No abstract available.
Cold Injury*

OBJECTIVETo evaluate the efficacy and the mechanism of application of selective head cooling on neuronal morphological damage during postischemic reperfusion in a rabbit model.

METHODS168 New Zealand rabbits were randomized into three groups. Group I [n = 24, (38 +/- 0.5) degrees C, non-ischemic control]; Group II [n = 72, (38 +/- 0.5) degrees C, normothermic reperfusion]; Group III [n = 72, (28 +/- 0.5) degrees C, selective head cooling, initiated at the beginning of reperfusion). Animals in three subgroups (n = 24, each) of Group II and Group III had reperfused lasting for 30, 180 and 360 min respectively. Using computerized image analysis technique on morphological changes of nucleus, the degree of neuronal damage in 12 regions were differentiated into type A (normal), type B (mild damaged), type C (severely damaged) and type D (necrotic). Fourteen biochemical parameters in brain tissues were measured.

RESULTSAs compared with Group I, the counts of type A neuron decreased progressively, and those of type B, C and D increased significantly in Group II during reperfusion (P < 0.01). In Group II, vasoactive intestinal peptide, b-endorphine, prostacyclin, T3 and Na+, K(+)-ATPase were correlated with the changes of type A; b-endorphine and thromboxane with type B; glucose and vasopressin with type C; Na+, K(+)-ATPase, glutamic acid, T3 and vasoactive intestinal peptide with type D (P < 0.05). As compared with Group II, the counts of type A increased, and those of type C and D significantly decreased in Group III (P < 0.01). In Group III, Ca2+, Mg(2+)-ATPase were correlated with the changes of type A, C and D (P < 0.01).

CONCLUSIONSelective head cooling for sex hours during postischemic reperfusion does improve neuronal morphological outcomes in terms of morphological changes.

Animals ; Brain Ischemia ; pathology ; Cold Temperature ; Neurons ; pathology ; Rabbits ; Reperfusion Injury ; prevention & control ; Resuscitation ; methods

The human capacity for physiologic adaptation to cold is minimal. A cold environment can be a threat to the skin, leading to a subsequent fall in core body temperature. Many physiologic, behavioral, and environmental factors predispose to the global effects of cold injuries. Physical injuries caused by cold have two forms: systemic forms such as hypothermia and localized forms such as frostbite. Reduced temperature directly damages the tissue, as in frostbite and cold immersion foot. Vasospasm of vessels perfusing the skin induces chilblain, acrocyanosis, and frostbite. The degree of damage caused by cold is related to four factors: temperature, exposure time, wind intensity (temperature sensation), and high altitude.
Adaptation, Physiological ; Altitude ; Body Temperature ; Chilblains ; Cold Injury ; Frostbite ; Humans ; Hypothermia ; Immersion Foot ; Skin ; Wind

Acute renal failure (ARF) secondary to immersion and near-drowning has rarely been described and it is poorly understood. ARF associated with immersion and near-drowning might be involved with systemic tissue hypoxia, hypovolemia and hypothermia. Some reports have shown that rhabdomyolysis could be involved. We report here on a 52 year old seaman who developed ARF after cold sea-water immersion. He had been swimming for one hour in cold sea-water because his ship became stuck on a rock. After 2 days, his serum creatinine level was increased to 7.8 mg/dL, and pulmonary edema was developed. The serum myoglobin level was 495.1 ng/mL. He was diagnosed as oliguric ARF and treated with hemodialysis. Thereafter, renal function was gradually recovered. We presumed that hypothermia-induced vasoconstriction, hypovolemia and rhabdomyolysis were involved in ARF in the patient. It should be considered that cold sea-water immersion for a long time could evoke ARF in healthy men.
Acute Kidney Injury ; Anoxia ; Cold Temperature ; Creatinine ; Humans ; Hypothermia ; Hypovolemia ; Immersion ; Male ; Myoglobin ; Near Drowning ; Pulmonary Edema ; Renal Dialysis ; Rhabdomyolysis ; Seawater ; Ships ; Swimming ; Vasoconstriction

OBJECTIVETo evaluate the protective effect of ischemic preconditioning against cold ischemia and reperfusion injury of rat intestinal graft following orthotopic transplantation.

METHODSEighty SD rats were randomly assigned into two groups with and without ischemic preconditioning, and each group was divided into 4 subgroups (n=10) according to the intestinal graft cold ischemia time of 3, 6, 12, and 18 h, respectively. Ischemic preconditioning model was established, and the small intestinal graft was preserved at 4 degrees celsius; in Ringer lactate solution for the corresponding time, followed by orthotopic transplantation of the graft. The graft samples were collected for histological examination 1 h after reperfusion, and nuclear factor-kappaB (NF-kappaB) expression in the epithelial cells was detected.

