Polyphenol (-)-epigallocatechin gallate targeting myocardial reperfusion limits infarct size and improves cardiac function / 대한마취과학회지

BACKGROUND: This experiment was performed to determine the effect of polyphenolic (-)-epigallocatechin (EGCG), the most abundant catechin of green tea, given at reperfusion period. METHODS: Isolated rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Green tea extract (GT) was perfused with the following concentrations; 0, 0.5, and 1 micrometer (GT-O, GT-0.5, and GT-1, respectively). In a next experiment, hearts were assigned randomly to one of the following groups; Control, EGCG-1 (1 micrometer of EGCG), and EGCG-10 (10 micrometer of EGCG). GT and EGCG were perfused for a period of 5 min before and 30 min after reperfusion. For comparison of cardioprotection among groups, morphometric measurement was performed by 2,3,5-triphenyltetrazolium chloride staning. RESULTS: GT 1 micrometer (10.3 +/- 2.1%, P < 0.05) significantly reduced infarct volume as a percentage of ischemic volume compared to untreated hearts (27.4 +/- 1.1%). EGCG 10 micrometer (13.2 +/- 4.0%) significantly reduced myocardial infarction compared to control hearts (27.2 +/- 1.4%, P = 0.002). After 2 h of reperfusion, cardiodynamic variables, including left ventricular developed pressure, rate-pressure produce, +dP/dt(max), and -dP/dt(min) were significantly improved by 10 micrometer of EGCG compared to control hearts (P = 0.01, 0.016, 0.009, and 0.019, respectively). CONCLUSIONS: EGCG treatment at an early reperfusion period reduces myocardial infarction and improves cardiodynamics in isolated rat hearts.

Polyphenol (-)-epigallocatechin gallate targeting myocardial reperfusion limits infarct size and improves cardiac function / 대한마취과학회지

BACKGROUND: This experiment was performed to determine the effect of polyphenolic (-)-epigallocatechin (EGCG), the most abundant catechin of green tea, given at reperfusion period. METHODS: Isolated rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Green tea extract (GT) was perfused with the following concentrations; 0, 0.5, and 1 micrometer (GT-O, GT-0.5, and GT-1, respectively). In a next experiment, hearts were assigned randomly to one of the following groups; Control, EGCG-1 (1 micrometer of EGCG), and EGCG-10 (10 micrometer of EGCG). GT and EGCG were perfused for a period of 5 min before and 30 min after reperfusion. For comparison of cardioprotection among groups, morphometric measurement was performed by 2,3,5-triphenyltetrazolium chloride staning. RESULTS: GT 1 micrometer (10.3 +/- 2.1%, P < 0.05) significantly reduced infarct volume as a percentage of ischemic volume compared to untreated hearts (27.4 +/- 1.1%). EGCG 10 micrometer (13.2 +/- 4.0%) significantly reduced myocardial infarction compared to control hearts (27.2 +/- 1.4%, P = 0.002). After 2 h of reperfusion, cardiodynamic variables, including left ventricular developed pressure, rate-pressure produce, +dP/dt(max), and -dP/dt(min) were significantly improved by 10 micrometer of EGCG compared to control hearts (P = 0.01, 0.016, 0.009, and 0.019, respectively). CONCLUSIONS: EGCG treatment at an early reperfusion period reduces myocardial infarction and improves cardiodynamics in isolated rat hearts.

Cardiomyopathy after local infiltration or application of epinephrine for plastic surgery under general anesthesia : Two cases report / 대한마취과학회지

Catecholamine-induced cardiomyopathy rarely occurs after local epinephrine infiltration. We experienced two patients with catecholamine induced cardiomyopathies. An 8-yr-old girl was scheduled for closed reduction of a nasal bone fracture. Propofol and rocuronium bromide were used for induction of anesthesia. After induction, lidocaine mixed with epinephrine was infiltrated to the block of supratrochlear and infraorbital nerves. About 10 sec later ventricular tachycardia, hypotension, hypoxemia, and pulmonary edema developed. The other case was a 23-yr-old woman with a nasal bone fracture. Propofol, rocuronium bromide, and fentanyl were used for the induction of anesthesia. After induction, epinephrine-containing wet gauze was packed in the nasal cavity for mucosal shrinkage. About 1 minute later, hypertension, tachycardia, and hypoxemia developed. After each operation, a transthorcic echo-cardiogram revealed hypokynesia of the myocardium.

