Varvara M. Byakhova

This article examines the issues of studying pathogenetic correlative links between various clinical and laboratory parameters in cats with cardiorenal syndrome. A significant correlation was found between the level of creatininemia and the pulse rate (r = 0.4), respiratory rate (r = 0.7), sleep breathing rate (r = 0.6), systolic (r = 0.3), diastolic (r = 0.3), mean arterial pressure (r = 0.3), QRS complex duration (r = 0.5), QT interval (r = 0.3), P wave voltage (r = 0.3) and R in the second standard lead (r = 0.4), left atrium size (r = 0.7), interventricular septum thickness in diastole (r = 0.7), left ventricular free wall thickness in diastole (r = 0.6), end-diastolic size (r = -0.6; p ≤ 0.05), end-systolic size of the left ventricular chamber (r = -0.5), serum alanine aminotransferase (r = 0.5), lactate dehydrogenase (r = 0.6), aspartic aminotransferase (r = 0.7), creatinine phosphokinase (r = 0.7), cardiac troponin (r = 0.5), serum concentration of urea (r = 0.7), ketone bodies (r = 0.7), malondialdehyde (r = 0.7), diene conjugates (r = 0.7), ceruloplasmin (r = 0.6), superoxide dismutase activity (r = -0.5), catalase (r = -0.7), glutathione peroxidase (r = -0.6). In the body of cats with cardiorenal syndrome, there is an activation of the sympathoadrenal system, myocardial remodeling processes in the form of concentric hypertrophy, oxidative stress and damage to the cell membranes of cardiomyocytes and other cells of the body, while there is an increase in the mass and number of cardiomyocytes, a violation of the diastolic function of the myocardium, a syndrome of damage to the cell membranes of cardiac cells occurs, progressive prerenal azotemia develops against the background of chronic decompensation of the circulatory organs. Changes in the correlative pathogenetic relationships between clinical and laboratory parameters in cats with cardiorenal syndrome can be considered as predictors of a more malignant course of the pathological process.

This research presents novel insights into the temporal dynamics of clinical and instrumental parameters pertaining to the emergence of cardiorenal syndrome in feline patients afflicted with hypertrophic cardiomyopathy. It elucidates that within pedigreed felines, the progression of congestive heart failure syndrome may precipitate the subsequent evolution and exacerbation of secondary renal damage, thus significantly complicating the trajectory of the primary pathological process. This study establishes, for the first time, theprevalence of cardiorenal syndrome, affecting 51.0% of the population within the broader cohort of cats afflicted with hypertrophic cardiomyopathy (n= 49). Moreover, it substantiates the role of the cardiorenal continuum in felines as apredictor of amore severe course of hypertrophic cardiomyopathy. Manifesting as concentric myocardial hypertrophy in domestic felines, cardiorenal syndrome is characterized by dyspnea, hypothermia, and circulatory insufficiency. Statistically significant findings include an elevated median nocturnal respiratory rate of 34.0 breaths/min (p0.001) compared to clinically healthy counterparts (18.0 breaths/min) in affected felines. Additionally, felines afflicted with hypertrophic cardiomyopathy and cardiorenal syndrome exhibit astatistically significant (p 0.001) elevation in median mean arterial blood pressure to 140.0 mmHg compared to clinically healthy counterparts (104.0 mmHg), sinus tachycardia at 199.0 beats/min (171.5 beats/min in healthy felines), resulting in astatistically significant (p 0.001) reduction in PQ intervals by 67.0 ms (75.5 ms in healthy felines), and an increase in QT interval by 204.0 ms (165.5 ms in healthy felines). Electrocardiographic assessments reveal indications of compromised intra-atrial and intraventricular conduction in hypertrophic cardiomyopathy-afflicted felines with cardiorenal syndrome, along with an augmented amplitude of the ventricular complex. Echocardiographic evaluations confirm alterations such as pulmonary vein dilation, pronounced left atrial anteroposterior enlargement, interventricular septal and left ventricular free wall hypertrophy, decreased longitudinal contractility of the left and right ventricles, and clinically significant diastolic dysfunction.

