Узагальнена патоморфологія вено-оклюзійної хвороби великої рогатої худоби молочних порід

Abstract

Вважається, що вено-оклюзійна хвороба тварин та людини – це судинна гепаральна патологія, яка складається із патологічних процесів, які виникають в печінці за дії на її структури трансформованих піролізідінових алкалоїдів або деяких інших отрут чи лікарських препаратів. Однак, доволі часто за патологоанатомічного розтину трупів тварин, що загинули за цієї хвороби, знаходять патології і в інших органах, зокрема А. В. Захар’єв виявляв їх у нирках великої рогатої худоби [1]. Він також отримував ці патології в експерименті, вводячи відповідні алкалоїди в артеріальне русло нирок.

It is considered that veno-occlusive disease of animals and people is a vascular hepatic pathology which consists of the pathological processes in liver caused by the transformed pyrrolizidine alkaloids and another toxicants or medicaments. However, quite often during postmortem dissection of corpses, pathologies in other organs can be found. In particular, Zakharyev A.V. discovered them in cattle kidneys. He could disclose these pathologies in experiments perfusing relevant pyrrolizidine alkaloids into kidneys arterial bed. In addition to this, extrahepatic pathologies were located in organs, such as mammary gland, ovaries, testicles, thyroid gland, suprarenal glands, hypothalamus, brain, spinal cord and organs of immune system. These changes are determined by properties of pyrrolizidine alkaloids. They are water soluble compounds which are absorbed in rumen, abomasum and intestinal tract after food consumption containing pyrrolizidine alkaloids. Then they get to the liver with blood. It is now clearly established that the first morphological change in veno-occlusive disease occurs in the sinusoidal endothelial cells, leading to the obstruction of the hepatic sinusoids in the hepatic acinus. In these early stages, histological examinations show thickening of the subintimal zone, which leads to the narrowing of the venular lumen and an increased resistance to blood flow. This contributes to the post-sinusoidal portal hypertension and as a result worsening liver dysfunction. The pyrrolizidine alkaloids, which have minimal toxicity in their original form, are metabolised in the liver through a CYP (P450 cytochrome) 3A-mediated transformation to N-oxides and conjugated dienic pyrroles. Pyrroles are alkylating compounds that are highly reactive with proteins and nucleic acids. The complex of pyrroles with proteins and nucleic acids may persist in tissues and generate chronic injury, whereas N-oxides may be transformed into epoxides and toxic necines. The enhanced oxidative stress can also affect collagen α1-transcription directly and/or through the activation of hepatic stellate cells, thus, ultimately leading to veno-occlusive disease. Because of this, new toxic substances can form and the only opportunity to remove these toxins from the body is to eliminate them with emunctories. But newly-formed products are much more harmful then their precursors - pyrrolizidine alkaloids so excretion them always is accompanied by cell damage – atrophy, dystrophy and necrosis in different organs. Disease status depends on its clinical form. It is known that veno-occlusive disease can have both acute and chronic forms involved with doze of pyrrolizidine alkaloids which animals consume. When organism receives small doses of pyrrolizidine alkaloids constantly we suppose the development of brand new form of the disease – latent form and the problem is to diagnose it in time because of unexpressed clinical features.