**3. Methods to assess microcirculation flow**

NO formed by the nitric oxide synthase enzyme found within endothelial cells is effective through paracrine routes. NO within the cell commonly shows the effect by ensuring calcium entry into the cell via guanosine monophosphate and protein kinase activation. In addition to vasodilatation, NO has anti-thrombogenic effects by reducing tissue factor expression, platelet aggregation, and adhesion molecule expression like VCAM. At the same time, proliferation in venous smooth

As a result of material like adrenalin, thrombin, and angiotensin II binding to receptors found in abluminal vascular smooth muscle cells, calcium entry into the cell is activated and due to the inositol triphosphate (IP3) pathway, endothelin released into the subendothelial interstitial areas causes the better-known vasoconstriction effect [17]. In situations where vasodilator materials pass through endothelial cells with increased permeability outside of the vein, the

Specific receptor expression available in endothelial and smooth muscle tissue found in the vein structures of organs affect agonist concentration and provide vasoactive material to luminal and abluminal vein structures affecting the concentration or dilatation response [3]. In 1922, August Krogh et al. first defined vasodilatation occurring due to the chemical stimulus. In 1971, Siggins and Weitsen showed that vasodilatation was caused by cholinergic stimulation. Khayutin et al. in 1991 showed that vasodilatation occurred due to myelin nerve stimulus. In 1959, Hilton showed that communication present between the smooth muscle

Gap junctions are structures formed by two half channels completing each other with nearly 9 nm size, allowing transfer between cells of ions and molecules with weight lower than 1 kDa isolated from the extracellular environment and linking two neighbouring cells. Just as gap junctions form between the same type of cells (endothelium-endothelium, smooth muscle-smooth muscle, etc.), they may also form between different cells (myoendothelial gap junctions). The channels allow transfer between cells of electrical stimuli and calcium [18].

Each half of gap junctions found in vein structures contain six connexins (Cx) proteins (Cx39, Cx40, Cx43, Cx45) [19]. Each connexin protein has effects with different clinical results [20]. In development-linked vasodilatation, each agonist has a different effect mechanism, with the best-described effect mechanism belonging to the agonist acetylcholine. When acetylcholine binds to a G protein-dependent muscarinic receptor, inositol triphosphate phosphorylation develops causing calcium release from endothelial endoplasmic reticulum [21, 22]. Simultaneously, calcium-dependent potassium channels open leading to hyperpolarization development in the cell [23]. After this flow, vasodilatation develops causing closure of voltage-dependent calcium channels within endothelial and vein smooth muscle cells [24]. At the same time, ion flows are communicated between cells via gap junctions with vasodilatation

Pericytes found in venules have regulatory effects on proliferation, differentiation and contractility of endothelial cells. During new vein creation, in situations where the endothelial layer is developing with tube shape contacts pericytes, endothelial growth and proliferation are suppressed, and maturation of the endothelial basal membrane structure is ensured [25, 26].

muscles is reduced and it limits neointimal hyperplasia development in vein walls [16].

54 Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus

vasodilator effect reverses and may cause vasoconstriction.

cells found in the vascular walls was effective on vasodilatation.

spreading distal and proximal to the point of acetylcholine binding [2].

The microcirculation performs the necessary oxygen distribution to meet the basic metabolic requirements of the tissues. Anatomically, it consists of arterioles, capillaries and venules. In situations where physiological or pathological stress develops, the balance between oxygen delivery and demand becomes very important. This delicate balance can play an important role in the progression of critical illnesses. In daily clinical practice, monitoring the microcirculation is essential for detection of potential organ dysfunctions. The ideal technique would allow quantification of vascular recruitment and the magnitude, heterogeneity, responsiveness, and efficiency of oxygen transfer to the tissues. There are a variety of methods and parameters available to evaluate the microcirculatory state of a patient.
