Blood Vessel Tone Research Articles

Phosphodiesterase 5A regulates the vomeronasal pump in mice.

The vomeronasal organ (VNO) is a specialized chemoreceptive structure in many vertebrates that detects chemical stimuli, mostly pheromones, which often elicit innate behaviors such as mating and aggression. Previous studies in rodents have demonstrated that chemical stimuli are actively transported to the VNO via a blood vessel-based pumping mechanism, and this pumping mechanism is necessary for vomeronasal stimulation in behaving animals. However, the molecular mechanisms that regulate the vomeronasal pump remain mostly unknown. In this study, we observed a high level of expression of phosphodiesterase 5A (PDE5A) in the vomeronasal blood vessel of mice. We provided evidence to support the potential role of PDE5A in vomeronasal pump regulation. Local application of PDE5A inhibitors-sildenafil or tadalafil-to the vomeronasal organ (VNO) reduced stimulus delivery into the VNO, decreased the pheromone-induced activity of vomeronasal sensory neurons, and attenuated male-male aggressive behaviors. PDE5A is well known to play a role in regulating blood vessel tone in several organs. Our study advances our understanding of the molecular regulation of the vomeronasal pump.

Ethyl alcohol. Influence on the dynamics of blood supply of skin and other soft tissues during their sudden cooling

It is shown that in norm (i.e. in sober people in the absence of ethyl alcohol in blood) sudden local cooling of skin and soft tissues of different parts of the body from +37 to +18 °С and below (but not below 0 °С) causes in the cooled tissues 2-phase change in the value of blood vessels tone, their blood filling, intensity of blood supply and feeling of painfulness. Thus from the first seconds of cooling the tone of blood vessels of muscular type begins to increase, their blood filling begins to decrease, skin color lightens and soon in the cooled area of the body there is a feeling of acute soreness. After a few tens of seconds of cooling, the spasm of blood vessels reaches maximum values, their filling with blood decreases to a minimum, the skin turns white, and the soreness reaches maximum values. These changes persist at their peak for a few minutes, after which they begin to disappear, despite the persisting hypothermia. But then, after 10-15 minutes of cooling, hyperemia inevitably develops in the hypothermia zone, as a result of which the soreness disappears and the skin reddens. It is established that in the norm, sudden cooling of tissues causes irritation of temperature receptors located in them. The resulting excitation of temperature receptors causes reflex spasm of blood vessels, which has an adaptive value, as it is evolutionarily developed for temperature homeostasis of warm-blooded organism. It has been found out that acute painfulness accompanying cold spasm of blood vessels arises due to mechanical squeezing of pain receptors located under the muscular layer in the wall of blood vessels. On the other hand, the presence of ethyl alcohol in the blood (the presence of alcohol intoxication) fundamentally changes the dynamics of blood supply of tissues at their sudden cooling: during cooling, blood vessels expand and overflow with blood without the initial phase of spasm and the appearance of a sense of pain. At the same time, hyperemia persists not only throughout the cooling period, but also after it. In other words, alcohol intoxication is manifested by the immediate development of hyperemia and redness of the skin in the cooled area of the body without the initial spasm of blood vessels, the appearance of a feeling of soreness and pallor of the skin in the area of cooling.

Effect of nitric oxide modulators on cerebrospinal fluid outflow through the cribriform plate of C57Bl/6 mice

