No Abstract available.
Anesthetics* ; Reperfusion Injury* ; Reperfusion*

No abstract available.
Anesthetics* ; Reperfusion Injury*

Humans ; Myocardial Reperfusion Injury

No abstract available.
Anesthetics, Local* ; Calcium* ; Hypothermia* ; Reperfusion Injury* ; Reperfusion*

No abstract available.
Animals ; Muscle, Skeletal* ; Rats* ; Reperfusion Injury* ; Reperfusion*

Autophagy ; Humans ; Myocardial Reperfusion Injury

BACKGROUND: Reoxygenation of an ischemic heart causes a decrease in the cardiac function, which is known as reperfusion injury that is associated with an increase in the concentration of reactive oxygen species (ROS). This study examined the effect of the propofol concentration on the generation of ROS during reoxygenation in rat embryonic heart H9c2 cells. METHODS: Cultured H9c2 cells were examined in the following sequences: Prehypoxic, Hypoxic and Reoxygenation period. Each period required 60 minutes. The cells were exposed to propofol at the beginning of the prehypoxic period. Thirty minutes later, DCFH-DA (dichlorofluorescin diacetate) 10 micrometer was added to detect the ROS. The propofol concentrations used were 0, 5, 25, 50, 250 micrometer in the first experiment and 0, 1, 2, 3, 4, 5 micrometer in the second experiment. The ROS level was estimated using a fluorometer at 5-minute intervals from 5 to 60 minutes after reoxygenation. RESULTS: When the propofol concentrations was > 5 micrometer, the ROS levels were significantly lower than those of the untreated group (P0) (P < 0.05). At propofol concentrations < 5 micrometer, the ROS levels 35 to 60 minutes after reoxygenation were significantly lower that in the untreated group (P < 0.05). Between 5 and 30 minutes after reoxygenation, the cells exposed to 1, 4 and 5 micrometer propofol also showed lower ROS levels than the untreated group P0. However, 2 and 3 micrometer propofol did not show any significant difference in ROS values to those observed in the untreated group except for 2 micrometer at 25 minutes after reoxygenation. CONCLUSIONS: During the reoxygenation period in H9c2 cells, propofol concentrations > 5 micrometer inhibited ROS production over the whole period, and even 1micrometer showed some inhibition of ROS.
Animals ; Heart* ; Propofol* ; Rats* ; Reactive Oxygen Species* ; Reperfusion ; Reperfusion Injury

The sinking skin flap syndrome is a rare complication after a large craniectomy. It consists of a sunken skin above the bone defect with neurological symptoms such as severe headache, mental changes, focal deficits, or seizures. In patient with sinking skin flap syndrome, cerebral blood flow and cerebral metabolism are decreased by sinking skin flap syndrome, and it may cause the deterioration of autoregulation of brain. We report a case of a patient with sinking skin flap syndrome who suffered from reperfusion injury after cranioplasty with review of pertinent literature.
Brain ; Headache ; Homeostasis ; Humans ; Reperfusion ; Reperfusion Injury ; Seizures ; Skin

OBJECTIVETo investigate the injury stress responses caused by ischemia reperfusion and its effects on the salivary secretory function of rat submandibular glands.

METHODSAn in situ ischemia reperfusion experimental model of rat submandibular glands was developed. The rat submandibular glands were subjected to 90 min of ischemia without denervation followed by reperfusion for 1, 12, 24, and 72 h. Salivary secretion, histological changes, reactive oxygen species (ROS) levels, and cellular apoptosis of the involved submandibular glands were detected after reperfusion.

RESULTSThe secretory function of the glands decreased at 1 and 12 h, and the saliva secretion gradually had the same value as that of the control sample 72 h after reperfusion. Increasing inflammatory cells infiltration, cellular atrophy, and tissue edema were observed especially after reperfusion for 12 h. The level of ROS and the number of apoptotic cells exhibited the same tendency, and higher ROS levels and more apoptosis cells 1 and 12 h after reperfusion were observed.

CONCLUSIONOur study suggests that ischemia reperfusion can cause a series of injury stress responses in submandibular glands, which might have an important function in the early phase dysfunction of transplanted submandibular glands.

Humans ; Myocardial Infarction ; physiopathology ; Myocardial Reperfusion Injury