RESULTSIschemia preconditioning obviously relieved the histological ischemia/reperfusion injury, as shown by regular alignment of the small intestinal villi, alleviated muscular layer edema and decreased expression of NF-kappaB in the epithelia of the graft in groups with cold preservation.

CONCLUSIONIschemic preconditioning can protect the intestinal graft from cold ischemia/reperfusion injury, and NF-kappaB is an important cytokine in ischemia preconditioning.

Animals ; Cold Ischemia ; Intestine, Small ; pathology ; transplantation ; Ischemic Preconditioning ; NF-kappa B ; metabolism ; Organ Preservation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control

BACKGROUND: The interaction between ischemic preconditioning (IPC) and propofol-induced cardioprotective effects during prolonged cold ischemia has not been studied yet. The purpose of this study is to investigate the effects of ischemic preconditioning and propofol on cardiac function and the development of endothelial injury after 4 hours of cold cardioplegia and reperfusion. METHODS: After suspension of the isolated heart on the Langendorff perfusion system, we took a stabilizing period for 15 minutes, perfusion period for 15 minutes, global cold (4oC) ischemic period for 4 hours, and then reperfusion period for 60 minutes. There were 4 groups: (1) CONTROL group, no intervention; (2) IPC group, two 2-minute total coronary occlusions interspaced with 5 minutes of normal reperfusion; (3) PROPOFOL group, propofol (2micrometer) was infused during reperfusion period; (4) BOTH group, ischemic preconditioning and postischemic propofol treatment group. The measurements of cardiac performances, such as left ventricular developed pressure (LVDP), rate of ventricular pressure generation (dp/dt), and heart rate (HR) was obtained at pre- and postischemic periods. For the evaluation of endothelial injury during reperfusion period, coronary flow responses to bradykinin were tested. Infarct size was measured using the triphenyl tetrazolium stain. RESULTS: IPC, PROPOFOL, and BOTH groups showed better outcome of LVDP, dp/dt, HR, and flow responses to bradykinin than CONTROL group did. But there is no statistically significant difference in variables among the three groups. CONCLUSIONS: Ischemic preconditioning and postischemic propofol have cardioprotective effect respectively but no additive effect after 4 hours cold cardioplegia and reperfusion.
Animals ; Bradykinin ; Cold Ischemia ; Coronary Occlusion ; Heart Arrest, Induced* ; Heart Rate ; Heart* ; Ischemic Preconditioning* ; Perfusion ; Propofol* ; Rats* ; Reperfusion Injury ; Reperfusion* ; Ventricular Pressure

OBJECTIVETo investigate the change of bile composition and its role in bile duct injury after orthotopic liver transplantation (OLT).

METHODSRats were randomly divided into 3 groups: group A (sham surgery), group B (OLT with 1 h cold preservation), group C (OLT with 12 h cold preservation). The arterialized rat liver transplantation model with biliary extra-drainage was used in group B and C. Animals were sacrificed at posttransplant 1, 3, 5, 7, 10 and 14 day. Routine bile chemistry and pathological assays were performed.

RESULTSCold preservation/reperfusion injury (CPRI) could repress the secretion of bile salts and phospholipid. However, in contrast with a rapid increase of bile salt secretion, the biliary secretion of phospholipid recovered more slowly, leading to an abnormal high bile salts/phospholipid ratio early after transplantation. Further analysis suggested that the secretion of bile salts correlated strongly with biochemical and histopathological signs of bile duct injury.

CONCLUSIONSCPRI can lead to great changes of graft bile composition, which plays a role in the pathogenesis of bile duct injury following liver transplantation.

Animals ; Bile ; metabolism ; Bile Acids and Salts ; metabolism ; Bile Duct Diseases ; etiology ; Bile Ducts, Intrahepatic ; pathology ; Cold Ischemia ; Disease Models, Animal ; Liver Transplantation ; Male ; Postoperative Complications ; etiology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; complications ; metabolism ; pathology