Introduction. Beside the excretion of metabolic wastes, the lymphatic system in CNS play a crucial role in the regulation of intracranial pressure that is vital for the organism. One of the possible pathways of cerebrospinal fluid (CSF) drainage is its flow through the foramen of the cribriform plate (CP) into the nasal cavity. Despite the significant contribution of the nasal tract to the overall dynamics of the liquor, not much is known about the mechanisms of this process and how it is regulated. Due to its influence on the tone of blood vessels and peristalsis of lymphatic vessels, nitric oxide (NO) is a powerful modulator of liquor outflow, but its effects on nasal CSF outflow have not been studied yet. Aim and Methods. Using diffusion-weighted magnetic resonance imaging (DW MRI), we characterized the changes in CSF outflow through the CP of C57Bl/6 mice influenced by intranasal application of NO synthesis modulators. Results. In our study, using DW MRI and computer tomography (CT) mapping of the CP, we detected significant CSF outflow through its large dorsal and ventral foramen located along the nasal septum. At the same time, the CSF flow rate through the dorsal orifices of the CP was the highest. In addition, we showed that intranasal introduction of NO donor after 30 min leads to a significant decrease of water diffusion through the CP whereas application of a nonspecific NO synthase inhibitor into the nasal cavity enhances nasal outflow. The effects of the NO modulators did not have any significant spatial patterns; CSF outflow was significantly altered across all CP orifices regardless of their size or localization. Conclusion. The obtained results demonstrate the potential possibility of noninvasive local regulation of liquor dynamics, which may be used in the development of new approaches to the therapy of intracranial hypertension of various etiologies and methods of CNS detoxification.

A computational model predicts sex-specific responses to calcium channel blockers in mammalian mesenteric vascular smooth muscle

The function of the smooth muscle cells lining the walls of mammalian systemic arteries and arterioles is to regulate the diameter of the vessels to control blood flow and blood pressure. Here, we describe an in silico model, which we call the ‘Hernandez–Hernandez model’, of electrical and Ca2+ signaling in arterial myocytes based on new experimental data indicating sex-specific differences in male and female arterial myocytes from murine resistance arteries. The model suggests the fundamental ionic mechanisms underlying membrane potential and intracellular Ca2+ signaling during the development of myogenic tone in arterial blood vessels. Although experimental data suggest that KV1.5 channel currents have similar amplitudes, kinetics, and voltage dependencies in male and female myocytes, simulations suggest that the KV1.5 current is the dominant current regulating membrane potential in male myocytes. In female cells, which have larger KV2.1 channel expression and longer time constants for activation than male myocytes, predictions from simulated female myocytes suggest that KV2.1 plays a primary role in the control of membrane potential. Over the physiological range of membrane potentials, the gating of a small number of voltage-gated K+ channels and L-type Ca2+ channels are predicted to drive sex-specific differences in intracellular Ca2+ and excitability. We also show that in an idealized computational model of a vessel, female arterial smooth muscle exhibits heightened sensitivity to commonly used Ca2+ channel blockers compared to male. In summary, we present a new model framework to investigate the potential sex-specific impact of antihypertensive drugs.

A computational model predicts sex-specific responses to calcium channel blockers in mammalian mesenteric vascular smooth muscle.

The function of the smooth muscle cells lining the walls of mammalian systemic arteries and arterioles is to regulate the diameter of the vessels to control blood flow and blood pressure. Here, we describe an in silico model, which we call the 'Hernandez-Hernandez model', of electrical and Ca2+ signaling in arterial myocytes based on new experimental data indicating sex-specific differences in male and female arterial myocytes from murine resistance arteries. The model suggests the fundamental ionic mechanisms underlying membrane potential and intracellular Ca2+ signaling during the development of myogenic tone in arterial blood vessels. Although experimental data suggest that KV1.5 channel currents have similar amplitudes, kinetics, and voltage dependencies in male and female myocytes, simulations suggest that the KV1.5 current is the dominant current regulating membrane potential in male myocytes. In female cells, which have larger KV2.1 channel expression and longer time constants for activation than male myocytes, predictions from simulated female myocytes suggest that KV2.1 plays a primary role in the control of membrane potential. Over the physiological range of membrane potentials, the gating of a small number of voltage-gated K+ channels and L-type Ca2+ channels are predicted to drive sex-specific differences in intracellular Ca2+ and excitability. We also show that in an idealized computational model of a vessel, female arterial smooth muscle exhibits heightened sensitivity to commonly used Ca2+ channel blockers compared to male. In summary, we present a new model framework to investigate the potential sex-specific impact of antihypertensive drugs.

