Background and Aim: It is known that during the early postpartum and lactation periods in dairy cows, metabolic disorders develop, that is, ketosis, which can lead to secondary damage to internal organs. Therefore, it is important to address the issues of changing the lactating cows' clinical, laboratory, and physiological parameters regarding the development of hepatocardial syndrome. This study aimed to provide clinical and diagnostic justification for developing hepatocardial syndrome in highly productive dairy cows.
Materials and Methods: The study was conducted on 20 black and white cows in the early postpartum period (7–10 days after birth), with a milk production level of >4500 kg of milk during the previous lactation period, a positive result in the formol colloid sedimentary test, the presence of deafness and splitting of heart sounds, changes in the size, or increased pain sensitivity of the percussion field of the liver. Clinically healthy dairy cows in the early postpartum period were used as controls (n = 24). Clinical, electrocardiographic, echocardiographic, and biochemical parameters were also evaluated.
Results: Dairy cows with hepatocardial syndrome developed arterial hypertension and sinus tachycardia, which led to a significant decrease in PQ and QT intervals at ECG. A significant increase in the diastolic size of the interventricular septum, systolic size of the free wall of the left ventricle, and diastolic and systolic sizes of the left ventricle and a significant decrease in the shortening fraction of the left ventricular myocardium were observed in the cows due to the development of hepatocardial syndrome. The affected cows demonstrated a significant increase in serum activity of gamma-glutamyl transferase, alanine aminotransferase, lactate dehydrogenase, creatine phosphokinase, alkaline phosphatase, troponin, malondialdehyde, diene conjugates, and ceruloplasmin and a decrease in glucose concentration. In addition, they demonstrated decreased activity of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase.
Conclusion: Hepatocardial syndrome in dairy cows occurs due to ketosis, characterized by arterial hypertension, sinus tachycardia, a moderate decrease in myocardial contractility, oxidative stress, and cytolysis of cardiomyocytes and hepatocytes. Therefore, the control and prevention of the development of hepatocardial syndrome will make it possible to maintain the productive health and longevity of dairy cows.
