**3.1. Glucose metabolism**

**2. Adenosine triphosphate depletion**

4 Artery Bypass

may lead to cell death and destruction of the parenchymal tissue.

tides, the precursors for ATP.

**3. Changes in metabolism (Figure 2)**

dation), amino acids and oxidative phosphorylation.

**Figure 1.** Hydrolysis of Adenosine-triphosphate provides energy (30.5 kJ per mole) for biochemical reactions

When devoid of ATP, the cell derives its energy from the pyrophosphate bonds of ADP as they are degraded to adenosine monophosphate (AMP) and then to adenosine. Adenosine diffuses freely out of the cell, dramatically reducing the intracellular pool of adenine nucleo‐

In the presence of oxygen, human cells respire and derive their energy from the complete degradation of food (fats, carbohydrates and amino acids) by specific oxidative processes that fuel oxidative phosphorylation. A lack of oxygen completely changes these metabolic pathways, disrupting glycolysis and inhibiting the degradation pathways of lipids (beta-oxi‐

Eukaryotic cells contain mitochondria, organelles whose main function is to produce adeno‐ sine triphosphate (ATP). ATP is an essential energy substrate, as its hydrolysis provides en‐ ergy for many metabolic and biochemical reactions involved in development, adaptation and cell survival. ATP production in an aerobic cell is particularly effective when the degra‐ dation of key nutrients such as glucose and fatty acids is coupled to a supramolecular com‐ plex located in the inner membrane of mitochondria to drive oxidative phosphorylation. Oxidative phosphorylation is mediated by an electron transport chain that consists of four protein complexes and establishes a transmembrane electrochemical gradient by supporting the accumulation of protons in the intermembrane space of the mitochondria. This gradient is used as an energy source by ATP synthase during the synthesis of an ATP molecule from a molecule of adenosine diphosphate (ADP) and an inorganic phosphate (Figure 1). Without oxygen, oxidative phosphorylation stops: the proton gradient between the intermembrane space and the inner mitochondria is abolished, and ATP synthesis is interrupted. The ensu‐ ing rapid fall in intracellular ATP induces a cascade of events leading to reversible cell dam‐ age. However, over time, the damage increases and gradually becomes irreversible, which

During ischemia, the cell will change not only its glucose supply routes but also its glycoly‐ sis pathways and transition from aerobic glycolysis to anaerobic glycolysis. When this hap‐ pens, the available cytosolic glucose is metabolized by anaerobic glycolysis and becomes the main source of ATP. The efficiency of this process is much lower than that of aerobic glycol‐ ysis coupled to oxidative phosphorylation; the anaerobic degradation of one molecule of glucose produces 2 ATP molecules compared to the 36 ATP molecules that are produced un‐ der aerobic conditions. Consumption quickly exceeds production, and the intracellular con‐ centration of ATP decreases. For example, in the heart, the degree of glycolysis inhibition is directly proportional to the severity of coronary flow restriction.[3]-[5]
