Table 3 Result summary
Figure | Interpretation |
|---|---|
Figure 4 | − Hypertrophic cardiomyopathy, a general observation in the use of slaughterhouse hearts (before) − Swelling of the cardiac tissue during reperfusion (after) |
Figure 5 | − Diminishing cardiac functions, possibly due to the initiation of waste product intoxication, reduction of essential nutrients, ion imbalances, cardiac necrosis and, most likely lastly, reperfusion injury and inflammation |
Figure 6 | − Hyperpotassemia (b), hypermagnesemia (g) and hyperphosphatemia(c) due to cardiac necrosis and washout of cardioplegia − Hypersodemia (a) due to sodium bicarbonate administration (pH balancing), while calcium chloride was administered to counterbalance the calcium reduction caused by bicarbonate, resulting in hypercalcemia (f) and hyperchloremia (e) − Hyperosmolarity (d) due to increase of ions |
Figure 7 | − General physiological aerobic cardiac metabolism, supported by free fatty acid (c) uptake and lactate (b) as well as glucose (a) metabolism − Amino acid catabolism, confirmed by rise of ammonia (d) − Decrease of essential cardiac nutrients (e.g. free fatty acids) and increase of toxic waste products (e.g. ammonia) over time − Rise of lactate after 180 min signalizes ischemia and acidosis − Hyperuremia (e) − Hypercreatininemia (f) − Static triglycerides (g) verifies the exclusion of fluid evaporation as a cause for the ion increase |
Figure 8 | − Hypoalbumia (a) due to blood dilution and potential cause for edema − Slight elevation of free hemoglobin (b) caused by the centrifugal pump − Hypercalcitriolemia (c) − Inconspicuous pH (e) and base excess(d) values and atrial oxygenation (f) |
Figure 9 | − Severe cardiac necrosis possibly due to reperfusion injury and inflammation and, heterogeneous cardioplegia delivery in the slaughterhouse |
− Physiological electrical activities of hearts during working mode − Unaltered electrical conduction pathways |