The issues of changes in clinical, laboratory and instrumental parameters in cats with hepatocardial syndrome formed against the background of hypertrophic cardiomyopathy were studied. It is known that in high-bred cats with congestive heart failure, secondary hepatopathy can develop and progress. It was shown that hepatocardial syndrome occurs in 33.7 % of cats, out of the total number of patients with hypertrophic cardiomyopathy (n = 83). It has been established that hepatocardial complications in cats are a risk factor for a more severe course of hypertrophic cardiomyopathy. Hepatocardial syndrome in cats with hypertrophic cardiomyopathy is characterized by severe hypothermia, circulatory and respiratory failure. In sick animals, an increase in frequency of breathing during sleep was recorded (33.39.3 versus 17.91.8 times/min; p 0.001). Domestic cats with hepatocardial syndrome had a decrease in mean arterial blood pressure (100.219.3 versus 107.219.1 mm Hg; p 0.05), sinus tachycardia (200.319.6 17.8 times/min; p 0.001), which leads to a significant decrease in PQ intervals (57.99.9 versus 64.99.9 ms; p 0.001) and QT intervals (168.917, 2 vs 157.518.6 ms; p 0.001). Sick cats had a significant increase in the time of refilling of capillaries with blood, slowdown in intraventricular conduction, increase in voltage of ventricular and atrial complex on electrocardiograms, expansion of pulmonary vein, significant dilatation of left atrium, extreme concentric hypertrophy of left ventricle, increase in transverse contractility of myocardium of left ventricle and decrease in longitudinal contractility myocardium of left and right ventricles, cardiomyocyte cytolysis syndrome, cholestasis, and hypoalbuminemia

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.

Background and Aim: Canine testicular tumors are among the most common reproductive tract tumors in male dogs and have been studied in many countries. However, to the best of our knowledge, studies with a large sample size have not been conducted in Russia. This study aimed to provide the latest information on the prevalence of canine testicular tumors in the Veterinary Oncology Scientific Center for Small Animals "Biocontrol" in Moscow, Russia, in 2010-2020 and the characteristics of the affected canine population. Materials and Methods: A retrospective review of patients and histological reports was collected and analyzed from 358 dogs with 447 testicular tumors within 11 years. Results: The mean age of the affected dogs was 10.4 years, whereas that of dogs with Sertoli cell tumors was 9.4 years p=0.009. This study includes mixed-breed dogs (18.4%), Yorkshire Terriers (8.8%), Labrador Retrievers (7.9%), Golden Retrievers (5.0%), and Fox Terriers (3.4%). The most common tumors were interstitial cell tumors (n=227, 50.8%). In contrast, 107 (23.9%) seminomas, 80 (17.9%) Sertoli cell tumors, 19 (7.4%) mixed germ cell-sex cord-stromal tumors, and 26 (7.6%) testicular tumors developed from cryptorchid testes, which included 16 (61.5%) Sertoli cell tumors, 10 (38.5%) seminomas, and no interstitial cell tumors. Conclusion: This study provides baseline information on the prevalence of canine testicular tumors in the described population, including the median age of each tumor type and overrepresented dog breeds. We further found that the most common scrotal testicular tumor was interstitial cell tumor, whereas Sertoli cell tumor was the most common in cryptorchid testicles.

Background and Aim: The present study investigated the influence of liver tumor structure on life expectancy in dogs. Diseases of the liver comprise 5-25% of all non-communicable diseases in dogs, and primary hepatic tumors account for 0.6-1.3% of tumors. This research aimed to study the post-operative life span of animals with primary or metastatic tumors of the liver. Materials and Methods: During the study period, 7124 oncological operations were performed in our clinic. In total, 128 liver tumors were detected in live animals, while 323 were detected posthumously. Forty animals underwent surgery for various liver tumors. In dogs with primary liver tumors, the average age was 11.9 years and the average body weight was 15.5 kg, while in dogs with liver metastases, the mean age was 11.4 years and the average body weight was 24 kg. Results: The ratio of males to females among dogs with primary liver tumors was about 1:1 (ten females and nine males), while that among dogs with metastatic liver damage was clearly predominantly female (14 females and two males) because females often undergo surgery for cancerous mammary glands or ovaries. Conclusion: The size of tumors and the number of affected lobes had a significant effect on the post-operative life span. With a tumor size of <5 cm and a lesion covering less than two lobes of the liver, life expectancy was significantly longer and the prognosis was more favorable. In cases of large tumors or those affecting more than two lobes, life expectancy was significantly reduced and the prognosis was cautious to unfavorable.

