scholarly journals Combined effects of the implementation of magnesium and ascorbic acid on myocardial ischemia-reperfusion in open heart surgery

2021 ◽  
Vol 3 (4) ◽  
pp. 319-326
Author(s):  
Yıldırım GÜLTEKİN ◽  
Abdulkadir GÜZEL ◽  
Atalay KARAKAYA ◽  
Yavuz BEŞOĞUL
2019 ◽  
Vol 22 (1) ◽  
pp. E027-E031 ◽  
Author(s):  
Naim Boran Tumer ◽  
Gokhan Erol ◽  
Atike Tekeli Kunt ◽  
Suat Doganci

Myocardial ischemia-reperfusion injury continues to be observed during open heart surgery. Various experimental models have been developed to overcome this injury and to increase postoperative prognosis. This study was conducted to assess the effect that iloprost, a prostacyclin analogue, can have on myocardial ischemia-reperfusion injury. We evaluated tissue damage by measuring the levels of malonyldialdehyde (MDA), glutathione, and nitric oxide (NO) in tissue and perfusates. In this study, 20 guinea pig hearts were prepared by using the modified Langendorff perfusion apparatus to form control (n = 10) and experimental study groups (n = 10). Following a preischemic period of perfusion and an ischemic period of 20 minutes, control hearts were perfused with Krebs–Henseleit solution. In the experimental group, iloprost (0.45 µg/kg per hour) was included in the perfusates for the last 10 minutes of the preischemic phase. Following cardiac stabilization, heart rate (pulse/min), contractility (mm), and aortic pressure (mmHg) values were recorded at the end of preischemia, postischemia, and reperfusion. Perfusate and tissue analyses for glutathione, MDA, and NO levels were made in each group at the end of experiments. Iloprost was found to have protective effects against myocardial ischemia by means of increased myocardial contractility, decreased tissue/perfusate glutathione levels and inhibited rise of tissue/perfusate MDA observed in the iloprost-treated experimental group. Future investigations on myocardial ischemia-reperfusion injury must evaluate iloprost-related mechanisms.


1995 ◽  
Vol 60 (3) ◽  
pp. 736-737 ◽  
Author(s):  
Ingrid Emerit ◽  
Jean-Noël Fabiani ◽  
Olivier Ponzio ◽  
Andrew Murday ◽  
Françoise Lunel ◽  
...  

1988 ◽  
Vol 46 (6) ◽  
pp. 619-624 ◽  
Author(s):  
Ingrid Emerit ◽  
Jean-Noël Fabiani ◽  
Olivier Ponzio ◽  
Andrew Murday ◽  
Françoise Lunel ◽  
...  

Perfusion ◽  
2010 ◽  
Vol 25 (1) ◽  
pp. 5-7 ◽  
Author(s):  
Laszlo Hejjel ◽  
Gabor Szluka ◽  
Laszlo Göbölös ◽  
Sandor Szabados ◽  
Tamas Varga ◽  
...  

Objectives: Besides low mortality and morbidity rates in cardiac surgery, the associated cognitive dysfunction is the focus of interest. One possible reason is microembolisation. Methods and results: The authors analysed the crystallogenesis in the calcium-containing prime, inspired by their observation that the fluid sometimes becomes turbid during the priming process. Lactated Ringer-based prime solutions were tested, adding mannitol, NaHCO3, and heparin. The oxygenator was ventilated with compressed medical air. Samples were taken for dynamic light scattering particulate level analysis. The priming was furthermore modelled in the laboratory by mixing the components and then ventilating the mixture through with compressed air. Turbid solutions from the operating room contained 100-6500 nm crystals, while clear solutions contained 20-473 nm particles. In the model, continuous pH measurement showed pH 6.4-7.4 after blending the solutions, which then elevated the pH to 7.5-8.0 after ventilation with concomitant turbidity. The pH of the prime can be stabilized by the addition of ascorbic acid (1-2 mg/ml) and, also, the turbidity may be prevented. Conclusion: Ventilating the lactated Ringer-based calcium-containing primes after blending is not advisible because of alkalization and crystallogenesis. Ascorbic acid stabilizes the pH and prevents crystallogenesis in the prime. Pre-bypass filtration is recommended.


1981 ◽  
Author(s):  
D S Rosenbaum ◽  
H Feinberg ◽  
S Levitsky

Recent evidence indicates that myocardial ischemia activates circulating platelets. Open heart surgery imposes global ischemia and platelet activation could lead to intravascular platelet deposition in ischemically injured myocardium. Platelets were labeled with111In and 51cr. The radioactive cells were injected into dogs prior to cardiopulmonary bypass. Following bypass the aorta was clamped to induce 60 min of global normothermic ischemia. The clamp was then removed to reperfuse the myocardium. Tissue biopsy 111In and 51cr activity indexed platelet content and the extent of perfusion respectively. The tissue platelet content in excess of that predicted from the tissue blood content was determined. A substantial increase in platelet content (X = 400%) was found during the reperfusion period following ischemic insult. Although platelets were sequestered in other organs the increases were moderate and unrelated to ischemia. Thus, the significant excess of platelets found in myocardium during coronary reperfusion indicates the presence of platelet thrombi. Low output failure, a complication of open heart surgery, may be the result of platelet microthrombi lodged in the small vasculature.


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