Dysfunctional vestibular system causes a blood pressure drop in astronauts returning from space.
Ontology highlight
ABSTRACT:
SUBMITTER: Hallgren E
PROVIDER: S-EPMC4680856 | biostudies-other | 2015 Dec
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Systemic diseases characterized by elevated levels of C-reactive protein (CRP), such as sepsis or systemic inflammatory response syndrome, are usually associated with hardly controllable haemodynamic instability. We therefore investigated whether CRP itself influences blood pressure and heart rate. Immediately after intravenous injection of purified human CRP (3.5 mg CRP/kg body weight) into anesthetized rabbits, blood pressure dropped critically in all animals, while control animals injected with bovine serum albumin showed no response. Heart rate did not change in either group. Approaching this impact on a cellular level, we investigated the effect of CRP in cell lines expressing adrenoceptors (CHO-α1A and DU-145). CRP caused a Ca2+ signaling being dependent on the CRP dose. After complete activation of the adrenoceptors by agonists, CRP caused additional intracellular Ca2+ mobilization. We assume that CRP interacts with hitherto unknown structures on the surface of vital cells and thus interferes with the desensitization of adrenoceptors.
| S-EPMC7483553 | biostudies-literature
Project description:Cytomegalovirus (CMV) infection is a common infection in adults (seropositive 60-99% globally), and is associated with cardiovascular diseases, in line with risk factors such as hypertension and atherosclerosis. Several viral infections are linked to hypertension, including human herpes virus 8 (HHV-8) and HIV-1. The mechanisms of how viral infection contributes to hypertension or increased blood pressure are not defined. In this report, the role of CMV infection as a cause of increased blood pressure and in forming aortic atherosclerotic plaques is examined. Using in vivo mouse model and in vitro molecular biology analyses, we find that CMV infection alone caused a significant increase in arterial blood pressure (ABp) (p<0.01 approximately 0.05), measured by microtip catheter technique. This increase in blood pressure by mouse CMV (MCMV) was independent of atherosclerotic plaque formation in the aorta, defined by histological analyses. MCMV DNA was detected in blood vessel samples of viral infected mice but not in the control mice by nested PCR assay. MCMV significantly increased expression of pro-inflammatory cytokines IL-6, TNF-alpha, and MCP-1 in mouse serum by enzyme-linked immunosorbent assay (ELISA). Using quantitative real time reverse transcriptase PCR (Q-RT-PCR) and Western blot, we find that CMV stimulated expression of renin in mouse and human cells in an infectious dose-dependent manner. Co-staining and immunofluorescent microscopy analyses showed that MCMV infection stimulated renin expression at a single cell level. Further examination of angiotensin-II (Ang II) in mouse serum and arterial tissues with ELISA showed an increased expression of Ang II by MCMV infection. Consistent with the findings of the mouse trial, human CMV (HCMV) infection of blood vessel endothelial cells (EC) induced renin expression in a non-lytic infection manner. Viral replication kinetics and plaque formation assay showed that an active, CMV persistent infection in EC and expression of viral genes might underpin the molecular mechanism. These results show that CMV infection is a risk factor for increased arterial blood pressure, and is a co-factor in aortic atherosclerosis. Viral persistent infection of EC may underlie the mechanism. Control of CMV infection can be developed to restrict hypertension and atherosclerosis in the cardiovascular system.
| S-EPMC2673691 | biostudies-literature
Project description:Real-time lab analysis is needed to support clinical decision making and research on human missions to the Moon and Mars. Powerful laboratory instruments, such as flow cytometers, are generally too cumbersome for spaceflight. Here, we show that scant test samples can be measured in microgravity, by a trained astronaut, using a miniature cytometry-based analyzer, the rHEALTH ONE, modified specifically for spaceflight. The base device addresses critical spaceflight requirements including minimal resource utilization and alignment-free optics for surviving rocket launch. To fully enable reduced gravity operation onboard the space station, we incorporated bubble-free fluidics, electromagnetic shielding, and gravity-independent sample introduction. We show microvolume flow cytometry from 10 μL sample drops, with data from five simultaneous channels using 10 μs bin intervals during each sample run, yielding an average of 72 million raw data points in approximately 2 min. We demonstrate the device measures each test sample repeatably, including correct identification of a sample that degraded in transit to the International Space Station. This approach can be utilized to further our understanding of spaceflight biology and provide immediate, actionable diagnostic information for management of astronaut health without the need for Earth-dependent analysis.
