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Biomedical subjects

J Amano

Publications and source records attributed to J Amano.

At least 217 records · Page 12Linked to original sources
PubMed1983

Metabolic effect of glucose, insulin and potassium cardioplegia.

Glucose-insulin-potassium (GIK) solution is widely used as a cardioplegic infusate for myocardial protection during aortic cross-clamping, to obtain rapid diastolic arrest and preservation of energy stores. Nine male patients with aorto-coronary bypass grafting procedure were studied with regard to the metabolic influence of GIK cardioplegia. Hyperglycemia was induced by the infusion of GIK solution for one week after surgery. The serum level of non-esterified fatty acid was high for one week while the triglyceride level was maintained at a high level only in the early post-operative period. Insulin, glucagon and growth hormone which influence carbohydrate and lipid metabolism were also elevated for one week after infusion of GIK solution. We conclude that the derangement of carbohydrate and lipid metabolism which is provoked by the use of GIK cardioplegia normalizes within two weeks after operation.

Blood Glucose↗
PubMed1983

Clinical pharmacokinetics and diuretic effect of furosemide in plain tablet and retard capsule with normal subjects and cirrhotic patients.

The dissolution profiles of furosemide in various solutions were studied with plain tablet and retard capsule of furosemide. The rate constant and percent dissolution in retard capsule were lower than that in plain tablet. Clinical pharmacokinetics and diuretic effect of furosemide after oral administration of two dosage forms were also studied with 3 normal subjects and 3 cirrhotic patients. In normal subjects, the extent of furosemide absorption from retard capsule was 45% of plain tablet. The daily urine volume after oral administration of two dosage forms was comparable, however, quite different profiles were observed between these dosage forms. In patients, the extent of furosemide absorption in retard capsule was one half that of plain tablet. The dose of retard capsule was increased without adverse reactions, thus decreasing of ascites, which was not observed with plain tablet, was achieved with increasing urine volume.

Adult↗
PubMed1982

Effect of glutathion pretreatment on hypothermic ischemic cardioplegia.

Glutathion (GSH) plays an important role in maintenance of the redox state of the myocardium and acts as the membrane stabilizer. Seventeen patients who underwent cardiac surgery were subjected to cardiopulmonary bypass (CPB) and ischemic cardioplegia. The effect of GSH on ischemic myocardium was evaluated by serum lysosomal enzymes (acid phosphatase, beta-glucuronidase), isoenzymes of creatine phosphokinase (MB-CPK) and aspartate aminotransferase (m-GOT). standard CPB was instituted and systemic hypothermia was employed. GSH was administered to 8 patients in a dose of 200 mg/kg i.v. prior to institution of CPB. Mixed venous blood was sampled before administration of GSH, 10 min after institution of CPB and 0, 1, 6, 24 and 48 hr of reperfusion period following cardioplegia. Activity of acid phosphatase and beta-glucuronidase were significantly suppressed in the GSH-treated group compared to the non-treated group at 24 hours of reperfusion and immediately after aortic unclamping, respectively. Serum MB-CPK levels remained stable during reperfusion, but in the non-treated group, the level increased significantly at 6 hours of reperfusion. Increment of serum m-GOT levels was significantly suppressed at 1, 6 and 24 hours of reperfusion, compared to the non-treated group. These data suggest that pretreatment of GSH can protect the myocardium subjected to CPB from ischemic insult.

Acid Phosphatase↗
PubMed1982

Myocardial protection by lidocaine hydrochloride in aorto-coronary bypass surgery.

Myocardial protective effect of lidocaine hydrochloride on the ischemic myocardium was evaluated by serum (MB-CK) and cardiac function in 48 patients; 24 patients in control (C) and 24 patients in lidocaine-treated group (L), who underwent aorto-coronary bypass surgery. Lidocaine hydrochloride, 1 mg/min was administered by continuous drip infusion from initiation of anesthesia, and throughout the operation and postoperative period for 24 hours. There were no significant differences between two groups with regard to duration of cardioplegia and cardiopulmonary bypass, hypothermic level and the number of grafts implanted. Serum MB-CK at 18-24 hours following cardioplegia was 39.5 +/- 15.2 I.U. (C) and 14.2 +/- 4.0 I.U. (L), (p less than 0.05). Cardiac index and stroke volume index were significantly increased in the lidocaine-treated group at 24 hours following aorto-coronary bypass surgery, as compared to the control group. Lidocaine thus appears to be beneficial in aorto-coronary bypass surgery to prevent ischemic changes in the myocardium.

