OBJECTIVE: To test cathepsin L as a biomarker of myocardial ischemia by examination of cathepsin L expression in plasma after myocardial ischemia and ischemia-reperfusion in rats. METHODS: The rat models were established and divided in acute myocardial ischemia model (myocardial ischemia 30 min, 1 h, 2 h groups), ischemia-reperfusion model (ischemia-reperfusion group), and isoflurane-pretreated ischemia-reperfusion model (isoflurane-pretreated group), respectively. Normal control group and sham-operated group were established as contrast. The contents of cathepsin L in plasma were examined by ELISA and myocardial infarction areas were measured after TTC staining. RESULTS: No statistical significant changes were found among the experimental groups compared with the normal control group and sham-operated group (P>0.05). The cathepsin L from the ischemia-reperfusion group increased to 2.37 times compared with the normal control group (P<0.05). The cathepsin L and myocardium infarction size of isoflurane-pretreated group decreased compared with the ischemia-reperfusion group (P<0.05). CONCLUSION The cathepsin L in plasma is not a promising biomarker of acute myocardial ischemia. Isoflurane preconditioning can reduce the cathepsin L in plasma caused by ischemia-reperfusion injury.
Animals ; Biomarkers/blood* ; Cathepsin L/analysis* ; Isoflurane ; Myocardial Infarction/metabolism* ; Myocardial Ischemia ; Myocardial Reperfusion Injury/metabolism* ; Myocardium ; Rats

AIMTo study the varies and effects of ischemic preconditioning of myocardium on every part of adrenergic receptor-adenyl cyclase system in rats in vivo.

METHODSSD rats were randomly divided into three groups: CON group (n = 6), IP group (n = 12) and I/R group (n = 12). Surgical procedure included intermittent left coronary artery occlusion and reperfusion. After the procedure, the hearts were extracted. We analyzed the infarct size by TTC staining, measured serum myocardial enzymes, studied the beta-AR Bmax and KD by radioligand binding assay of receptors (RAB), and checked the activity of AC and the content of cAMP by radioimmunoassay (RIA).

RESULTSInfarct area were much smaller in IP group than in I/R group (P < 0.05). CK, CK-MB, LDH were significantly higher in I/R group (P < 0.01). The Bmax of beta-AR in IP group were much higher than in I/R group (P < 0.01). No difference of KD could be seen between IP and I/R group. In IP group, the activity of AC and the content of cAMP were higher than I/R group (P < 0.05).

CONCLUSIONIschemic preconditioning can protect the heart from necrosis and reduce endo-enzyme leakage. Ischemic preconditioning can increase the density of beta-AR, the activity of AC and the content of cAMP, which shows that the system of adrenergic receptor-adenyl cyclase system probably takes part in the protection of IP.

Adenylyl Cyclases ; metabolism ; Animals ; Female ; Ischemic Preconditioning, Myocardial ; Myocardial Ischemia ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta ; metabolism

OBJECTIVE: To explore the effect of Kuanxiong Aerosol (KXA) on isoproterenol (ISO)-induced myocardial injury in rat models. METHODS: Totally 24 rats were radomly divided into control, ISO, KXA low-dose and high-dose groups according to the randomized block design method, and were administered by intragastric administration for 10 consecutive days, and on the 9th and 10th days, rats were injected with ISO for 2 consecutive days to construct an acute myocardial ischemia model to evaluate the improvement of myocardial ischemia by KXA. In addition, the diastolic effect of KXA on rat thoracic aorta and its regulation of ion channels were tested by in vitro vascular tension test. The influence of KXA on the expression of calcium-CaM-dependent protein kinase II (CaMK II)/extracellular regulated protein kinases (ERK) signaling pathway has also been tested. RESULTS: KXA significantly reduced the ISO-induced increase in ST-segment, interventricular septal thickness, cardiac mass index and cardiac tissue pathological changes in rats. Moreover, the relaxation of isolated thoracic arterial rings that had been precontracted using norepinephrine (NE) or potassium chloride (KCl) was increased after KXA treatment in an endothelium-independent manner, and was attenuated by preincubation with verapamil, but not with tetraethylammonium chloride, 4-aminopyridine, glibenclamide, or barium chloride. KXA pretreatment attenuated vasoconstriction induced by CaCl₂ in Ca²⁺-free solutions containing K⁺ or NE. In addition, KXA pretreatment inhibited accumulation of Ca²⁺ in A7r5 cells mediated by KCl and NE and significantly decreased p-CaMK II and p-ERK levels. CONCLUSION KXA may inhibit influx and release of calcium and activate the CaMK II/ERK signaling pathway to produce vasodilatory effects, thereby improving myocardial injury.
Aerosols ; Animals ; Aorta, Thoracic ; Calcium/metabolism* ; Endothelium, Vascular/metabolism* ; Myocardial Ischemia/metabolism* ; Rats ; Vasodilation