Case discussion: The effect of extreme temperatures on an older adult

Climate change can cause high temperatures that can affect the older adult in significant ways. Older adults may not be aware of the dangers of high temperature days and may continue with old habits such as staying in the sun to garden without sunscreen or a hat as they may have done in years past. High temperatures can cause impairment of the tone and structure of blood vessels by interfering with nitric oxide synthesis and cytokine production and can cause systemic inflammation, all of which significantly contribute to dehydration in older adults, who are known to have a decreased sense of thirst, resulting in increased blood viscosity and the risk of heat induced shock and thrombotic strokes.This case discussion highlights the effects of high temperatures due to climate change on an older adult, and what nurse practitioners need to be aware of when assessing older adults who may be suffering from heat exhaustion or heat stroke, and how to manage appropriately.

MicroRNAs (miRNAs) role in hypertension: pathogenesis and promising therapeutics.

MicroRNAs (miRNAs) are small, non-coding RNA molecules that play a crucial role in regulating various cellular processes, including cell proliferation, differentiation, apoptosis, and disease development. Recent studies have highlighted the importance of miRNAs in the development and progression of essential hypertension, a common form of high blood pressure that affects millions of individuals worldwide. The molecular mechanisms by which miRNAs regulate hypertension are complex and multifaceted. MiRNAs target the 3' untranslated regions of mRNA molecules, thereby regulating the synthesis of specific proteins involved in cardiovascular function. For instance, miRNAs are known to regulate the expression of genes involved in blood vessel tone, cardiac function, and inflammation. The growing body of research on miRNAs in hypertension has highlighted their potential as therapeutic targets for managing this condition. Studies have shown that miRNA-based therapies can modulate the expression of key genes involved in hypertension, leading to improvements in blood pressure and cardiovascular function. However, more research is needed to fully understand the mechanisms of miRNA-mediated hypertension and to develop effective therapeutic strategies. In summary, this review highlights the current understanding of the role of miRNAs in essential hypertension, including their molecular mechanisms and potential therapeutic applications. Further research is needed to fully understand the impact of miRNAs on hypertension and to develop new treatments for this common and debilitating condition.

Minor age difference substantially affects renal function in conscious and anaesthetized rats*

Abstract In this study we re-examined the postulate that in the rat age-related body metabolism and kidney function changes progress only slowly. Thus we checked whether a moderate between-animal age distance may cause any marked difference, which could affect interpretation of experimental results. Food and water consumption, renal sodium and potassium excretion and haemodynamics were lower in rats aged 15 versus 9 weeks. In turn, hematocrit, mean arterial pressure, and renal vascular resistance were significantly higher in older animals, whereas renal excretion of NO3-/NO2- and vascular endothelial growth factor A and in situ renal tissue NO signal did not differ. Evidently, an age older by 6 weeks was associated with decreased hydration, tone of systemic and renal blood vessels, and renal excretion. In conclusion, since the actual age is an important determinant of the animal’s functional status, accurate age-matching of experimental groups is a necessary pre-condition for correct data interpretation.

The Role of Reactive Oxygen Species in the Regulation of Blood Vessel Tone in Perinatal and Early Postnatal Ontogenesis

Reactive oxygen species (ROS) have been considered for many years as negative regulators in the cardiovascular system. Indeed, excessive production of ROS characterizes many cardiovascular diseases. The damaging effect of ROS can be especially pronounced in a newborn organism, since during this period their contractile effect in pulmonary arteries remains as high as in the pre-term fetus arteries and the antioxidant systems have not yet formed. Therefore, in the first hours and days of independent life, pulmonary arteries tend to contract, primarily due to the low bioavailability of endothelial NO, which increases the risk of developing pulmonary hypertension in newborns. At the same time, during the perinatal period, ROS play an important role in the adaptive reactions of the circulatory system. ROS provide occlusion of the ductus arteriosus and separation of the pulmonary and systemic circulations soon after birth, and also contribute to the contraction of peripheral vessels during hypoxia, which often accompanies the delivery, and therefore provide priority blood supply to the brain in these conditions. The vasomotor effect of ROS is also pronounced in early postnatal ontogenesis, but it has a different character. In the first weeks of life, the action of ROS serves as one of the mechanisms for increasing endothelium-dependent relaxation of pulmonary vessels. In addition, during early postnatal ontogeny, ROS may play an important role in the regulation of systemic vascular tone. This review outlines the current understanding of the vasomotor role of ROS in the vessels of the pulmonary and systemic circulation and considers the mechanisms of ROS effects on the functioning of vascular endothelial and smooth muscle cells in the perinatal and early postnatal periods.

