Serum enzyme profile characteristics of victims following the Wenchuan earthquake in China.

BACKGROUND: Earthquakes are major causes of morbidity and mortality. The Wenchuan region of China was devastated by a catastrophic earthquake on May 12, 2008, at 02:28 p.m. (Beijing time), registering magnitude 8.0 on the Richter scale and causing more than 69,181 deaths. As a first-line general hospital in the disaster area, Mianyang Central Hospital admitted a large number of the victims. METHODS: A total of 534 victims (246 males, 288 females) were categorized as non-crush injury patients (n=239), simple crush injury patients (n=136), and crush syndrome patients (n=69) according to their traumatic conditions. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), cholinesterase (CHS), and creatine kinase (CK) levels were measured. RESULTS: ALT, AST, LDH, CHS, and CK levels showed significant differences among the three groups by one-way analysis of variance (ANOVA). Pearson correlation analysis showed that correlative changes between any two of the following: ALT, AST, GGT, ALP, LDH, and CHS were similar among three groups, with the following exceptions. The correlation coefficients of ALT-GGT, AST-GGT, and ALP-CHS changed from positive to negative values, and ALP-LDH changed from a negative value to a positive value. Receiver-operating characteristic (ROC) curve analysis showed the highest diagnostic effectiveness of 99.4% for CK, with 100% specificity [positive predictive value (PPV)=100%] and 99.4% sensitivity [negative predictive value (NPV)=99.0%] in distinguishing crush injury (including crush syndrome) from non-crush injury. AST had the best diagnostic effectiveness in distinguishing crush syndrome from crush injury; 53.8%, with 85.5% specificity (PPV=64.4%) and 77.9% sensitivity (NPV=90.7%). Multivariate logistic analysis revealed that CK was best at distinguishing crush injury (including crush syndrome) from non-crush injury (OR 409.636, 95% CI 382.96-438.17), and AST was best for distinguishing crush syndrome from crush injury (OR 50.08, 95% CI 46.84-53.55). CONCLUSIONS: Crush injury and crush syndrome are severe in victims following accidents or natural catastrophes. Serum CK, LDH, AST, ALT, GGT, and ALP activities were all helpful biochemical parameters in estimating the severity of crush injury and/or crush syndrome and preventing the development of further complications.

The study of Na+, K(+)-ATPase activity of rat brain during Crush syndrome.

Crush syndrome (CS) results from severe traumatic damage to the organism that is characterized by stress, acute homeostatic failure of the tissues, and myoglobinuria with severe intoxication. This leads to an acute impairment of kidneys and heart. The peripheral and central nervous systems are also the subject of significant changes in CS. Na(+), K(+)-ATPase is a critical enzyme in neuron that is essential for the regulation of neuronal membrane potential, cell volume as well as transmembrane fluxes of Ca(++) and Excitatory Amino Acids. In the present study, Na(+), K(+)-ATPase activity of rat brain regions [Olfactory lobes (OL), Cerebral cortex (CC), Cerebellum (CL), and Medulla oblongata (MO)] during CS was investigated. Experimental model of CS in albino rats was induced by 2-h of compression followed by 2, 24, and 48-h of decompression of femoral muscle tissue. In this study, we have observed elevation in Na(+), K(+)-ATPase activity above normal/control levels in all parts of brain (OL: 34.4%; CC: 1.0%; CL: 3.3% and MO: 45%) during 2-h compression in comparison to controls.

[The liver monooxygenase system activity in the long-term compression syndrome and treatment with benzonal in prepubertal rats and rabbits]. / Aktivnost' monooksigenaznoi sistemy pecheni nepolovozrelykh krys i krolikov pri sindrome dlitel'nogo zdavlivaniia i korrektsii ego narushenii benzonalom.

A compression syndrome was reproduced in rats and rabbits aged one month. Efficacy of the benzonal treatment in the postcompression period was evaluated by measuring the parameters of antipyrin pharmacokinetics, hexenal sleep duration, and the level of medium-molecular-weight (MMW) peptides in the blood serum. It was established that benzonal restored the detoxicating liver function (significantly reduced in animals with the compression syndrome) and eliminated the pronounced endotoxemia manifestations.

