Hypertensive patients features of the microcirculation type after new coronavirus infection of COVID-19

Introduction. The COVID-19 pandemic multiplies the incidence of long-term adverse events. Family history of heart disease predicates the necessity of study hemostasis in hypertensive patients. The purpose was to study the microcirculation in hypertensive COVID-19 survivors. Materials and methods. We selected patients treated at the hospitals of Samara from January to March 2021. COVID-19 survivors (diagnosis was confirmed by polymerase chain reaction analysis) were divided into 2 groups and analysed: the group with family history of hypertension (167 patients) and control group with no relevant past medical history (68 patients). The main microcirculation characteristics were evaluated by laser Doppler flowmetry of skin blood flow. Results. The average age of COVID-19 survivors was 52.3±14.2 years, n=86 (51.4 %) – male. The majority of patients (n=61/36.5 %) were 45 to 54 years. A fifth of the patients (n=35/20.9 %) showed no complaints about the underlying disease, the clinical manifestations of the rest were general weakness, fever, shortness of breath, cough, headaches, unstable blood pressure, inflammation of the ENT organs. By comparison the microcirculation parameters of the case patients and control group, a decreased perfusion was detected. It requires a preventive medicine to prevent from early and distant micro and macrothrombosis. Conclusion. The study of microcirculation essential features by the LDF of skin blood flow revealed a pathological type with a predominance of vasoconstrictions in patients with a history of hypertension. Taking into account the proven increase in the incidence of thrombotic events in COVID-19 survivors, the noticed changes in microcirculation require a new approach to prevent from adverse events concerning the hypercoagulation process, especially in patients with famil y history of heart disease.

Reactive Oxygen Species Are Essential for Vasoconstriction upon Cold Exposure

Purpose. We explored the role of ROS in cold-induced vasoconstriction and corresponding mechanism. Methods. Three experiments were performed. First, we measured blood flow in human hands before and after cold exposure. Second, 24 mice were randomly divided into 3 groups: 8 mice received saline injection, 8 received subcutaneous Tempol injection, and 8 received intrathecal Tempol injection. After 30 min, we determined blood flow in the skin before and after cold exposure. Finally, we used Tempol, CCG-1423, and Go 6983 to pretreat HAVSMCs and HUVECs for 24 h. Then, cells in the corresponding groups were exposed to cold (6 h, 4°C). After cold exposure, the cytoskeleton was stained. Intracellular Ca2+ and ROS levels were measured by flow cytometry and fluorescence microscopy. We measured protein expression via Western blotting. Results. In the first experiment, after cold exposure, maximum skin blood flow decreased to 118.4 ± 50.97 flux units. Then, Tempol or normal saline pretreatment did not change skin blood flow. Unlike intrathecal Tempol injection, subcutaneous Tempol injection increased skin blood flow after cold exposure. Finally, cold exposure for 6 h shrank the cells, making them narrower, and increased intracellular Ca2+ and ROS levels in HUVECs and HAVSMCs. Tempol reduced cell shrinkage and decreased intracellular Ca2+ levels. In addition, Tempol decreased intracellular ROS levels. Cold exposure increased RhoA, Rock1, p-MLC-2, ET-1, iNOS, and p-PKC expression and decreased eNOS expression. Tempol or CCG-1423 pretreatment decreased RhoA, Rock1, and p-MLC-2 levels in HAVSMCs. Furthermore, Tempol or Go 6983 pretreatment decreased ET-1, iNOS, and p-PKC expression and increased eNOS expression in HUVECs. Conclusion. ROS mediate the vasoconstrictor response within the cold-induced vascular response, and ROS in blood vessel tissues rather than nerve fibers are involved in vasoconstriction via the ROS/RhoA/ROCK1 and ROS/PKC/ET-1 pathways in VSMCs and endothelial cells.

Caffeine alters thermoregulatory responses to exercise in the heat only in caffeine-habituated individuals: a double-blind placebo-controlled trial

We provide empirical evidence that acute caffeine ingestion exerts a thermoregulatory effect during exercise in the heat in caffeine-habituated individuals but not in nonhabituated individuals. Specifically, caffeine habituation was associated with a greater rise in esophageal temperature with caffeine compared with placebo, which appears to be driven by a blunted skin blood flow response. In contrast, no thermoregulatory differences were observed with caffeine in nonhabituated individuals. Caffeine did not affect sweating responses during exercise in the heat.

