Effect Of Limb Ischemic Preconditioning Research Articles

Limb ischemic preconditioning attenuates cerebral ischemic injury in rat model

Ischemic brain injury is not uncommon after open-heart surgery with cardiopulmonary bypass and seriously undermines the patients' life quality. Therefore, potential protective effects of limb ischemic preconditioning (LIP) on subsequent ischemic injury of the brain were investigated by evaluating anti-inflammatory effects and apoptosis of pyramidal neurons in the CA1 hippocampus. One hundred and eight Sprague-Dawley rats were divided into the middle cerebral artery occlusion (MCAO) group (n=54) and the LIP group (n=54). A thread was used to occlude the middle cerebral artery in the MCAO group and the LIP group animals were pretreated with LIP followed by MCAO. In the two groups, nine samples were collected at each time-point of 0, 6, 12, 24, 48 and 72 h after MCAO to detect IL-6 and IL-17 and their mRNA levels. Neurological severity scores (NSS) were examined before the animals were sacrificed. Compared with the LIP group, cerebral histopathological changes in the MCAO group were most distinct and significantly more infiltrated inflammatory and apoptotic neuronal cells were observed at 24, 48 and 72 h post-surgery. IL-17 and IL-6 mRNA levels analyzed by quantitative real-time polymerase chain reaction (PCR) (qRT-PCR) were significantly reduced in the LIP group compared with the MCAO group at the 12, 24 and 48 h time-points. A significant reduction in IL-17 expression level was determined by enzyme-linked immunosorbent assay (ELISA) in the LIP group at 12, 24 and 48 h, while IL-6 was significantly reduced at the 24 and 48 h time-points. The NSSs were not significantly different between the groups. Therefore, in a MCAO rat model, we have proved that LIP pretreatment can protect the brain from infarction after ischemic injury and induce ischemic tolerance, potentially, by reducing IL-17 to provide anti-inflammatory effects and attenuate apoptosis of hippocampal neuronal cells.

Effect of limb ischemic preconditioning on myocardial apoptosis-related proteins in ischemia-reperfusion injury

The aim of this study was to investigate the effect of limb ischemic preconditioning (LIPC) on myocardial apoptosis in myocardial ischemia-reperfusion injury (MIRI), as well as the regulation of caspase-3 and the B cell lymphoma 2 (Bcl-2) gene in LIPC. A total of 50 rats were divided randomly into 5 groups (n=10). Four rats in each group were drawn out for detection of apoptosis. The sham, MIRI and LIPC groups underwent surgery without additional treatment. In the LY294002 group, LY294002 preconditioning was administered 15 min before reperfusion. In the LY294002+LIPC group, following LIPC, LY294002 was administered 15 min before reperfusion. The relative expression of myocardial Bcl-2 and caspase-3 mRNA and the apoptotic index for each group were determined by reverse transcription-polymerase chain reaction (RT-PCR) and terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL), respectively. The ultrastructure of the cardiac muscle tissues was observed by election microscopy. Compared with the sham group, the expression of caspase-3 mRNA in the MIRI group significantly increased (P<0.05) and the expression of Bcl-2 mRNA clearly decreased. Compared with the MIRI group, LIPC reduced the expression of caspase-3 and increased the expression of Bcl-2 mRNA (P<0.05). There were no significant differences between the LY294002+LIPC group and the MIRI group. Compared with the sham group, the apoptotic index of myocardial cells in the MIRI group significantly increased (P<0.05). Compared with the MIRI group, LIPC significantly decreased the apoptotic index of myocardial cells (P<0.05) and LY294002 increased the apoptotic index of myocardial cells. Compared with the LIPC group, LY294002+LIPC significantly increased the apoptotic index of myocardial cells (P<0.05). There were no significant differences between the LY294002+LIPC and MIRI groups. In conclusion, LIPC increased the expression of Bcl-2 and decreased caspase-3 mRNA and apoptosis in myocardial tissue following MIRI. Therefore, LIPC plays a protective role in myocardial tissue.