BACKGROUND: Chronic post-ischemia pain (CPIP) model is reported to represent the complex regional pain syndrome type I. The administration of non-specific free radical scavengers reduced mechanical allodynia, but it is not evident which type of free radical is responsible for the development of CPIP. This study was investigated to elucidate the role of superoxide on the development of CPIP and the relationship with the expression of c-fos gene. METHODS: Male Sprague-Dawley rats weighing 290-310 g were housed in one cage with food and water ad libitum. CPIP model was made by placing a tourniquet on the left hindpaw of rats. The tourniquet maintained for 3 hours, then released to allow reperfusion. Thirty minutes before reperfusion, superoxide dismutase (SOD) or normal saline (control group) was injected. Mechanical allodynia and cold allodynia were measured at 1, 3, 5, 7, 14 and 28 days after reperfusion and compared. Also, spinal cord was harvested and the expression of c-fos gene was measured through the real time reverse transcription polymerase chain reaction. RESULTS: Superoxide dismutase reduced mechanical allodynia (1, 3, 5 and 14 day) and cold allodynia (1, 3 and 7 day) compared with control rats in left hindpaw. Expression of c-fos was significantly reduced in the SOD rats at the day 14 and 28 compare to the control rats. CONCLUSIONS: The administration of superoxide dismutase suppressed the allodynia and c-fos gene expression of CPIP model rats and it may be suggested that the superoxide has an important role in the development of CPIP.
Animals ; Cold Temperature ; Free Radical Scavengers ; Genes, fos ; Humans ; Hyperalgesia ; Inositol Phosphates ; Male ; Prostaglandins E ; Rats ; Rats, Sprague-Dawley ; Reperfusion ; Reperfusion Injury ; Reverse Transcription ; Spinal Cord ; Superoxide Dismutase ; Superoxides ; Tourniquets ; Water

We present a case of orthotopic liver transplantation in 63 year-old female patient with liver cirrhosis, who is the record of the oldest recipient in Korea. The donor was 20 year-old male patient with subarachnoidal hemorrhage. The operation time was 12 hours. The duration of cold ischemic time and anhepatic phase were 8 hours and 85 minutes respectively. After operation the patient resumed clear consciousness. The ventilator was weaned and removed. On the third postoperative day, reoperation was required due to hemoperitoneum. Splenectomy was performed for a tearing in the hilum. After reoperation, acute renal failure and sepsis developed. Continous arteriovenous hemofiltration was continued for 3 weeks. The patient was discharged on postoperative 59th day. The patient is doing well with normal liver function. No episode of acute rejection occurred until now. More aggressive approach has been feasible in organ transplantation for older patients by advanced knowledge of perioperative management. We conclude that age over 60 years should not be a barrier to liver transplantation.
Acute Kidney Injury ; Cold Ischemia ; Consciousness ; Female ; Hemofiltration ; Hemoperitoneum ; Hemorrhage ; Humans ; Korea* ; Liver Cirrhosis ; Liver Transplantation* ; Liver* ; Male ; Middle Aged ; Organ Transplantation ; Reoperation ; Sepsis ; Splenectomy ; Tissue Donors ; Transplants ; Ventilators, Mechanical ; Young Adult

OBJECTIVETo investigate the role of IL-6/STAT3 pathway in the proliferation of cholangiocyte induced by cold ischemia and reperfusion injury.

METHODSRats were randomized into CP 1 h and CP 12 h groups (supplied livers were preserved for 1 or 12 h), anti-IL-6R (rats in CP 12 h group were administrated with anti-rat soluble IL-6 receptor antibody), and control group. At 1, 3, 7, 14 d postoperative, IL-6 concentration in liver homogenate and cholangiocyte proliferation were detected by enzyme linked immunosorbent assay and histochemistry respectively. Expressions of IL-6 mRNA, phosphorylated-STAT3 and cyclin D1 protein in cholangiocytes were determined by real-time PCR or Western blot analysis. Serum concentrations of ALP and GGT and histology analysis were also performed.

RESULTSMinimal expressions of IL-6, p-STAT3 and cyclin D1 were detected in CP 1 h group, with a slight cholangiocytes proliferation. Cholangiocytes responded to extended cold preservation with severe bile duct injures and marked increase in IL-6 secretion, p-STAT3 and cyclin D1 protein expression, followed by compensatory cholangiocytes regeneration. Parallel to this observation, biochemical index and morphology indicated that bile duct injury was recovery at 14 d postoperative. However, anti-sIL-6R inhibited cholangiocytes proliferation and reduced the expressions of IL-6, STAT3 and cyclin D, with the cellular injury and increase of serum ALP or GGT.

CONCLUSIONSIL-6/STAT3 pathway might participate to initiate cholangiocytes regeneration after cold ischemia and preservation injury, which might benefit biliary recovery after liver transplantation.

Animals ; Bile Ducts, Intrahepatic ; pathology ; Cell Proliferation ; Cold Ischemia ; Disease Models, Animal ; Epithelial Cells ; pathology ; Interleukin-6 ; metabolism ; Liver ; metabolism ; pathology ; Liver Transplantation ; Male ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; pathology ; STAT3 Transcription Factor ; metabolism