The purpose of our study is to evaluate aggravation of arrhythmia induced byantiarrhythmic drugs during electrophysiologic testing In 266 tests, patients with arrhythmia weretreated with quinidine, procainamide, mexil...The purpose of our study is to evaluate aggravation of arrhythmia induced byantiarrhythmic drugs during electrophysiologic testing In 266 tests, patients with arrhythmia weretreated with quinidine, procainamide, mexiletine amicdarone, locainide pirmenol flacainide andnorpace and the results were analysed. Aggravation of arrhythmia induced by antiarrhythmic drugswas common, involving almost all antiarrhythmic drugs The incidence of aggravation was 21. 8%.There was no definite relationship between arrhythrnic aggravation and underlying heart diseases. Inno circumstances were blood levels in toxic range at the time of arrhythmic aggravation. Combinedwith antiarrhythmic drugs Ia+Ib (?) the incidence of aggravation of arrhythmia. Greatly wid-ened QRS might he a due to recognizing the danger of quinidine-induced arrhythmic aggravation.展开更多
Objective: To observe the inhibitory effect of calcitonin gene--related peptide (CGRP) on adriamycininduced acute cardiotoxicity. Methods: Primarily cultured rat myocardial cells were treated with 10-6 mol/Ladriamycin...Objective: To observe the inhibitory effect of calcitonin gene--related peptide (CGRP) on adriamycininduced acute cardiotoxicity. Methods: Primarily cultured rat myocardial cells were treated with 10-6 mol/Ladriamycin and 10-6mol/L adriamycin + 10 8mol/I. CGRP. Lactate dehydrogenase (LDH ) activity in the mediumand the contents of malondialdehyde (MDA ). calcium. and magnesium in the myocardial cells were assayed.Results: In the adriamycin group, LDH activity in medium and calcium, MDA contents in myocardial cells weresignificantly increased compared with those in control group, and magnesium content in the myocardial cells wassignificantly reduced. In the adriamycin group. there was a positive correlation between LDH activity in themedium and MDA content in the myocardial cells. Meanwhile, in the adriamycin + CGRP group,- CGRP mightsignificantly reduce the leakage of LDH from myocardial cells, lessen the increase in calcium and MDA contentsand prevent the loss of magnesium. Conclusion: CGRP may inhibit adriamycin induced acute cardiotoxicity byinhibiting lipid peroxidation, attenuating calcium overload, magnesium loss, and protecting enzyme activity.展开更多
Objective:To observe the effects of inhibition of glycolysis with iodoacetate (IAA) on calcium homeostasis and functional recovery of stunned myocardium in anesthetized dogs. Methods: Atomic absorption spectrophotomet...Objective:To observe the effects of inhibition of glycolysis with iodoacetate (IAA) on calcium homeostasis and functional recovery of stunned myocardium in anesthetized dogs. Methods: Atomic absorption spectrophotometry was employed to measure myocyte calcium and magnesium contents. Hemodynamics were monitored with a multichannel electrophysiologic recorder. Results: In nonischemic canine hearts (control), IAA's inhibition of glycolysis failed to change the [Ca2+] and [Mg2+] levels and cardiac functional conditions, whereas in hearts subjected to 15-minute ischemia , [Ca2+] increased from nonischemic 1.40±0. 20μmol/g to ischemic 1.80±0.17 μmol/g (P<0. 05), while [Mg2+] decreased. After 30 min of reperfusion,[Ca2+] continued to increase from 1.57±0.21 μmol/g (nonischemic area)to 2. 26±0. 09 μmol/g (abnormal area) and 60 min of reperfusion saw a slight restoration (1.54±0. 16 μmol/g in nonischemic area and 2. 21±0.20 μmol/g in abnormal area). In the glycolysis-inhibiting group, the calcium level registered a significant rise after 30 min of reperfusion: 1.57±0.07 μmol/g in nonischemic area and 2. 90? 0.25 μmol/g in abnormal area (P<0. 01).There was a significant difference between the glycolysis-inhibiting group and the group to which IAA was not applied. [Mg2+] maintained at a relatively low level and registered a more remarkable drop during inhibition of glycolysis, P<0.01 in comparison with the non IAA-administered group,suggesting that inhibition of glycolysis could cause severe calcium overload to sustain, in addition to an obvious harm to cardiac function. Left ventricular end-diastolic pressure and diastolic factor T were augmented andp/dt(max)declined. Conclusion: Since in vivo inhibition of glycolysis seemed to lead to severe calcium overload and hemodynamics changes,it might indicate that glycolysis played an importent role in the restoration of calcium homeostasis in postischemic myocardium,and that ATP derived from glycolysis took a significant part in myocardial ion transport both at the stage of ischemia and the early stage of reperfusion and in cardiac functional recovery.展开更多
文摘The purpose of our study is to evaluate aggravation of arrhythmia induced byantiarrhythmic drugs during electrophysiologic testing In 266 tests, patients with arrhythmia weretreated with quinidine, procainamide, mexiletine amicdarone, locainide pirmenol flacainide andnorpace and the results were analysed. Aggravation of arrhythmia induced by antiarrhythmic drugswas common, involving almost all antiarrhythmic drugs The incidence of aggravation was 21. 8%.There was no definite relationship between arrhythrnic aggravation and underlying heart diseases. Inno circumstances were blood levels in toxic range at the time of arrhythmic aggravation. Combinedwith antiarrhythmic drugs Ia+Ib (?) the incidence of aggravation of arrhythmia. Greatly wid-ened QRS might he a due to recognizing the danger of quinidine-induced arrhythmic aggravation.
