Application of warm cardioplegia early in reperfusion resuscitates the ischemic rat heart (part 10)

 ischemic rat heart (part 10)

Metabolic results: For each group, changes were recorded in the steady state cellular pools of phosphocreatine and ATP that occurred during the experimental protocol (Table 2). As expected, and confirmed by the spectra, a drastic decrease in cellular phosphocreatine and ATP with concurrent increase in Pi was indicated during myocardial ischemia (Figure 1). The phosphocreatine signal disappeared from the spectrum early in the ischemic episode, while the ATP signal was slower to disappear and became undetectable at the end of the ischemic interval.Application of warm cardioplegia early in reperfusion resuscitates the ischemic rat heart Once you have read all the information given above, you may be thinking about getting the drug that will solve the problem. At our canadian pharmacy family viagra you will find best deals on the medicine required getting it delivered very soon.

Figure 1 Representative 31P nuclear magnetic resonance spectra obtained from an isolated perfused rat heart throughout the experimental protocol (control group 1, perfused with Krebs-Henseleit [KH] buffer). Peak assignments are marked on top trace. Spectrare-corded are A, control, baseline; B, after 10 mins of ischemia; C, at the end of the ischemic period; D, early in the postischemic KH reperfusion (10 mins); E, after 30 mins of reperfusion; and F,following 50 mins reperfusion. Two inorganic phosphate (Pi) signals, one corresponding to normal tissue pH and the other (*) to acidic tissue pH, are visible in all spectra accumulated during the reperfusion interval. The left-most resonance appearing in traces D to F corresponds to monophosphoesters. PCr Phosphocreatine

Table 2 Preischemic hemodynamic parameters of perfused rat hearts and their percentage recovery values (± SEM) at the end of 50 mins of postischemic perfusion

Phosphocreatine ATP
GroupTime (mins) Stage10 120 Stage30 250 Stage10 120 Stage30 250
1 63±4 61±4.5 54±4 55±3.5 27±3 28±2.5 27±1.5 26±1.5
2 77±9 43±5* 49±3 51±5 52±2* 42±3.5* 37±2.5* 28±2
3 129±10*+ 140±7.5*+ 66±5*+ 55±4.5 50±3* 52±4.5* 32±4.5 30±3.5
4 121±9* 136±8.5* 81±9* 79±7* 55±3.5* 47±6* 38±3* 31±3.5
5 99±15* 124±15* 73±13* 62±10 45±4* 60±6* 43±12 37±8

*Significant at P<0.05 compared with group 1; fSignificant at P<0.05 compared with group 2. Group 1: Krebs-Henseleit (KH) buffer (control); group 2: warm blood diluted with normal KH buffer (control); group 3: warm blood diluted with modified St Thomas’ cardioplegic solution; group 4: high potassium KH cardioplegic solution; group 5: modified St Thomas’ cardioplegic solution

This entry was posted in Ischemic heart and tagged 31P-NMR spectroscopy, Blood cardioplegia, Ischemic heart.