[The preliminary study on change of serum enzyme level in crush syndrome rat].

OBJECTIVE: To study the changes of serum creatinine kinase(CK) and its cardiac-specific isoenzyme compound(CK-MB) levels in crush injury rats. METHODS: Crush injury was produced in SD rats, the serum levels of CK and CK-MB were studied by automated biochemical analyzer. RESULTS: The levels of plasma CK and CK-MB were much higher in crush injury rats than those of the control group. CONCLUSIONS: Cardiomyocyte injury may be induced in the early stage of crush injury rats.

The preliminary study on change of serum enzyme level in crush syndrome rat / 法医学杂志

OBJECTIVE@#To study the changes of serum creatinine kinase(CK) and its cardiac-specific isoenzyme compound(CK-MB) levels in crush injury rats.@*METHODS@#Crush injury was produced in SD rats, the serum levels of CK and CK-MB were studied by automated biochemical analyzer.@*RESULTS@#The levels of plasma CK and CK-MB were much higher in crush injury rats than those of the control group.@*CONCLUSIONS@#Cardiomyocyte injury may be induced in the early stage of crush injury rats.

Activity of enzymes of adenyline compounds metabolism during crush and decompression of muscle tissue. Part I. Adenylate deaminase activity at experimental crush syndrome.

INTRODUCTION: The number of works on investigation of crush syndrome (CS) pathogenesis, of organs and enzymatic systems at traumatic toxicosis is rather limited. While the clinical current of trauma and the lethality prognosis depend on a degree of violations in them. Such investigations are necessary for opportune diagnosis and definition of a treatment tactic. To complete this deficiency, adenylate deaminase (AMPD) level was studied in twelve tissues at experimental CS in vivo. RESULTS: The experimental model of CS on white rats was caused by crush and decompression of femoral muscle tissue. The CS influence on AMPD activity was investigated in hemisphere, cerebellum, hypothalamus, pituitary body, heart, lung, liver, spleen, kidney, adrenal, crushed and not crushed muscles. In muscles, kidney, pituitary body and adrenal the activity decreased in 2 hours crush but the compensation of effect is observed after 5 hours crush. In cerebellum, hemisphere, heart, liver and lung it decreased during both of crush times. After 2 and 5 hours crush in hypothalamus and in spleen AMPD activity appeared much higher than in control. After 2 hours crush at the end of 48 hours decompression, the activity in muscles, kidney, adrenal and pituitary body was lower, in cerebellum, hypothalamus, hemisphere and heart--higher than, in lung, spleen and liver--close to control. After 5 hours crush in the majority of studied tissues at the end of decompression, the activity was below of control. The greatest deviance was observed in muscles. As to brain in cerebellum and hemisphere the parameter was close to, in pituitary body and in hypothalamus it was 1,5-fold of control. CONCLUSION: AMPD level in the most of studied tissues differs from the control at definite time of crush and decompression. These results mean the possibility of nucleotides pool balance distortion and intermediates accumulation.

Activity of enzymes of adenyline compounds metabolism during crush and decompression of muscle tissue. Part II. Adenosine deaminase activity at experimental crush syndrome.

INTRODUCTION: Publications on investigation of crush syndrome pathogenesis, particularly of enzymatic systems upon traumatic toxicosis are rather limited. Such investigations are necessary for opportune diagnosis and definition of a treatment tactic. To replenish this deficiency, the adenosine deaminase level was studied in 12 rat tissues at experimental crush syndrome in vivo. RESULTS: The experimental model of crush syndrome on white rats was induced by crush and decompression of femoral muscle tissue. The crush syndrome influence on activity of adenosine deaminase isoenzymes was investigated in hemisphere, cerebellum, hypothalamus, pituitary body, heart, lung, liver, spleen, kidney, adrenal, as well as in crushed and native muscles. In 2 and 5 hours after compression, the enzyme activity decreased in muscles, lung and heart; increased in hypothalamus; remains near the control value in kidney and spleen. In cerebellum the parameter practically does not vary during 2 hours compression, while increased in 5 hours. In adrenal, liver, pituitary body and hemisphere the data after 5 hours compression approximated the level of control value in account of compensating mechanism. In 48 hours decompression after 2 hours crush, the adenosine deaminase activity becomes higher than control value in hemisphere, hypothalamus, cerebellum, liver, heart, adrenal, intact muscle, lung and kidney; in the crushed muscle and spleen the activity is reduced down to 60% of control value. In 48 hours decompression after 5 hours compression, the enzyme activity is higher than control value in hypothalamus, pituitary body, hemisphere, cerebellum, kidney, adrenal, heart and lung. The activity is reduced in muscles, spleen and liver. CONCLUSION: The level of adenosine deaminase in most of studied tissues differs from the control value depending on compression and decompression time. It is worthy of note that namely during decompression, the enzyme level deviates from the control in the majority of tissues.