Effect of A Kappa-opioid Receptor Agonist U50488H Given at Early Reperfusion Phase in Isolated Rat Hearts / 대한마취과학회지

BACKGROUND: The experiment was performed to determine the role of kappa-opioid receptor (OR) agonist U50488H given at early reperfusion. METHODS: Isolated hearts were subjected to 30 minutes of regional ischemia and 120 minutes of reperfusion.Hearts were assigned randomly to one of the three groups:1) Control (n = 9), 2) U50-1 (n = 8); 10micrometer of U50488H, and 3) U50-10 (n = 8); 10micrometer of U50488H.U50488 was perfused for a period of 5 min before and 30 min after reperfusion. RESULTS: U50488H significantly reduced infarct size as a percentage of ischemic area (12.2 +/- 1.9% in U50-1 and 7.2 +/- 1.7% in U50-10, P < 0.001) compared to the control hearts (27.2 +/- 1.2%). After 2 hrs of reperfusion, left ventricular developed pressure was significantly recovered by U50488H (62.6 +/- 5.7% in U50-1 and 68.6 +/- 4.7% in U50-10, P = 0.018 and 0.002, respectively) compared to the control (46.3 +/- 4.4%).Rate-pressure product was improved by 100micrometer U50488H (62.3 +/- 5.5%, P = 0.007) but not by 1micrometer U50488H (50.0 +/- 4.1%) compared to the control (44.7 +/- 4.5%).U50488H significantly increased the + dP/dt(max) (77.9 +/- 5.5% in U50-1 and 78.0 +/- 4.3 in U50-10, P = 0.005 and 0.001 vs. control, respectively).The -dP/dt(min) also improved by 10micrometer U50488H (64.7 +/- 4.8%, P = 0.003) compared to control (47.0 +/- 2.7%). CONCLUSIONS: U50488H given at early reperfusion phase reduces both infarct size and myocardial stunning in isolated rat hearts.

Cardioprotective signaling cascade of A2 adenosine receptor agonist 5'-N-ethylcarboxaminidoadenosine against myocardial reperfusion injury / 대한마취과학회지

BACKGROUND: This experiments investigated the signaling cascade responsible for anti-infarct effect by an A2 adenosine receptor (AR) agonist 5'-N-Ethylcarboxaminidoadenosine (NECA). METHODS: Langendorff perfused isolated rat hearts were subjected to 30 minutes of regional ischemia and 120 minutes of reperfusion. Drugs were perfused for a period of 5 minutes before and 60 minutes after reperfusion. For comparison of cardioprotection among groups, area at necrosis (AN) and area at risk (AAR) were measured by triphenyltetrazolium chloride staining. RESULTS: NECA significantly attenuated AN/AAR (14.1 +/- 1.9%, P < 0.001) compared with control hearts (30.7 +/- 2.8%). Anti-infarct effect by NECA was attenuated by an A(2A)AR antagonist 8-(3-chlorostyryl)caffeine (23.7 +/- 3.4%, P < 0.05) and an A(2B)AR antagonist MRS1706 (29.9 +/- 3.3%, P < 0.001). Cardioprotection by NECA was blocked by a guanylyl cyclase inhibitor (23.1 +/- 2.9%, P < 0.05) and a protein kinase G (PKG) inhibitor KT5823 (30.3 +/- 3.2%, P < 0.001). Glycogen synthase kinase-3beta (GSK-3beta) inhibitor SB216763 attenuated the AN/AAR in both NECA with MRS (17.8 +/- 2.7%, P < 0.01 vs. control) and NECA with KT5823 treated hearts (8.2 +/- 1.8%, P < 0.001 vs. control). The mitochondrial permeability transition pore (mPTP) opener atractyloside also aborted NECA's anti-infarct effect (24.7 +/- 2.4% P < 0.05). CONCLUSIONS: The signaling pathway by NECA administered at reperfusion involves the activation of both A2AAR and A2BAR and cGMP/PKG pathway, which in turn depends on inactivation of GSK-3beta and inhibition of mPTP opening.