Features of neuroimmune and genetic profile in men with clinical manifestations of vegetative vascular dystonia of hypertensive type

Background. Identification of immune, neurohumoral and genetic markers of vegetative vascular dystonia of the hypertensive type is relevant in the aspect of prevention and early diagnosis of cardiovascular pathology in middle-aged men.
 Aim. To study the features of the immune and neurohumoral profile in middle-aged men with clinical manifestations of vegetative vascular dystonia of the hypertensive type, associated with polymorphic variants of candidate genes for blood vessel tone regulation.
 Material and methods. 113 middle-aged men (mean age 46.13.9 years) were examined. The observation group included 65 men (average age 45.34.6 years) with clinical manifestations of vegetative vascular dystonia of the hypertensive type. The comparison group included 48 men without signs of autonomic regulation dysfunction (average age 48.33.2 years). The groups were comparable in age (p=0.593), ethnic and social composition. The content of CD3+CD95+ lymphocytes was determined by flow cytometry; interleukin-6, total immunoglobulin E, adrenaline, serotonin by enzyme immunoassay. Polymorphic variants of the genes ADRB2 (rs1042713), ADD1 (rs4961), GNB3 (rs5443), HTR2A (rs7997012) were identified by real-time polymerase chain reaction. Statistical processing: comparison of arithmetic means using Student's t-test or MannWhitney U-test, calculation of odds ratio (OR) and 95% confidence interval (CI).
 Results. The immune profile of men with disorders of autonomic regulation was characterized by a deficiency of CD3+CD95+ lymphocytes against the background of overproduction of total immunoglobulin E and interleukin-6. The neurohumoral profile was characterized by excessive synthesis of adrenaline and serotonin. The development of symptoms of vegetative vascular dystonia of the hypertensive type was associated with the G allele of the ADRB2 gene (rs1042713) (OR=1.80; 95% CI=1.053.08; p 0.05), the G allele of the ADD1 gene (rs4961) (OR=3.51; 95% CI=1.279.67; p 0.05), C allele of the GNB3 gene (rs5443) (OR=2.30; 95% CI=1.214.37; p 0.05), A allele of the HTR2A gene (rs7997012) (OR=2.38; 95% CI=1.374.15; p 0.05).
 Conclusion. Changes in the immune profile were identified (deficiency of CD3+CD95+ lymphocytes, excess of total immunoglobulin E, interleukin-6), associated with hyperproduction of adrenaline and serotonin against the background of polymorphism of candidate genes for vascular tone regulation [ADRB2 (rs1042713), ADD1 (rs4961), HTR2A (rs7997012 ), GNB3 (rs5443)].

The Role of Reactive Oxygen Species in the Regulation of Blood Vessel Tone in Perinatal and Early Postnatal Ontogenesis

The Role of Reactive Oxygen Species in the Regulation of Blood Vessel Tone in Perinatal and Early Postnatal Ontogenesis

Perivascular Adipose Tissue and Vascular Smooth Muscle Tone: Friends or Foes?

