Oscillations of Hemodynamic Parameters Induced by Negative Pressure Breathing in Healthy Humans.

INTRODUCTION: Negative pressure breathing is breathing with decreased pressure in the respiratory tract without lowering pressure acting on the torso. We lowered air pressure only during inspiration (NPBin). NPBin, used to increase venous return to the heart, is considered a countermeasure against redistribution of body fluids toward the head during spaceflight. We studied NPBin effects on circulation in healthy humans with an emphasis on NPBin-induced oscillations of hemodynamic parameters synchronous with breathing. We propose an approach to analyze the oscillations based on coherent averaging.METHODS: Eight men ages 24-42 yr participated in the NPBin and control series. During the series, to reproduce fluids shift observed under microgravity, subjects were supine and head down (-8°). Duration of NPBin was 20 min, rarefaction -20 cm H2O. Hemodynamic parameters were measured by Finometer. Electrical impedance measurements were used to estimate changes in blood filling of cerebral vessels.RESULTS: Mean values of hemodynamic parameters virtually did not change under NPBin, but NPBin induced oscillations of the parameters synchronous with respiration. Peak-to-peak amplitude under NPBin were: mean arterial pressure, 4 ± 1 (mmHg); stroke volume, 7 ± 3 (mL); and heart rate, 4 ± 1 (bpm). Electrical impedance of the head increased during inspiration. The increase under NPBin was three times greater than under normal breathing.DISCUSSION: Analysis of oscillations gives more information than analysis of mean values. NPBin induces short-term decrease in left ventricle stroke volume and arterial blood pressure during each inspiration; the decrease is compensated by increase after inspiration. NPBin facilitates redistribution of body fluids away from the head.Semenov YS, Melnikov IS, Luzhnov PV, Dyachenko AI. Oscillations of hemodynamic parameters induced by negative pressure breathing in healthy humans. Aerosp Med Hum Perform. 2024; 95(6):297-304.

Kinetics of platelet adhesion to a fibrinogen-coated surface in whole blood under flow conditions.

AIM: To test a novel method of assessment of platelet adhesion to a fibrinogen-coated surface in whole blood under flow conditions. METHODS: We developed a fluidic device that mimics blood flow in vessels. The method of detection of platelet adhesion is based on recording of a scattered laser light signal from a fibrinogen-covered surface. Testing was performed in platelet-rich plasma (PRP) and whole blood of healthy volunteers. Control measurements were performed, followed by tests with inhibition of platelet GPIIa/IIIb and GPIb receptors. Then, the same testing sequence was performed in whole blood of persons with autoimmune thrombocytopenia and type 3 von Willebrand disease. RESULTS: The change in intensity of scattered light was 2.7 (2.4; 4.1) times higher in whole blood (0.2 ± 0.08V, n = 7) than in PRP (0.05 ± 0.02 V, n = 7), p < 0.01. The blocking of GP IIb/IIIa receptors decreased the intensity of scattered light to 8.5 (6.5;12)%; the blocking of GPIb receptors decreased it to 34 (23;58)%, p < 0.01. In the whole blood of a person with autoimmune thrombocytopenia, the inhibition of GPIb receptors decreased platelet adhesion, but no effect was observed in type 3 von Willebrand disease. Inhibition of platelet GPIIb/IIIa receptors alone or combined inhibition of GPIb and GPIIb/IIIa receptors resulted in almost total suppression of adhesion in both cases. CONCLUSION: Our system effectively registers platelet adhesion to a fibrinogen-coated surface under controlled-flow conditions and may successfully be applied to the investigation of platelet adhesion kinetics.

Current Position on the Role of Monomeric C-reactive Protein in Vascular Pathology and Atherothrombosis.

C-reactive Protein (CRP) is an acute phase reactant, belonging to the pentraxin family of proteins. Its level rises up to 1000-fold in response to acute inflammation. High sensitivity CRP level is utilized as an independent biomarker of inflammation and cardiovascular disease. The accumulating data suggests that CRP has two distinct forms. It is predominantly produced in the liver in a native pentameric form (nCRP). At sites of local inflammation and tissue injury it may bind to phosphocholine-rich membranes of activated and apoptotic cells and their microparticles, undergoing irreversible dissociation to five monomeric subunits, termed monomeric CRP (mCRP). Through dissociation, CRP deposits into tissues and acquires distinct proinflammatory properties. It activates both classic and alternative complement pathways, binding complement component C1q and factor H. mCRP actively participates in the development of endothelial dysfunction. It activates leukocytes, inducing cytokine release and monocyte recruitment. It may also play a role in the polarization of monocytes and T cells into proinflammatory phenotypes. It may be involved in low-density lipoproteins (LDL) opsonization and uptake by macrophages. mCRP deposits were detected in samples of atherosclerotic lesions from human aorta, carotid, coronary and femoral arteries. mCRP may also induce platelet aggregation and thrombus formation, thus contributing in multiple ways in the development of atherosclerosis and atherothrombosis. In this mini-review, we will provide an insight into the process of conformational rearrangement of nCRP, leading to dissociation, and describe known effects of mCRP. We will provide a rationalization for mCRP involvement in the development of atherosclerosis and atherothrombosis.