Background: There are multiple studies showing the effect of severe heat stress on systemic functions. Severe heat stress has been known to affect almost every organ in the body. It is well proved that liver is the organ which is severely affected by heat stress and the biochemical, morphological, and morphometric changes of liver following severe heat stress are well documented. But, the effect of repetitive heat stress of moderate level on the liver has not been studied extensively.
Aims & Objective: In the present study, the effect of repetitive heat stress of moderate level was assessed on biochemical [Serum Glutamic Pyruvate Transaminase (SGPT); Serum Glutamic Oxaloacetic Transaminase (SGOT); and Alkaline phosphatase (ALKP)], morphological, and morphometric changes of liver of adult albino male rats (wistar strain).
Materials and Methods: The experimental animals were subjected to repetitive heat stress for 4 hours daily, at 37 ± 0.5ºC in a Biological Oxygen Demand (BOD) incubator (relative humidity 65 - 82%) for 2, 5, and 10 consecutive days. Biochemical assessment (SGPT, SGOT, and ALKP) was done on blood collected from left ventricle of beating heart of rats. Morphometric and morphological studies were conducted under light microscope on paraffin sections (H&E) of liver from control and experimental animals. The morphometric analysis was done by intersection point counting method, using simple square lattice test system.
Results: The serum levels of liver enzymes were elevated in all heat exposed animals (statistically significant in five and ten days exposed animals) in comparison to controls. Morphological changes of anisocytosis at some sites, disruption of cell plates in lobules, mild Kupffer cell hyperplasia were present in rats exposed to heat for two consecutive days. After five days heat exposure ballooning degeneration, single cell necrosis along with small foci of necrosis disrupting cell plates in lobules, and sinusoidal compression were noticed. Kupffer cell hyperplasia was observed. At various sites, hepatocytes showed regenerative changes as binucleate cells and anisocytosis. After 10 days exposure, changes became more marked. The volume density of hepatocytes (Vvh) and numerical density of hepatocytes (Nvh) increased with the increase in heat exposure, despite increasing degenerative changes, confirming regenerative power of liver by hepatocyte proliferation. The increasing numerical density of Kupffers cells on area (Nak) indicated progressive liver damage.
Conclusion: All the observations confirmed that exposure to repetitive heat stress, even of moderate level, leads to liver damage.
Key words: Anisocytosis; Heat Exposure; Liver; Rat; Regenerative Changes; Sinusoidal Compression