Cold Temperature↗
PubMed1982

Superior action of magnesium-lidocaine-1-aspartate cardioplegia to glucose-insulin-potassium cardioplegia in experimental myocardial protection.

The effect of 2 hours of hypothermic Mg-lidocaine cardioplegia upon left ventricular function, myocardial high-energy stores, edema, and ultrastructure was studied as compared to glucose-insulin-potassium (GIK) cardioplegia in 12 mongrel dogs. The myocardial temperature recorded in the ventricular septum was kept at 20 degrees C during the cardioplegia. The heart was re-warmed up to 37 degrees C by the support of cardiopulmonary bypass, then, observations were made during a 60 minutes reperfusion. Left ventricular function was preserved at a more physiological level in cases of Mg-lidocaine cardioplegia. Myocardial ATP as preserved at significantly higher levels following Mg-lidocaine cardioplegia than in cases of GIK cardioplegia (p < 0.05). However, content of myocardial creatine phosphate was higher in the GIK cardioplegia group than that in Mg-lidocaine group in the subendocardium and the ventricular septum. Myocardial edema was significantly suppressed following Mg-lidocaine cardioplegia, and such was significantly lower than in cases of GIK cardioplegia (p < 0.05). The myocardial ultrastructure was protected from ischemic insult in the Mg-lidocaine cardioplegia group. These data suggest that Mg-lidocaine-1-aspartate solution is superior to GIK solution as a cardioplegic solution, and that such will feasibly provide myocardial protection for 2 hours of hypothermic cardiac arrest, in an experimental reperfused model.

Adenosine Triphosphate↗
PubMed1982

Studies on the significance of serum mitochondrial aspartate aminotransferase activity following ischemic cardiac arrest.

Aspartate aminotransferase (EC 2.6.1.1:AST) is known to have two isoenzymes, one associated with the cytoplasm (c-AST) and the other with the mitochondria (m-AST). We studied the relationships of m-AST activity in the coronary sinus blood to left ventricular function, coronary blood flow, water content and high-energy phosphate stores of the left ventricle following hypothermic ischemic cardiac arrest. Under cardiopulmonary bypass with hypothermia of 20 degrees C of myocardial temperature, 120 min of aortic occlusion was employed in 15 mongrel dogs. Left ventricular function (peak left ventricular pressure, left ventricular end-diastolic pressure, max dp/dt, cardiac index, left ventricular stroke work index), coronary blood flow, myocardial oxygen consumption, myocardial enzyme activity (m-AST, CK-MB), myocardial water content and high-energy phosphate stores (adenosine triphosphate, creatine phosphate) of the subendocardium of the left ventricle were measured. Data was obtained in the control state, and after 0, 30 and 60 min of reperfusion. Significant negative correlations were obtained between m-AST activity and peak left ventricular pressure (r = -0.81, p less than 0.001), max dp/dt (r = -0.83, p less than 0.001), cardiac product (r = -0.73, p less than 0.01), coronary blood flow (r = -0.59, p less than 0.05), adenosine triphosphate level (r = 0.72, p less than 0.01) and creatine phosphate level (r = -0.72, p less than 0.02) after 60 min of reperfusion. Significant positive correlations were obtained between m-AST activity and left ventricular end-diastolic pressure (r=0.75, p less than 0.01) and water content (r = 0.78, p less than 0.01) after 60 min of reperfusion. These results led to the assumption that serum m-AST activity in the coronary venous blood is a useful index to evaluate the degree of myocardial injury.

Adenosine Triphosphate↗
PubMed1982

The optimal flow rate during reperfusion after hypothermic ischemic arrest.

This experiment was designed to determine the optimal flow rate during early reperfusion after ischemic arrest for one hour at 28 degrees C of myocardial temperature, assessed by cardiac function, biochemistry and fine structure of the left ventricle. Under cardiopulmonary bypass (CPB) at a flow rate of 80 ml/kg/min, the ascending aorta was clamped for one hour at 28 degrees C of myocardial temperature in 19 mongrel dogs. After the aorta was declamped, the perfusion pressure was maintained at 50 mmHg and dogs were divided into 3 groups by flow rate of 50 (Group A), 80 (Group B) and 150 ml/kg/min (Group C) for 15 min of reperfusion. The left ventricular function was measured and calculated before the institution of CPB and 30 and 60 min after the declamping of the aorta. Myocardial isoenzymes (m-GOT, MB-CPK) in the coronary sinus venous blood were measured. Myocardial adenosine triphosphate (ATP), creatine phosphate (CP) and water content were measured by the samples of the epicardial and endocardial layers of the left ventricle and the ventricular septum at the end of experiment. The subendocardium of the left ventricle was examined by electron microscopy. Mortality rates were 1/6 (16.7%) in Group A, 2/7 (28.6%) in Group B and 4/6 (66.7%) in Group C. The myocardial water content was the lowest, and ATP was significantly higher in Group A compared to others. Left ventricular endodiastolic pressure was the lowest and the ultrastructure was well maintained in Group A. These data suggest that a high flow rate is detrimental to myocardial recovery during early reperfusion, and the optimal flow rate during early reperfusion after ischemic arrest (60 min, 28 degrees C) appears to be 50 ml/kg/min.