Background: Dilated cardiomyopathy is common in dogs. This form of cardiomyopathy is the main cause of death due to heart disease in dogs. Death can occur suddenly in clinically normal animals as a result of the progression of congestive heart failure (CHF). The pathogenesis of heart failure syndrome in dogs with dilated cardiomyopathy involves activation of the neurohumoral system and immune-mediated inflammation, which leads to further progression of the condition. Heart failure syndrome in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, the involvement of other key internal organs, and intestinal dysbiosis. Aim: This study aimed to determine the immunological and inflammatory mechanisms surrounding the development of heart failure syndrome in dogs with dilated cardiomyopathy. Materials and Methods: The subjects of this study were dogs with a dilated form of cardiomyopathy (n=159), complicated by various functional classes of heart failure syndrome. Evaluation of myocardial remodeling, systolic function, and systemic hemodynamics was performed using EMP-860 Vet and PU-2200V ultrasound scanners according to the standard technique. Electrocardiography was performed with all dogs in right lateral recumbency using the EK1T-04 Midas electrocardiograph (50 mm/s speed and 1 mV gain = 1 cm). Results: In some affected animals, especially in cases of compensated dilated cardiomyopathy, leukocytosis was noted. In patients with dilated cardiomyopathy complicated by heart failure syndrome of various functional classes, the number of neutrophils was significantly increased, and the number of lymphocytes was decreased by 1.9-2.1 times when compared with those in clinically normal animals. In dogs with dilated cardiomyopathy, neutrophilic leukocytosis develops with a simple regenerative shift to the left. The results of immunological studies indicate that dogs with dilated cardiomyopathy develop T lymphocytopenia as compared with clinically normal animals. Conclusion: The central component of heart failure syndrome in dogs with dilated cardiomyopathy is the activation of the neurohumoral system and immune-mediated inflammation. The development of CHF in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, involvement of other key internal organs, and intestinal dysbiosis.

Aim: The work aimed to study the morphology of colonies and their comparison by features of the formation of Yersinia enterocolitica biofilms. Materials and Methods: Bacteria were cultured on a Yersinia Selective Agar medium ("CIN-agar") at 28°C for 24 h. The microorganisms were grown in meat-peptone broth with 1.0% glucose to measure the absolute values of the optical density of the culture. The optical density of the liquid was determined in a microplate photometric analyzer Immunochem-2100 (HTI, USA) at a wavelength of 490 nm. For the study of biofilms, the specimens were fixed for 3-5 h in pairs of 25.0% solution of glutaraldehyde (according to DV), and pairs of a 1.0% aqueous solution of osmic acid (OSO4) were used for contrasting for 2-3 min. The specimens were examined with stereoscopic microscopy "BIOMED MS-1 Stereo" (Russia) and scanning electron microscope "TM 3030 plus" (Holland). Results: With stereoscopic microscopy of the colonies of Y. enterocolitica, the S-forms had an elevated intensely colored center, radial striation along the periphery, smooth edges, d ≤ 1.0 mm. R-form colonies had a dark color and a dry surface, were tuberous and had a dense center with a peripheral ridge, rugged edges, d ≥ 1.5 mm. The optical density of the Y. enterocolitica S-form showed that this type of microorganism belongs to the moderate producers of biofilms since the optical density of the sample (density of the sample - Ds) exceeded the optical density of control (density of the control - Dc) by 3 times. In Y. enterocolitica R-form (D ≤ 0.197) weakly produced biofilms, the optical density of the sample exceeded the optical density of the control by