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Thyroid hormones have an effect on every tissue of the organism because they carry out the functions of a catalyst of the oxidize reaction and the main regulator of metabolism. The thyroid hormones have an effect on the heart and cardiovascular system through β-receptors and they are synergistic with catecholamine. The excess and the deficiency of thyroid hormones in an organism is a cause of disorders in the cardiovascular system. These disorders are demonstrated as strong and nagging signs in animals and humans with hyperthyroidism and hypothyroidism. The disorders of heart functioning in hyperthyroidism may result in congestive heart failure (CHF). The development of heart failure in hyperthyroidism is connected with multidirectional changes in the cardiovascular system.
The purpose of this article is to present immunosuppressive and immunostimulating properties of antimicrobial drugs, particularly of antibiotics. Among the former, also known as the adverse effects of these substances on the immune response, the article discusses chemotaxis, lymphocyte transformation, delayed hypersensitivity, antibody production, phagocytosis and the microbial activity of phagocytes. The immunostimulatory effects of antimicrobial drugs, including antibiotics, can occasionally be therapeutically useful, at present in human medicine. In a general sense, immunomodulatory effects of antimicrobial drugs fall into the following categories: stimulation of the inflammatory response, inhibition of the anti-inflammatory response, and promotion of the anti-inflammatory response. The immunomodulatory effects of antibiotics have mainly been shown in vitro or in experiments with laboratory animals. Until now, there has been little evidence from clinical observations, particularly in relation to infectious diseases of domestic animals, that these modulatory actions of antibiotics play a significant role. As far as humans are concerned, the most convincing in this respect are the anti-inflammatory effects of macrolides and tetracyclines. Considering the importance of antibiotics that - in addition to their antimicrobial action - would also stimulate the innate and specific immunity in the control of bacterial diseases of animals, further research in this area is needed.
The attention recently being paid to strain induction of oxidative stress has resulted in numerous studies, conducted mainly on sportsmen and laboratory animals, the majority of which focused on performing tests during a strenuous endurance effort (15, 31, 41, 54). As a consequence, the disturbance of the pro-oxidative/ anti-oxidative balance has been noted, which in most cases was manifested by a drop of activity of the main anti-oxidative enzymes in erythrocytes and muscle cells (65, 68), as well as an increase in content of products of lipid peroxidation in blood (11, 15, 58, 68). In spite of some discrepancies between them, the results of the research so far seem to indicate that the level of oxidative stress remains closely connected with the intensity and duration of physical strain (20, 42, 62). The aim of the paper was to present the impact of physical effort on the induction of oxidative stress in horses and to describe the features of anti-oxidative protection, in spite of some discrepancies between them, of the organism.
Cannabinoids, the active components of Cannabis sativa, and their derivatives produce a wide spectrum of physiological effects mediated by two different types of receptors: G protein coupled cannabinoid receptor CB1 and transient receptor potential vanilloid type 1 (TRPV1). The afferent vagal pathway modulates the cardio-respiratory response to cannabinoids. The present article summarizes the cardio-respiratory effects of selected cannabinoids: endogenous anandamide and a novel drug arvanil, a metabolically stable hybrid between anandamide and capsaicin. An intravenous administration of anandamide in rats induces apnoea coupled with hypotension and evokes the decrease in the tidal volume at the early phase of reinitiated breathing. The inhibition of respiration and depression of blood pressure produced by anandamide are mediated via vagal peripheral input to the respiratory center in the medulla, while the nodose ganglia are essential in the observed phenomena. Post-anandamide apnoea and hypotension are mediated by both TRPV1 and CB1 receptors but the decline of tidal volume evoked by anandamide might depend on receptors of a different type. An administration of arvanil produced an increase of tidal volume and diaphragm activity, hypertension coupled with a fall in respiratory rate. The post-arvanil rise of tidal volume was mediated by both TRPV1 and CB1 receptors. Only vanilloid receptors seemed to be involved in the increase of diaphragm activity and decrease of respiratory frequency. Hypertensive response to arvanil might depend on receptors of a different type. The respiratory effects elicited by arvanil require intact midcervical vagi. Supranodose vagotomy failed to eliminate the hypertension evoked by arvanil. This implies that post-arvanil hypertension could be co-mediated by both vagal and extravagal pathways. The mechanism of cardio-respiratory effects of cannabinoids is worth exploring on account of their anti-tumor and anti-inflammatory actions and the possible usage of cannabinoids and their derivatives as drugs.
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