This study aimed to explore the role of CIHH in preventing contrast-induced acute kidney injury (CI-AKI) in rats and its mechanism. Rats mean arterial pressure, heart rate, serum creatinine, and blood urea nitrogen levels were measured. The kidney tissue pathological changes, superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, hypoxia-inducible factor-1α, Bcl-2/adenovirus E1B-19kDa-interacting protein3 (BNIP3), cysteiny aspartate specific protease3(caspase3) and poly(ADP-ribose) polymerase (PARP) expression levels were tested. The results showed that CIHH prevented CI-AKI group mean arterial pressure, heart rate, serum creatinine and blood urea nitrogen levels were reduced, kidney tissue SOD activity was increased, MDA levels were reduced, HIF-1α, BNIP3, caspase3 and PARP levels were increased than the CI-AKI group. This study indicates that CIHH pretreatment may have a protective effect on contrast-induced early kidney injury by activating the HIF-1α/BNIP3 signaling pathway to regulate mitochondrial autophagy and enhance cellular anti-apoptotic and renal antioxidant capacity, for the first time.