How do rats die from pituitary adenoma? - briefly
Rats die from pituitary adenomas because the growing tumor compresses the gland and deregulates hormone secretion, leading to severe metabolic, cardiovascular, and electrolyte disturbances. These systemic failures ultimately result in organ collapse and death.
How do rats die from pituitary adenoma? - in detail
Pituitary adenomas in rodents develop from the anterior lobe cells and grow slowly, eventually displacing normal tissue and altering hormone secretion. Tumor expansion produces a mass effect that compresses adjacent hypothalamic and brain‑stem structures, while the altered endocrine output creates systemic imbalances.
The principal pathways leading to mortality are:
- Hormonal hypersecretion – excess prolactin, growth hormone, or ACTH drives metabolic disturbances, insulin resistance, and severe hyperglycemia, which can precipitate ketoacidosis and organ dysfunction.
- Hormonal insufficiency – loss of normal pituitary function reduces cortisol, thyroid hormone, and gonadotropins, resulting in adrenal crisis, hypothyroidism, and electrolyte abnormalities that compromise cardiovascular stability.
- Intracranial pressure elevation – tumor mass increases intracranial pressure, causing cerebral edema, herniation, and brain‑stem compression, which can lead to respiratory arrest.
- Hemorrhage and necrosis – rapid tumor growth may outstrip vascular supply, causing intra‑tumoral hemorrhage or necrotic cavitation; the resulting intracranial bleed can be fatal.
- Cardiovascular complications – chronic hypertension and left‑ventricular hypertrophy, driven by excess growth hormone or ACTH, predispose rats to arrhythmias, myocardial infarction, and sudden death.
- Renal failure – hypercortisolism and hyperglycemia increase glomerular filtration pressure, leading to proteinuria, tubular injury, and eventual renal insufficiency.
In experimental models, death typically occurs weeks to months after tumor onset, reflecting the cumulative impact of endocrine disruption and mechanical compression. Pathological examination frequently reveals enlarged pituitary glands, hemorrhagic necrosis, and secondary lesions in the adrenal cortex, heart, and kidneys. Management of the condition in laboratory settings focuses on early detection of hormonal abnormalities and humane endpoints to prevent prolonged suffering.