# Heart Rate and Rhythm Changes in Dogs Treated in a Hyperbaric Oxygen Chamber
## 4 Discussion  
Hyperbaric chamber therapy has found application in many fields of veterinary and human medicine. However, in order to assess the safety and validity of this therapy in humans, different animal species have been used for studies. They describe the body's response in cerebral ischemic conditions in rats [21], cats [22], or pigs [23]. Furthermore, they show the benefits of HBOT in different animal species in the healing of burn wounds in guinea pigs [24] as well as mechanical trauma in pigs [25; 26], mice [27], rats [28], or dogs, being one of the most important clinical indications used in veterinary practice [29; 30]. They also describe ototoxicity reactions in guinea pigs [31] or induced endotoxemia in horses [32]. Finally, they describe the hemodynamic mechanisms associated with high oxygen exposure under high-pressure conditions. Admittedly, the detailed mechanism is not known; however, it was indicated that bradycardia induction occurs through two mechanisms: (1) an oxygen-dependent mechanism and (2) a non-oxygen-dependent mechanism. In the oxygen-dependent mechanisms, rapid vasoconstriction of the peripheral vasculature occurs due to the direct effect of oxygen on the vessel wall. The mechanisms of vasoconstriction are not fully understood; however, high plasma oxygen concentrations lead to the displacement of nitric oxide from the vascular wall, one of the best known vasodilators [33]. Additional hypotheses are based on the inhibition of prostaglandin synthesis [34] or the enhancement of the activity of endothelin 1 [35; 36]. Furthermore, this results in hypertension and activation of the baroreceptor reflex of the aortic arch and carotid sinuses. This leads to a decrease in sympathetic nervous system activity in favor of increased vagal nerve tone. The result is bradycardia, reduced myocardial contractility, and, consequently, reduced cardiac output [37; 38; 39]. Furthermore, it has been shown that 100% oxygen saturation, regardless of the prevailing pressures, leads to bradycardia mainly due to the direct effect of high oxygen pressure on the myocardium [40]. The oxygen-independent mechanism is mainly due to a reduction in sympathetic nervous system tone associated with lower levels of circulating catecholamines, which further enhances the bradycardia effect [41; 42]. Nevertheless, due to the high concentration of pure oxygen dissolved in blood serum, tissue oxygenation remains at a similar level despite severe peripheral vasoconstriction [5]. Furthermore, blood distribution in the parenchymal organs increases in favor of peripheral circulation [43], sustaining vital organs with sufficient blood perfusion; thus, it is a safe and well-tolerated procedure. Standard conditions in the HBOT involve pressures ranging between 2 and 3 ATA with 100% oxygen saturation as they bring numerous benefits without much risk of adverse effects [44]. Some protocols are based on sessions at conditions above 3 ATA; their main aim is to rapidly counteract gas embolism. For this reason, treatment sessions can even take place under 6 ATA conditions [45]. Nevertheless, many studies prove that HBOT therapy with a pressure equal to or greater than 1.4 ATA with 100% oxygen saturation leads to similar changes in the body as in the case of the standard procedures. These are associated with a significant increase in the production of ROS and antioxidant reactions, as well as with the cardiovascular system [37; 46]. They are mainly attributed to conditions associated with 100% oxygen saturation, but it has been indicated that hyperbaric conditions with a normal physiological oxygen concentration mobilize proangiogenic and hematopoietic stem progenitor cells, which may be another therapeutic target [47]. Positive aspects of modified hyperbaric chamber therapy are also indicated.