Post-exercise Body Cooling: Skin Blood Flow, Venous Pooling, and Orthostatic Intolerance

Athletes and certain occupations (e.g., military, firefighters) must navigate unique heat challenges as they perform physical tasks during prolonged heat stress, at times while wearing protective clothing that hinders heat dissipation. Such environments and activities elicit physiological adjustments that prioritize thermoregulatory skin perfusion at the expense of arterial blood pressure and may result in decreases in cerebral blood flow. High levels of skin blood flow combined with an upright body position augment venous pooling and transcapillary fluid shifts in the lower extremities. Combined with sweat-driven reductions in plasma volume, these cardiovascular alterations result in levels of cardiac output that do not meet requirements for brain blood flow, which can lead to orthostatic intolerance and occasionally syncope. Skin surface cooling countermeasures appear to be a promising means of improving orthostatic tolerance via autonomic mechanisms. Increases in transduction of sympathetic activity into vascular resistance, and an increased baroreflex set-point have been shown to be induced by surface cooling implemented after passive heating and other arterial pressure challenges. Considering the further contribution of exercise thermogenesis to orthostatic intolerance risk, our goal in this review is to provide an overview of post-exercise cooling strategies as they are capable of improving autonomic control of the circulation to optimize orthostatic tolerance. We aim to synthesize both basic and applied physiology knowledge available regarding real-world application of cooling strategies to reduce the likelihood of experiencing symptomatic orthostatic intolerance after exercise in the heat.

Spectral analysis of blood flow oscillations to assess the plantar skin blood flow regulation in response to preconditioning local vibrations

BACKGROUND: Local vibration has been shown promise in improving skin blood flow and wound healing. However, the underlying mechanism of local vibration as a preconditioning intervention to alter plantar skin blood flow after walking is unclear. OBJECTIVE: The objective was to use wavelet analysis of skin blood flow oscillations to investigate the effect of preconditioning local vibration on plantar tissues after walking. METHODS: A double-blind, repeated measures design was tested in 10 healthy participants. The protocol included 10-min baseline, 10-min local vibrations (100Hz or sham), 10-min walking, and 10-min recovery periods. Skin blood flow was measured over the first metatarsal head of the right foot during the baseline and recovery periods. Wavelet amplitudes after walking were expressed as the ratio of the wavelet amplitude before walking. RESULTS: The results showed the significant difference in the metabolic (vibration 10.06 ± 1.97, sham 5.78 ± 1.53, p < 0.01) and neurogenic (vibration 7.45 ± 1.54, sham 4.78 ± 1.22, p < 0.01) controls. There were no significant differences in the myogenic, respiratory and cardiac controls between the preconditioning local vibration and sham conditions. CONCLUSIONS: Our results showed that preconditioning local vibration altered the normalization rates of plantar skin blood flow after walking by stimulating the metabolic and neurogenic controls.

Monitoring skin blood flow to rapidly identify alterations in tissue perfusion during fluid removal using continuous veno-venous hemofiltration in patients with circulatory shock

Background Continuous veno-venous hemofiltration (CVVH) can be used to reduce fluid overload and tissue edema, but excessive fluid removal may impair tissue perfusion. Skin blood flow (SBF) alters rapidly in shock, so its measurement may be useful to help monitor tissue perfusion. Methods In a prospective, observational study in a 35-bed department of intensive care, all patients with shock who required fluid removal with CVVH were considered for inclusion. SBF was measured on the index finger using skin laser Doppler (Periflux 5000, Perimed, Järfälla, Sweden) for 3 min at baseline (before starting fluid removal, T0), and 1, 3 and 6 h after starting fluid removal. The same fluid removal rate was maintained throughout the study period. Patients were grouped according to absence (Group A) or presence (Group B) of altered tissue perfusion, defined as a 10% increase in blood lactate from T0 to T6 with the T6 lactate ≥ 1.5 mmol/l. Receiver operating characteristic curves were constructed and areas under the curve (AUROC) calculated to identify variables predictive of altered tissue perfusion. Data are reported as medians [25th–75th percentiles]. Results We studied 42 patients (31 septic shock, 11 cardiogenic shock); median SOFA score at inclusion was 9 [8–12]. At T0, there were no significant differences in hemodynamic variables, norepinephrine dose, lactate concentration, ScvO2 or ultrafiltration rate between groups A and B. Cardiac index and MAP did not change over time, but SBF decreased in both groups (p < 0.05) throughout the study period. The baseline SBF was lower (58[35–118] vs 119[57–178] perfusion units [PU], p = 0.03) and the decrease in SBF from T0 to T1 (ΔSBF%) higher (53[39–63] vs 21[12–24]%, p = 0.01) in group B than in group A. Baseline SBF and ΔSBF% predicted altered tissue perfusion with AUROCs of 0.83 and 0.96, respectively, with cut-offs for SBF of ≤ 57 PU (sensitivity 78%, specificity 87%) and ∆SBF% of ≥ 45% (sensitivity 92%, specificity 99%). Conclusion Baseline SBF and its early reduction after initiation of fluid removal using CVVH can predict worsened tissue perfusion, reflected by an increase in blood lactate levels.