Adenosine Triphosphate↗
PubMed1982

Optimal calcium concentration for a cardioplegic solution and "calcium paradox".

This study was performed to determine the optimal calcium concentration for a cardioplegic solution and to examine the effect of hypothermia on the occurrence of "calcium paradox." Under cardiopulmonary bypass with moderate hypothermia, 90 min of aortic occlusion was employed, and cardioplegic solutions of different calcium concentrations were infused continuously from the aortic root. The myocardial temperature was kept around 28 degrees C in 36 mongrel dogs (Group A) and 20 degrees C in six dogs (Group B). Calcium concentrations of the infused cardioplegic solutions were 0, 1, 2, 3, 4, and 5 mEq/liter in Group A and 0 in Group B. Hemodynamics, myocardial enzymes, and myocardial ultrastructure were evaluated in each group. In Group A, severe myocardial damage was observed in the hearts perfused with calcium-free solution. In the group employing the solution with 5 mEq/liter of calcium, the left ventricle was extraordinarily contracted during aortic clamping and was unable to survive 60 min after unclamping in all cases. However, in the group with 2 mEq/liter calcium, myocardial function and structure were well preserved. These results suggested that the optimum calcium concentration of a cardioplegic solution was 2 mEq/liter and that hypothermia at 20 degrees C of myocardial temperature prevents "calcium paradox."

Animals↗
PubMed1981

Relationship between hemodynamics and cardiac metabolism in the reperfusion period following hypothermic global ischemia.

Ten mongrel dogs were subjected to hypothermic ischemic cardioplegia for two hours followed by 30 minutes of reperfusion to characterize the relationship between hemodynamic parameters during reperfusion and the recovery of high energy store of the post-ischemic left ventricular myocardium. Dogs were anesthetized with intravenous pentobarbital 30 mg/kg, and standard cardiopulmonary bypass was instituted with the flow rate of 80 ml/min/kg and perfusion pressure around 80 mmHg. Ischemic cardioplegia was obtained by cross-clamping of the aorta for 2 hours under 20 degrees C of myocardial temperature. After termination of cardioplegia, the heart was rewarmed by the support of cardiopulmonary bypass with the flow rate of 80 ml/min/kg until the myocardial temperature was reached 36 degrees C. Hemodynamic parameters were measured throughout the experiment and myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) were measured at the end of experiment. Correlation was significant between myocardial ATP and coronary blood flow and myocardial oxygen consumption. However, myocardial creatine phosphate correlated poorly to coronary blood flow, myocardial oxygen consumption and other hemodynamic parameters. These results indicate that the recovery of myocardial high energy store is partly related to coronary blood flow and myocardial oxygen consumption, but other parameters are probably involved in the process of early recovery of the myocardium from ischemic cardioplegia.

Adenosine Triphosphate↗
PubMed1980

Additive protection of aprotinin, protease inhibitor to cold cardioplegia from ischemic myocarium.

Protective action of aprotinin froom ischemic myocardial damage was evaluated in 9 patients compared to non-treated 18 patients, who underwent open heart surgery (22 ACB, 3 AVR and 2 MVR) with respect to the alterations of beta-glucronidase, acid-phosphatase, MB-CPK and m-GOT. Cold cardioplegia with glucose-insulin-potassium solution was used in this investigation. Average arrest time was 78.6 +/- 4.9 minutes associated with hypothermia between 25 and 28 degrees C in rectal temperature. Aprotinin was administered in 9 patients intravenously with 5,000 KIU/Kg 30 minutes prior to CPB and then 5,000 KIU/Kg in the prime solution. Activity of beta-glucronidase was significantly suppressed in the aprotinin-treated group compared to the non-treated group following cardioplegia and in the reperfusion period up to 6 hours, however, acid-phosphatase failed to demonstrate significant difference among two groups. Serum MB-CPK and m-GOT levels in the aprotinin-treated group did not elevate the beginning of reperfusion following cardioplegia. These data suggest that aprotinin add myocardial protection to cold cardioplegia.

Acid Phosphatase↗