Influence of delayed hyperbaric oxygenation on recovery from mechanically induced damage.

This study examined whether subjecting a crushed muscle to a delayed intermittent hyperbaric oxygenation protocol would facilitate healing, the marker for healing being a return toward 100% uncrushed muscle in selected mechanical, morphologic, and biochemical parameters. Thirty-six rabbits (4 groups of 9) had the right lateral head of their gastrocnemius muscle surgically crushed. After surgery, the rabbits were exposed daily for 90 min 5 days/wk to either 100% O2 at 243 kPa, 8.5% O2 and 91.5% N2 at 243 kPa, 100% O2 at 101 kPa, or 21% O2 at 101 kPa. Initial treatments were administered 16-18 h post-muscle crush. After 10 days of treatment, maximal twitch and tetanic tension of the crushed muscle and its contralateral counterpart were measured. The muscles were then removed and analyzed morphologically, and the activity of citrate synthase, phosphofructokinase, and glucose-6-phosphate dehydrogenase were measured. The treatment group means for any of the parameters measured were not significantly different from each other. The extent of muscle damage, however, was determined to be minor as the control group recovery threshold was approximately 80%. Thus, it seems that the treatment protocol used does not facilitate healing for this type of muscle crush injury.

[Effect of adrenaline on kidney lysosome function in rats during prolonged soft tissue crushing]. / Vliianie adrenalina na funktsional'noe sostoianie lizosom pochek krys pri dlitel'nom sdavlenii miagkikh tkanei.

The total and unsedimentable activity of acid DNase, RNase, phosphatase and arylsulfatases A and B was examined in the rat kidneys during long-term compression of soft tissues in the presence of high excitability of the sympathoadrenal system. Injection of adrenalin to rats with trauma reduced the total activity of DNase, acid phosphatase and arylsulfatases A and B, particularly at the late periods of soft tissue compression, whereas the total activity of acid RNase slightly increased as compared with control. Compression of soft tissues after adrenalin preinjection was accompanied by a substantial rise of unsedimentable activity of the lysosomal enzymes under study in the kidneys. The activity of the enzymes in cytosol progressively ascended as the time of soft tissue injury increased.

[Effect of acetylcholine on the lysosome function of liver and kidneys in severe mechanical trauma]. / Vliianie atsetilkholina na funktsional'noe sostoianie lizosom pecheni i pochek krys pri tiazheloi mekhanicheskoi travme.

The functions of rat hepatic and renal lysosomes were explored during severe mechanical trauma caused by soft tissue compression in the presence of acetylcholinesterase induction by multiple acetylcholine administration. The increase of the trauma severity entailed the accumulation of non-hydrolyzed acetylcholine, thereby producing an injurious action on lysosomal membranes. Varying intensity of the changes in the activity of lysosomal hydrolases under study is likely to be related to the structural features of hepatic and renal lysosomes.

[Effect of serotonin on the lysosomal apparatus of liver cells and on hydrolase activity in the blood in severe mechanical injury]. / Vliianie serotonina na lizosomal'nyi apparat kletok pecheni i aktivnost' gidrolaz v krovi pri tiazheloi mekhanicheskoi travme.

A study was made of the pattern of changes in overall and non-sedimented activity of lysosomal hydrolases of the liver of rats injected with serotonin under grave mechanical trauma. Lability of the lysosomal membranes was found to be twice as increased, with remarkable hyperfermentemia being seen starting from the 3rd hour of compression in the presence of an appreciable rise of overall enzymatic activity. The role of serotonin in the mechanism of exocytosis of lysosomal enzymes is discussed.