Perivascular adipose tissue (PVAT) is a specialized type of adipose tissue that surrounds most mammalian blood vessels. PVAT is a metabolically active, endocrine organ capable of regulating blood vessel tone, endothelium function, vascular smooth muscle cell growth and proliferation, and contributing critically to cardiovascular disease onset and progression. In the context of vascular tone regulation, under physiological conditions, PVAT exerts a potent anticontractile effect by releasing a plethora of vasoactive substances, including NO, H2S, H2O2, prostacyclin, palmitic acid methyl ester, angiotensin 1-7, adiponectin, leptin, and omentin. However, under certain pathophysiological conditions, PVAT exerts pro-contractile effects by decreasing the production of anticontractile and increasing that of pro-contractile factors, including superoxide anion, angiotensin II, catecholamines, prostaglandins, chemerin, resistin, and visfatin. The present review discusses the regulatory effect of PVAT on vascular tone and the factors involved. In this scenario, dissecting the precise role of PVAT is a prerequisite to the development of PVAT-targeted therapies.

Conversion From Hypothyroidism to Hyperthyroidism and Back After Anti-SARS-CoV-2 Vaccination

Cases presenting with changes in various organs caused by anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination are rare. In particular, after such instances of vaccination, onset of subacute thyroiditis, Hashimoto thyroiditis, and Graves’ disease was observed. We present the case of a 55-year-old woman whose hypothyroidism converted to hyperthyroidism after vaccination with Gam-COVID-Vac (Sputnik V). After the first dose of vaccine, a hormonal metabolism alteration was noted, i.e., conversion from hypothyroidism to euthyroidism. After the second dose of vaccine, onset of hyperthyroidism with thyrotoxicosis was noted without signs of subacute thyroiditis. Hyperthyroidism persisted for several weeks before reverting to hypothyroidism. Assessments did not reveal an increase in the patient’s thyroid-stimulating hormone receptor antibody levels throughout the indicated period. However, after hyperthyroidism reverted to hypothyroidism, a significant increase in the peak systolic velocity of the superior thyroid arteries was observed, which is characteristic of hyperthyroidism. Owing to the known involvement of the autonomic nervous system (ANS) in blood vessel tone regulation, thyroid hormonogenesis, and stress, the ANS-mediated conversion from hypothyroidism to hyperthyroidism in certain individuals after receiving a vaccine, which may serve as a sufficient stimulus for ANS nerve centers, is highly probable. Therefore, diagnostic assessment of ANS condition should be performed before vaccination in patients with chronic thyroid disorders or diseases of other organs or organ systems. If changes in ANS are found, providing preemptive treatment before vaccination is recommended. J Endocrinol Metab. 2022;12(6):202-208 doi: https://doi.org/10.14740/jem833

The Role of Amino Acids in Endothelial Biology and Function.

The vascular endothelium acts as an important component of the vascular system. It is a barrier between the blood and vessel wall. It plays an important role in regulating blood vessel tone, permeability, angiogenesis, and platelet functions. Several studies have shown that amino acids (AA) are key regulators in maintaining vascular homeostasis by modulating endothelial cell (EC) proliferation, migration, survival, and function. This review summarizes the metabolic and signaling pathways of AAs in ECs and discusses the importance of AA homeostasis in the functioning of ECs and vascular homeostasis. It also discusses the challenges in understanding the role of AA in the development of cardiovascular pathophysiology and possible directions for future research.

Patient Specific Numerical Modeling for Renal Blood Monitoring Using Electrical Bio-Impedance.

Knowledge of renal blood circulation is considered as an important physiological value, particularly for fast detection of acute allograft rejection as well as the management of critically ill patients with acute renal failure. The electrical impedance signal obtained from kidney with an appropriate electrode system and optimal electrode system position regarding to the kidney projection on skin surface reflects the nature of renal blood circulation and tone of renal blood vessels. This paper proposes a specific numerical modelling based on prior information from MRI-data. The numerical modelling was conducted for electrical impedance change estimation due to renal blood distribution. The proposed model takes into the account the geometrical and electrophysiological parameters of tissues around the kidney as well as the actual blood distribution within the kidney. The numerical modelling had shown that it is possible to register the electrical impedance signal caused by renal blood circulation with an electrode system commensurate with the size of kidney, which makes it possible to reduce the influence of surrounding tissues and organs. Experimental studies were obtained to prove the numerical modelling and the effectiveness of developed electrode systems based on the obtained simulation results. The obtained electrical impedance signal with the appropriate electrode system shows very good agreement with the renal blood change estimated using Doppler ultrasound. For the measured electrical impedance signal, it is possible to obtain the amplitude-time parameters, which reflect the hemodynamic characteristics of the kidneys and used in diagnostics, which is the subject of further research.

