"Heart" - what is it, definition of the term
The cardiac organ is a muscular cavity that contracts rhythmically to propel blood throughout the circulatory system of mammals such as rats and mice, extracting oxygen from pulmonary exchange and delivering it to tissues while returning deoxygenated fluid to the lungs for re‑oxygenation.
Detailed information
The cardiac organ of rats and mice is a compact, four‑chambered structure weighing approximately 0.5 g in mice and 1.0 g in rats. The left ventricle dominates the mass, accounting for roughly 70 % of the total. Wall thickness averages 0.8 mm in mice and 1.2 mm in rats, reflecting the high metabolic demand of these small mammals.
Blood supply originates from paired coronary arteries that branch from the aortic root. The left coronary artery divides into anterior and circumflex branches, while the right coronary artery supplies the posterior wall. Capillary density reaches 1,200 mm⁻², ensuring efficient oxygen delivery during rapid heart rates that exceed 500 bpm in mice and 400 bpm in rats.
Electrical activity is governed by a well‑defined conduction system. The sinoatrial node initiates impulses that travel through the atrial myocardium to the atrioventricular node, then through the His‑Purkinje network to the ventricles. Electrocardiographic recordings display a short PR interval (≈15 ms in mice, ≈20 ms in rats) and a narrow QRS complex, consistent with rapid depolarization.
Key physiological parameters measured in laboratory studies include:
- Resting heart rate: 600–700 bpm (mouse), 350–450 bpm (rat)
- Stroke volume: 0.02 µL (mouse), 0.05 µL (rat)
- Cardiac output: 12–15 mL/min (mouse), 20–30 mL/min (rat)
- Ejection fraction: 70–80 % in both species
Experimental models exploit genetic manipulation, pharmacological intervention, and pressure overload to investigate disease mechanisms. Transgenic lines permit tissue‑specific expression of fluorescent reporters, facilitating real‑time imaging of contractile dynamics. Pressure overload, induced by aortic constriction, leads to hypertrophic remodeling that mirrors human pathological growth.
Comparative analysis reveals notable differences from human anatomy. The absence of a true interventricular septal muscle bundle and the proportionally larger atria affect hemodynamic calculations. Nonetheless, the rodent cardiac organ provides a reproducible platform for studying molecular pathways, drug efficacy, and regenerative strategies.