OBJECTIVE: To explore expression of the glycoprotein in early myocardial ischemic. METHODS: The glycoprotein changes occurred at the early acute cardiac ischemic area induced experimentally by ligation of left coronary artery of 32 SD rats. 6 lectins were measured by means of immunohistochemical methods. RESULTS: Positive staining of PNA could be observed in ischemic area at 5 min after ischemia, and the positive area increased with the prolongation of ischemic period. It became the strongest for 2 h and then decreased. CONCLUSION This experiment proved that myocardial cell membrane in ischemia expressed D-galactose. This may be of some value in forensic medicine practice.
Animals ; Female ; Immunohistochemistry ; Male ; Membrane Glycoproteins/biosynthesis* ; Myocardial Ischemia/metabolism* ; Myocardium/metabolism* ; Rats ; Rats, Sprague-Dawley

Fatty Acids ; metabolism ; Humans ; Myocardial Ischemia ; diagnostic imaging ; metabolism ; Tomography, Emission-Computed, Single-Photon

Humans ; Ischemia ; metabolism ; pathology ; therapy ; Ischemic Postconditioning ; methods ; Myocardial Reperfusion Injury ; metabolism ; pathology ; therapy

OBJECTIVETo explore the relationship between α-actinin content and cardiac function in rats during myocardial ischemia-reperfusion.

METHODSThirty-two rats were randomized equally into sham-operated group, 30 min ischemia group, 1 h ischemia group, and 1 h ischemia with 2 h reperfusion group. Acute myocardial ischemia was induced in the 3 ischemia groups by ligation of the left anterior descending coronary artery, and the cardiac functions were evaluated. The myocardial contents of α-actinin was measured by immunohistochemistry, and phospholipase C (PLC) and phosphatidylinositol-3-kinase (PI3K) contents were determined by ELISA after the operations.

RESULTSThe left ventricular systolic pressure (LVSP), +dp/dt max, and -dp/dt max tended to decrease during myocardial ischemia, and increased after reperfusion, and the left ventricular end-diastolic pressure (LVEDP) showed reverse changes. The levels of α-actinin decreased with prolonged ischemia, showing a significant difference in 1 h ischemia group from those in the other 3 groups. PI3K and PLC contents were significantly increased with prolonged myocardial ischemia. Stimulation by LY-294002 and U-73122 caused enhanced contraction of single cardiomyocytes, and also increased the fluorescence intensity of α-actinin in the cardiomyocytes compared with that in 1 h ischemia group.

CONCLUSIONSThe cardiac dysfunction during acute ischemia-reperfusion in rats may be related with the changes of myocardial α-actinin content, which are probably a result of increased PI3K and PLC contents in the ischemic myocardium.