Does breathing pattern affect cerebrovascular reactivity?

What is the central question of this study? Is cerebrovascular reactivity affected by isocapnic changes in breathing pattern? What is the main finding and its importance? Cerebrovascular reactivity does not change with isocapnic variations in tidal volume and frequency. Deviations of arterial carbon dioxide tension from resting values affect cerebral blood vessel tone and thereby cerebral blood flow. Arterial carbon dioxide tension also affects central respiratory chemoreceptors, adjusting respiratory drive. This coincidence raises the question: does respiratory drive also affect the cerebral blood flow response to carbon dioxide? A change in cerebral blood flow for a given change in the arterial carbon dioxide tension is defined as cerebrovascular reactivity (CVR). Two studies have reached conflicting conclusions on this question, using voluntary control of breathing as a disturbing factor during measurements of CVR. Here, we address some of the methodological limitations of both studies by using sequential gas delivery and targeted control of carbon dioxide and oxygen to enable a separation of the effects of carbon dioxide on CVR from breathing vigour. We confirm that there is no detectable superimposed effect of breathing efforts on CVR.

Changes in Body Surface Temperature Play an Underappreciated Role in the Avian Immune Response.

AbstractFever and hypothermia are well-characterized components of systemic inflammation. However, our knowledge of the mechanisms underlying such changes in body temperature is largely limited to rodent models and other mammalian species. In mammals, high dosages of an inflammatory agent (e.g., lipopolysaccharide [LPS]) typically leads to hypothermia (decrease in body temperature below normothermic levels), which is largely driven by a reduction in thermogenesis and not changes in peripheral vasomotion (i.e., changes in blood vessel tone). In birds, however, hypothermia occurs frequently, even at lower dosages, but the thermoeffector mechanisms associated with the response remain unknown. We immune challenged zebra finches (Taeniopygia guttata) with LPS, monitored changes in subcutaneous temperature and energy balance (i.e., body mass, food intake), and assessed surface temperatures of and heat loss across the eye region, bill, and legs. We hypothesized that if birds employ thermoregulatory mechanisms similar to those of similarly sized mammals, LPS-injected individuals would reduce subcutaneous body temperature and maintain constant surface temperatures compared with saline-injected individuals. Instead, LPS-injected individuals showed a slight elevation in body temperature, and this response coincided with a reduction in peripheral heat loss, particularly across the legs, as opposed to changes in energy balance. However, we note that our interpretations should be taken with caution owing to small sample sizes within each treatment. We suggest that peripheral vasomotion, allowing for heat retention, is an underappreciated component of the sickness-induced thermoregulatory response of small birds.

Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis.

Arteriogenesis is one of the primary physiological means by which the circulatory collateral system restores blood flow after significant arterial occlusion in peripheral arterial disease patients. Vascular smooth muscle cells (VSMCs) are the predominant cell type in collateral arteries and respond to altered blood flow and inflammatory conditions after an arterial occlusion by switching their phenotype between quiescent contractile and proliferative synthetic states. Maintaining the contractile state of VSMC is required for collateral vascular function to regulate blood vessel tone and blood flow during arteriogenesis, whereas synthetic SMCs are crucial in the growth and remodeling of the collateral media layer to establish more stable conduit arteries. Timely VSMC phenotype switching requires a set of coordinated actions of molecular and cellular mediators to result in an expansive remodeling of collaterals that restores the blood flow effectively into downstream ischemic tissues. This review overviews the role of VSMC phenotypic switching in the physiological arteriogenesis process and how the VSMC phenotype is affected by the primary triggers of arteriogenesis such as blood flow hemodynamic forces and inflammation. Better understanding the role of VSMC phenotype switching during arteriogenesis can identify novel therapeutic strategies to enhance revascularization in peripheral arterial disease.