文摘Objective: To observe the inhibitory effect of calcitonin gene--related peptide (CGRP) on adriamycininduced acute cardiotoxicity. Methods: Primarily cultured rat myocardial cells were treated with 10-6 mol/Ladriamycin and 10-6mol/L adriamycin + 10 8mol/I. CGRP. Lactate dehydrogenase (LDH ) activity in the mediumand the contents of malondialdehyde (MDA ). calcium. and magnesium in the myocardial cells were assayed.Results: In the adriamycin group, LDH activity in medium and calcium, MDA contents in myocardial cells weresignificantly increased compared with those in control group, and magnesium content in the myocardial cells wassignificantly reduced. In the adriamycin group. there was a positive correlation between LDH activity in themedium and MDA content in the myocardial cells. Meanwhile, in the adriamycin + CGRP group,- CGRP mightsignificantly reduce the leakage of LDH from myocardial cells, lessen the increase in calcium and MDA contentsand prevent the loss of magnesium. Conclusion: CGRP may inhibit adriamycin induced acute cardiotoxicity byinhibiting lipid peroxidation, attenuating calcium overload, magnesium loss, and protecting enzyme activity.
文摘Objective:To observe the effects of inhibition of glycolysis with iodoacetate (IAA) on calcium homeostasis and functional recovery of stunned myocardium in anesthetized dogs. Methods: Atomic absorption spectrophotometry was employed to measure myocyte calcium and magnesium contents. Hemodynamics were monitored with a multichannel electrophysiologic recorder. Results: In nonischemic canine hearts (control), IAA's inhibition of glycolysis failed to change the [Ca2+] and [Mg2+] levels and cardiac functional conditions, whereas in hearts subjected to 15-minute ischemia , [Ca2+] increased from nonischemic 1.40±0. 20μmol/g to ischemic 1.80±0.17 μmol/g (P<0. 05), while [Mg2+] decreased. After 30 min of reperfusion,[Ca2+] continued to increase from 1.57±0.21 μmol/g (nonischemic area)to 2. 26±0. 09 μmol/g (abnormal area) and 60 min of reperfusion saw a slight restoration (1.54±0. 16 μmol/g in nonischemic area and 2. 21±0.20 μmol/g in abnormal area). In the glycolysis-inhibiting group, the calcium level registered a significant rise after 30 min of reperfusion: 1.57±0.07 μmol/g in nonischemic area and 2. 90? 0.25 μmol/g in abnormal area (P<0. 01).There was a significant difference between the glycolysis-inhibiting group and the group to which IAA was not applied. [Mg2+] maintained at a relatively low level and registered a more remarkable drop during inhibition of glycolysis, P<0.01 in comparison with the non IAA-administered group,suggesting that inhibition of glycolysis could cause severe calcium overload to sustain, in addition to an obvious harm to cardiac function. Left ventricular end-diastolic pressure and diastolic factor T were augmented andp/dt(max)declined. Conclusion: Since in vivo inhibition of glycolysis seemed to lead to severe calcium overload and hemodynamics changes,it might indicate that glycolysis played an importent role in the restoration of calcium homeostasis in postischemic myocardium,and that ATP derived from glycolysis took a significant part in myocardial ion transport both at the stage of ischemia and the early stage of reperfusion and in cardiac functional recovery.