Independent and combined impact of hypoxia and acute inorganic nitrate ingestion on thermoregulatory responses to the cold

Purpose This study assessed the impact of normobaric hypoxia and acute nitrate ingestion on shivering thermogenesis, cutaneous vascular control, and thermometrics in response to cold stress. Method Eleven male volunteers underwent passive cooling at 10 °C air temperature across four conditions: (1) normoxia with placebo ingestion, (2) hypoxia (0.130 FiO2) with placebo ingestion, (3) normoxia with 13 mmol nitrate ingestion, and (4) hypoxia with nitrate ingestion. Physiological metrics were assessed as a rate of change over 45 min to determine heat loss, and at the point of shivering onset to determine the thermogenic thermoeffector threshold. Result Independently, hypoxia expedited shivering onset time (p = 0.05) due to a faster cooling rate as opposed to a change in central thermoeffector thresholds. Specifically, compared to normoxia, hypoxia increased skin blood flow (p = 0.02), leading to an increased core-cooling rate (p = 0.04) and delta change in rectal temperature (p = 0.03) over 45 min, yet the same rectal temperature at shivering onset (p = 0.9). Independently, nitrate ingestion delayed shivering onset time (p = 0.01), mediated by a change in central thermoeffector thresholds, independent of changes in peripheral heat exchange. Specifically, compared to placebo ingestion, no difference was observed in skin blood flow (p = 0.5), core-cooling rate (p = 0.5), or delta change in rectal temperature (p = 0.7) over 45 min, while nitrate reduced rectal temperature at shivering onset (p = 0.04). No interaction was observed between hypoxia and nitrate ingestion. Conclusion These data improve our understanding of how hypoxia and nitric oxide modulate cold thermoregulation.

Age-Related Changes in the Response of Finger Skin Blood Flow during a Braille Character Discrimination Task

We hypothesized that age-related changes in sensory function might be reflected by a modulation of the blood flow response associated with tactile sensation. The aim of the present study was to clarify how the blood flow response of the fingers during concentrated finger perception is affected by aging. We measured the tactile-pressure threshold of the distal palmar pad of the index finger and skin blood flow in the finger (SBF) during Braille reading performed under blind conditions in young (n = 27) and older (n = 37) subjects. As a result, the tactile-pressure threshold was higher in older subjects (2.99 ± 0.37 log10 0.1 mg) than in young subjects (2.76 ± 0.24 log10 0.1 mg) (p < 0.01). On the other hand, the SBF response was markedly smaller in older subjects (−4.9 ± 7.0%) than in young subjects (−25.8 ± 15.4%) (p < 0.01). Moreover, the peak response arrival times to Braille reading in older and young subjects were 12.5 ± 3.1 s and 8.8 ± 3.6 s, respectively (p < 0.01). A decline in tactile sensitivity occurs with aging. Blood flow responses associated with tactile sensation are also affected by aging, as represented by a decrease in blood flow and a delay in the reaction time.

EFFECTS OF PHYSICAL ACTIVITY ON VASCULAR FUNCTION IN AUTOIMMUNE RHEUMATIC DISEASES: A SYSTEMATIC REVIEW AND META-ANALYSIS

Objectives To summarise existing evidence and quantify the effects of physical activity on vascular function and structure in autoimmune rheumatic diseases (ARDs). Methods Databases were searched (up to March 2020) for clinical trials evaluating the effects of physical activity interventions on markers of micro- and macrovascular function and macrovascular structure in ARDs. Studies were combined using random-effects meta-analysis, which was conducted using the Hedge's g. Meta-analyses were performed on each of the following outcomes: (1) microvascular function (i.e., skin blood flow or responses to acetylcholine [ACh] or sodium nitropusside [SNP] administration); (2) macrovascular function (i.e., brachial flow-mediated dilation [FMD%] or brachial responses to glyceryl trinitrate [GTN%]; and (3) macrovascular structure (i.e., aortic pulse wave velocity [PWV]). Results Ten studies (11 trials), with a total of 355 participants, were included in this review. Physical activity promoted significant improvements in micro- (skin blood flow responses to ACh [g = 0.92; 0.42 to 1.42]) and macrovascular function (FMD% [g = 0.94; 0.56 to 1.02]; GTN% [g = 0.53; 0.09 to 0.98]). Conversely, there was no evidence for beneficial effects of physical activity on macrovascular structure (PWV [g = -0.41; -1.13 to 0.32]). Conclusions Overall, the available clinical trials demonstrated a beneficial effect of physical activity on markers of micro- and macrovascular function, but not on macrovascular structure, in patients with ARDs. The broad beneficial impact of physical activity across the vasculature identified in this review support its role as an effective non-pharmacological management strategy for patients with ARD.