Actinin ; metabolism ; Animals ; Myocardial Ischemia ; metabolism ; physiopathology ; Myocardial Reperfusion Injury ; metabolism ; physiopathology ; Myocardium ; metabolism ; Phosphatidylinositol 3-Kinase ; metabolism ; Rats ; Rats, Wistar ; Type C Phospholipases ; metabolism

BACKGROUND: Lidocaine is a well known antiarrhythmic agent. However, recent reports indicate that indocaine has myocardial protective effects on acute myocardial ischemia and reperfusion. The exact mechanism of myocardial protection of lidocaine is still not clearly understood. In this study we intended to assess the effects of lidocaine on high energy phosphate metabolism in cats subjected to myocardial ischemia-reperfusion by using 31P MR spectroscopy. Effect of lidocaine on size of infarct will also be evaluated by 2, 3, 5-triphenyltetrazolium chloride(TTC) staining. METHODS: Twenty-seven cats were used for this study. The animals were divided into three groups : for group 1(n=10) and group 2(n=7), animals were subjected to a 90 min of LAD occlusion followed by a 90 min of reperfusion ; for group 3(n=10), a 20 min of occlusion followed by a 90 min of reperfusion. In group 2 and group 3, lidocaine(5mg/kg/hr) was infused continuously during the occlusion and reperfusion periods with an initial bolus injection(1mg/kg) before ligation of LAD. In-vivo MR spectroscopy was performed on a 4.7T Biospec System(Bruker, Switzerland). A home-made surface coil(diameter : 1.5cm) was used to receive31p signals from the myocardium underwent ischemic and reperfusion damage. RESULTS: Decrease of PCr during ischemic period was not different between each groups : PCr showed less than 30% of the baseline value at L-30 in group 1 and group 2 and at L-20 in group 3. More than 90% recovery of PCr was achieved at R-30 in group 2 and group 3, whereas less than 50% of PCr was recovered in group 1. Decrease of ATP during ischemic period was less pronounced in group 2 than in group 1 : in group 2 ATP depleted down to 25% of the baseline at L-90, whereas in group 1 ATP decreased to 50% of the baseline. Recovery of ATP during reperfusion period was not signiflcant in all three groups. On TTC staining, evidence of infarct was seen in all cases of group 1 : the area of infarct was 12.3+/-2.7% of the left ventricular mass and 23.9+/-6.1% of the area at risk. On the contrary, there was no evidence of infact in any case of group 2 and group 3. CONCLUSION: In this study, we found that lidocaine has myocardial protecitve effects on ischemia-reperfusion in cats. Lidocaine improves high energy phosphorous metabolism during ischemia and reperfusion as well as reduces infarct size.
Adenosine Triphosphate ; Animals ; Cats* ; Ischemia ; Lidocaine* ; Ligation ; Magnetic Resonance Spectroscopy ; Metabolism ; Myocardial Ischemia ; Myocardium ; Polymerase Chain Reaction ; Reperfusion ; Reperfusion Injury

Aged ; Biomarkers ; blood ; Cobalt ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; diagnosis ; Myocardial Ischemia ; diagnosis ; Serum Albumin ; metabolism ; Spectrophotometry

OBJECTIVETo investigate the role of calcium-sensing receptor (CaR) on ischemia/reperfusion-induced rat cardiomyocyte apoptosis.

METHODSThe isolated rat hearts were subjected to 40 min ischemia followed by 2h of reperfusion with or without CaR agonist GdCl3 at the beginning of reperfusion. Control hearts (without ischemia) and ischemic hearts (40 min ischemia without reperfusion) served as controls. The protein expressions of CaR, Bcl-2 and cyt C were detected by Western blot. Cardiomyocyte apoptosis was detected by TUNEL. Mitochondrial potential (Deltaphim) was detected by laser confocal microscopy.

RESULTSCompared to controls groups, the expressions of CaR and apoptotic cells were significantly increased, Deltaphim and expressions of mitochondria cyt C and Bcl-2 were significantly reduced in ischemia/reperfusion hearts with or without GdCl3.

CONCLUSIONCaR was involved in the induction of cardiomyocyte apoptosis during ischemia/reperfusion via mitochondrial pathway.

Animals ; Apoptosis ; Disease Models, Animal ; Female ; Male ; Mitochondria, Heart ; metabolism ; Myocardial Ischemia ; metabolism ; Myocardial Reperfusion Injury ; metabolism ; Myocytes, Cardiac ; cytology ; Rats ; Rats, Wistar ; Receptors, Calcium-Sensing ; metabolism