitation, and 0.5, 2 and 4 hours after resuscitation. In sham operation control group, hemodynamics monitoring and plasma contents of NO, TNF-alpha and IL-6 were also determined. Tissue samples of the liver and intestine were obtained after experiments for microscopic examination. RESULTS: Compared with NS group, hemodynamics was stable in MB group. The levels of plasma NO in rabbits after traumatic shock were much higher than those of before shock. In NS group, the levels of plasma NO were progressively increased after resuscitation, reaching peak level at 0.5 hour after resuscitation, then decreased thereafter but still remaining higher than those of before shock. But in MB group, the levels of plasma NO after resuscitation were obviously decreased. In sham operation group, the levels of plasma NO showed no significant changes during the whole course. The levels of plasma TNF-alpha and IL-6 in rabbits after traumatic shock were much higher than those of before shock. But after intravenous administration of MB, the levels of plasma TNF-alpha and IL-6 after resuscitation showed no significant difference compared with the baseline levels. In sham operation group, the levels of plasma TNF-alpha and IL-6 showed no significant changes during the entire course. In NS group, the organs showed prominent pathologic changes. But in MB group, less pathologic changes in the organs were milder, and in sham operation group, there was no obvious pathologic changes in the organs. CONCLUSION: NO, TNF-alpha and IL-6 play important roles in the pathologic process of traumatic shock and the administration of MB after resuscitation can decrease the levels of plasma NO, TNF-alpha and IL-6, improve hemodynamics in traumatic shock, and protect the important organs.
Animals↗
[Effect of acupuncture on the contents of enkephalins in different brain regions of rats with traumatic shock].
The study was carried out on the animal model of traumatic shock which induced by ligating bilateral hind legs. The contents of enkephalins in hippocampus, striatum, hypothalamus, diencephalon and brain stem were determined with radioimmunoassay. The results show that: (1) when traumatic shock occurs, the contents of Met-enkephalin are not obvious change in the above 5 brain regions, and also not significant change after acupuncture; (2) there is a tendency to increase the content of Leu-enkephalin in each brain region described above of shock animal, while it is decreased in hypothalamus after acupuncture. The result suggests that the occurrence of traumatic shock may be related to the functional activities of Leu-enkephalinergic system in the central nervous system; the anti-shock of acupuncture may be through a decrease in the level of central Leu-enkephalin to improve micro-circulation and raise the blood pressure.
Animals↗
Beneficial actions of CP-0127, a novel bradykinin receptor antagonist, in murine traumatic shock.
We studied the effects of CP-0127, a novel bradykinin receptor 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-free amino-nitrogen (8.6 +/- 0.97 vs. 2.3 +/- 0.15 U/ml in control rats) and intestinal myeloperoxidase (MPO) activity (2.7 +/- 0.33 vs. 0.08 +/- 0.03 U/100 mg control rats, intestinal tissue), and a survival time of only 110 +/- 9 min. Moreover, superior mesenteric artery (SMA) rings isolated from rats subjected to traumatic shock relaxed to the endothelium-dependent vasodilator acetylcholine (ACh) significantly less than rings isolated from control rats (21 +/- 4 vs. 92 +/- 4%, P < 0.001). Administration of CP-0127 at a dose of 10 mg/kg subcutaneously completely blocked the hypotensive response to 2.5 micrograms/kg bradykinin injected intravenously in sham traumatic shock rats. CP-0127 given immediately posttrauma prolonged survival time to 219 +/- 27 min (P < 0.01) and attenuated the increases in plasma-free amino-nitrogen (3.7 +/- 0.41 U/ml, P < 0.01) and tissue MPO activities (1.2 +/- 0.71 U/100 mg intestinal tissue, P < 0.05). Furthermore, SMA endothelial function was significantly preserved (relaxation to ACh: 57 +/- 6%, P < 0.01) in CP-0127-treated traumatic shock rats. These results indicate that bradykinin plays an important role in tissue injury associated with traumatic shock and that CP-0127 affords significant protection, which may be achieved through inhibition of neutrophil-endothelial interaction and protection of vascular endothelial function.
Animals↗
[Therapeutic effect of L-arginine on traumatic shock in rats].
OBJECTIVE: To evaluate the therapeutic effect of L-arginine (L-Arg) on traumatic shock in rats and explore the possible mechanisms. METHODS: Rat models of traumatic shock were established in Sprague-Daulay rats, which were randomly divided into two groups either to receive L-Arg treatment or not. The plasma concentration of endothelin (ET) and oxygen partial pressure in the tissues from the skeletal muscles, liver and small intestine were measured before and after the shock and 1, 3, and 5 h after resuscitation. The hemodynamics of the rats and their survival rates at 12 and 24 h were recorded. RESULTS: The changes of plasma ET levels and oxygen partial pressure in tissues of both groups were statistically significant after traumatic shock (P<0.05). Plasma ET concentration at 5 h after resuscitation was significantly lower in the treatment group than in the non-treatment shock group (P<0.05), while oxygen partial pressure in the liver and small intestine after resuscitation were significantly higher in the treatment group (P<0.05). The survival rates at 12 and 24 h were also significantly different between the 2 groups. CONCLUSION: Adscititious L-Arg can decrease plasma ET levels, improve oxygen partial pressure of internal organs and significantly increase the survival rate of the rats with traumatic shock.
Animals↗