Haematological Alterations in Heat-Stressed Male Wistar Rats

Abstract

Background: Heat stress (HS) occurs due to global rising temperatures and the exposure of certain industrial workers to hot ambient temperatures. Physiological adaptability to heat stress involves long-term hemorheological modifications. Objectives: The present study evaluated the effect of heat stress on haematological profile using heat-stressed Wistar rat models. Materials and Methods: The study involved using twenty (20) male apparently healthy Wistar rats, with a weight range of 200-250g and an age range of 12-16 weeks. Before the study, the rats were acclimated for two weeks under standard animal husbandry conditions. To simulate heat stress (HS), a heating chamber was utilized and maintained at a temperature of 38±1˚C. The animals were randomly grouped into five (5), comprising five (5) animals per group. Group 1 served as the control and was not exposed to HS, while Groups 2, 3 and 4 were exposed to HS inside the heating chamber, regulated at  38±1˚C for 2, 4 and 8 hours respectively for thirty 30 days. Animals were anaesthetized by cervical dislocation and blood was collected by cardiac puncture for haematological analysis: packed cell volume (PCV), haemoglobin concentration (Hb),  red blood cell (RBC), white blood cell (WBC), MID cells percentage (MID), lymphocytes, neutrophil and platelet counts were determined using a haematology auto-analyzer. Other haematological indices: mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH), mean corpuscular haemoglobin concentration (MCHC), neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), total lymphocyte count (TLC), plateletcrit (PCT), mean platelet volume (MPV), platelet distribution width (PDW) and platelet large ratio (PCLR) were determined in line with standard formulae. Results: Data from the study indicated a significantly raised PCV, RBC, Hb, NLR and PLR among the heat-exposed groups compared to the control (p<0.05). Also, mean values of WBC, TLC, lymphocytes and MPV significantly decreased compared to the control (p<0.05). Conclusion: Long-term hemorheological changes are involved in the physiological adaptation to heat stress. According to the information from the current study, it appears that HS caused a rise in the PVC, Hb RBC, NLR, and PLR levels and a decrease in WBC, TLC, lymphocytes, and MPV. The data points to HS as a potential cause of increased blood viscosity, inflammation, and tissue damage, as well as immune system suppression and disruption of platelet synthesis and activation.