The Optimal Strategy of Noninvasive Limb Ischemic Preconditioning for Protecting Heart Against Ischemia-Reperfusion Injury in Rats

Limb ischemic preconditioning (LIPC) induced by prior brief periods of ischemia-reperfusion (I/R) to a limb is a simple and convenient strategy to protect the heart from I/R injury. However, the optimal strategy is unknown. Therefore, the present study was conducted to test the most effective method of LIPC for clinical applications. Male Wistar rats were randomized into the following groups: control groups, consecutive LIPC groups, intermittent LIPC groups. The control groups, including the sham operation group, the ischemia-reperfusion (I/R)-control group, the myocardial ischemic preconditioning (MIPC) group, the femoral artery ischemic preconditioning (FAIP) group; the consecutive LIPC groups, including continuously using for 1 d, 3 d, and 7 d groups. Each group was tested on the first, third, and fifth d after LIPC; intermittent LIPC groups, including 1-d LIPC + 1-d interval group, 1-d LIPC + 2-d interval group, 3-d LIPC + 3-d interval group, 3-d LIPC + 5-d interval group. Left ventricular function, incidence of ventricular arrhythmia, and ST-segment were measured during I/R. Myocardial infarct size, creatine kinase isoenzyme MB (CK-MB), and cardiac troponins I (cTnI) were determined at the end of experiment. Compared with the I/R-controls, the MIPC, FAIP, continuous LIPC for 3 and 7 d and 1-d LIPC + 1-d interval groups showed amelioration of ventricular arrhythmia, improved left ventricular function, lower ST-segment elevation, reduced myocardial infarct size, decreased CK-MB, and cTnI activity. The protective effects of LIPC persisted for 72 h. Our results suggest that a 1-d LIPC + 1-d interval provides optimal cardioprotection from I/R.

Effect of Limb Ischemic Preconditioning on Myocardial Injury in Patients Undergoing Mitral Valve Replacement Surgery - A Randomized Controlled Trial -

Whether limb ischemic preconditioning (LIPC) is beneficial for patients undergoing mitral valve replacement (MVR) surgery is unknown. Seventy-five adult patients undergoing MVR surgery were randomly assigned to 3 groups: control group (n=25), LIPC group I (3 × 5-min cycles of right upper arm ischemia and 5-min reperfusion; n=25) and LIPC group II (3 × 5-min cycles of right upper arm ischemia and 5-min reperfusion combined with 2 × 10-min cycles of right upper leg ischemia and 10-min reperfusion; n=25). Cardiopulmonary bypass (CPB) time, cross-clamp time, cardiac index, cumulative postoperative dosage of dobutamine, intensive care stay, postoperative hospital stay were not statistically different. Although the cumulative postoperative dosage of dobutamine was not different, there was a significantly lower inotropic requirement in LIPC II compared with the control group at 4 and 8h after surgery. Plasma levels of cardiac troponin-I in the 3 groups significantly increased during CPB and peaked at 4h after surgery. Levels of cTnI in LIPC II were significantly lower than in the control group at each time point after surgery. Myocardial injury is obvious after MVR surgery. LIPC can protect the myocardium from ischemia-reperfusion injury and decrease the inotropic requirement after surgery. The data also confirmed the requirement for the preconditioning stimulus to cross a threshold.

Protective effect of limb ischemic preconditioning on acute lung injury induced by lipopolysaccharide in rats

To explore the protective effect of noninvasive limb ischemic preconditioning (N-LIP) on acute lung injury (ALT) induced by lipopolysaccharide (LPS) in rats. Fifteen female SD rats were randomly divided into a control group, an acute lung injury group (ALI group), an acute lung injury and noninvasive limb ischemic preconditioning group (ALI+N-LIP group). After ALI rats were treated with N-LIP, the changes of airway resistance (AR) and dynamic compliance (Cdyn) were tested by invasive pulmonary function system and recorded. Blood samples and bronchoalveolar lavage fluid (BALF) were collected, the amounts of white blood cell (WBC) in BALF were counted by cytometry, and the level of lactate dehydrogenase (LDH) in BALF was also examined by automatic biochemistry analyzer. The level of serum superoxide dismutase (SOD) and malondialdehyd (MDA) was examined by chromatometry. The lung tissues were acquired to observe the expression of pulmonary surfactant-associated protein-A (SP-A) and pathological changes. After being stimulated by methacholine (Mch), the increasing rate of AR and decreasing rate of Cdyn in the ALI+N-LIP group were less than those in the ALI group (P<0.01). The levels of WBC and LDH in BALF in the ALI+N-LIP group were much lower than those in the ALI group (P<0.05). Meanwhile, the activity of serum SOD in the ALI+N-LIP group was higher, and the level of serum MDA was lower than that in the ALI group (P<0.05). The expression of SP-A in the lung tissue in the ALI+N-LIP group was the highest in the 3 groups, while that in the ALI group was the weakest (P<0.01). Injury of the lung tissue in the ALI+N-LIP group was less than that in the ALI group, but more severe than that in the control group. N-LIP has protective effect on acute lung injury induced by LPS in rats. The possible mechanism is related to improving the secretion of SP-A and antioxidation.