ЖАНУАРЛАРДА ҰЙҚЫ БЕЗІ ҚЫЗМЕТІНІҢ БҰЗЫЛУЫ КЕЗІНДЕГІ ҚАН АҒЫСЫНДАҒЫ ӨЗГЕРІСТЕР

the article examines the blood supply of tissues and organs during pancreatic disorders, changes in blood flow. When modeling acute pancreatitis, the functions of blood circulation and blood indicators are considered. In acute pancreatitis in the blood, there was an increase in the indicators of total amylase, lipase, alkaline phosphatase, ALT, AST, and a decrease in the indicators of total protein and cholesterol. With pancreatitis in experimental animals, the rheological parameters of blood changed, the viscosity increased, the blood clotting time was shortened, the number of blood platelets increased, which worsened the fluidity of both blood and lymph and showed the phenomenon of a chronic inflammatory process. In pancreatitis, changes in the ionic composition of blood, lymph, and urine are noted. A decrease in Na+, K+, Ca+2 in blood and urine, a decrease in K+, Ca+2 in lymph, and an increase in Na+ indicate changes in ion exchange in the body. With a violation of the pancreas, characterized by a lack of cell activity in it, there is a violation of the balance system, cellular and humoral components of the blood, accompanied by changes in metabolism and the presence of endogenous poisoning. The circulatory system consists in maintaining the stability of the body in the environment during the destruction of internal organs and tissues. There was a blood clot in the small blood vessels of the pancreas, which in the future will lead to a violation of the blood supply to the microcirculatory core of the pancreas. The rate of blood flow in the trunk vein in acute pancreatitis decreased compared to the control group. The resistance Index RI in the trunk root decreased by 35% due to the fact that it is accompanied by an increase in the diameter of the trunk root. In acute pancreatitis, an increase in the rate of blood flow in the upper secondary artery was recorded, and in the case of posture, the rate of blood flow was 28±0.02 cm/s. As a result of a decrease in the tone of blood vessels after pancreatic disorders, the blood supply to the abdominal cavity and pancreas decreased. As a result of a decrease in the functional properties of the arteries and veins, which led to a decrease in blood flow in the pancreas, which, in turn, is manifested as a result of the preservation of microcirculatory disorders.

Critical Role of LSEC in Post-Hepatectomy Liver Regeneration and Failure.

Liver sinusoids are lined by liver sinusoidal endothelial cells (LSEC), which represent approximately 15 to 20% of the liver cells, but only 3% of the total liver volume. LSEC have unique functions, such as fluid filtration, blood vessel tone modulation, blood clotting, inflammatory cell recruitment, and metabolite and hormone trafficking. Different subtypes of liver endothelial cells are also known to control liver zonation and hepatocyte function. Here, we have reviewed the origin of LSEC, the different subtypes identified in the liver, as well as their renewal during homeostasis. The liver has the exceptional ability to regenerate from small remnants. The past decades have seen increasing awareness in the role of non-parenchymal cells in liver regeneration despite not being the most represented population. While a lot of knowledge has emerged, clarification is needed regarding the role of LSEC in sensing shear stress and on their participation in the inductive phase of regeneration by priming the hepatocytes and delivering mitogenic factors. It is also unclear if bone marrow-derived LSEC participate in the proliferative phase of liver regeneration. Similarly, data are scarce as to LSEC having a role in the termination phase of the regeneration process. Here, we review what is known about the interaction between LSEC and other liver cells during the different phases of liver regeneration. We next explain extended hepatectomy and small liver transplantation, which lead to “small for size syndrome” (SFSS), a lethal liver failure. SFSS is linked to endothelial denudation, necrosis, and lobular disturbance. Using the knowledge learned from partial hepatectomy studies on LSEC, we expose several techniques that are, or could be, used to avoid the “small for size syndrome” after extended hepatectomy or small liver transplantation.