| S-EPMC10963801 | biostudies-literature
Project description:Salt sensitivity of blood pressure is an independent risk factor for cardiovascular morbidity. Mechanistically, abnormal mineralocorticoid action and subclinical renal impairment may blunt the natriuretic response to high sodium intake, causing blood pressure to rise. 11β-Hydroxysteroid dehydrogenase type 2 (11βHSD2) controls ligand access to the mineralocorticoid receptor, and ablation of the enzyme causes severe hypertension. Polymorphisms in HSD11B2 are associated with salt sensitivity of blood pressure in normotensives. In this study, we used mice heterozygote for a null mutation in Hsd11b2 (Hsd11b2(+/-)) to define the mechanisms linking reduced enzyme activity to salt sensitivity of blood pressure. A high-sodium diet caused a rapid and sustained increase in blood pressure in Hsd11b2(+/-) mice but not in wild-type littermates. During the adaptation to high-sodium diet, heterozygotes displayed impaired sodium excretion, a transient positive sodium balance, and hypokalemia. After 21 days of high-sodium feeding, Hsd11b2(+/-) mice had an increased heart weight. Mineralocorticoid receptor antagonism partially prevented the increase in heart weight but not the increase in blood pressure. Glucocorticoid receptor antagonism prevented the rise in blood pressure. In Hsd11b2(+/-) mice, high-sodium feeding caused suppression of aldosterone and a moderate but sustained increase in corticosterone. This study demonstrates an inverse relationship among 11βHSD2 activity, heart weight, and blood pressure in a clinically important context. Reduced activity causes salt sensitivity of blood pressure, but this does not reflect illicit activation of mineralocorticoid receptors by glucocorticoids. Instead, we have identified a novel interaction among 11βHSD2, dietary salt, and circulating glucocorticoids.
| S-EPMC4830399 | biostudies-literature
Project description:The recent consensus by the Perioperative Quality Initiative (POQI) on intraoperative hypotension (IOH) stated that mean arterial pressure (MAP) below 60-70 mmHg is associated with myocardial infarction (MI), acute kidney injury (AKI), death and also that IOH is a function of not only severity but also of duration. However, most of the data come from large, heterogeneous cohorts of patients who underwent different surgical procedures and types of anaesthesia. We sought to assess how various definitions of IOH can predict clinically significant hypoperfusive outcomes in a homogenous cohort of generally anesthetised patients undergoing abdominal surgery, taking into account thresholds of MAP and their time durations. The data for this study come from a prospective cohort study in which patients who underwent abdominal surgery between 1 October 2018 and 15 July 2019 in the university hospital in Katowice were included in the analysis. We analysed perioperative data to assess how various IOH thresholds can predict hypoperfusive outcomes (defined as myocardial injury, acute kidney injury or stroke). 508 patients were included in the study. The total number of cases of clinically significant hypoperfusion was 38 (7.5%). We found that extending durations of low MAP, i.e., below 55 mmHg, 60 mmHg, 65 mmHg and 70 mmHg, were associated with the development of either AKI, MI or stroke. It was observed that for narrower and lower hypotension thresholds, the time required to induce complications is shorter. Patients who suffered from AKI/MI/Stroke experienced more episodes of any of the IOH definitions applied. Absolute IOH thresholds were superior to the relative definitions. For patients undergoing abdominal surgery, it is vital to prevent the extended durations of intraoperative mean arterial pressure below 70 mmHg. Finally, there appears to be no need to guide intraoperative haemodynamic therapy based on pre-induction values and, consequently, on relative drops of MAP.
| S-EPMC8584611 | biostudies-literature
Project description:Introduction"Man-in-the-barrel syndrome" is a neurological phenotype with brachial diplegia, normal sensation, and preserved motor function of the lower limb. It has been described in various neuropathological conditions affecting the cerebral hemispheres, pons, upper spinal cord, and peripheral neurons. Severe hypotension leading to watershed infarctions leading to this phenotype has been reported. We describe the first case of "man-in-the-barrel syndrome" in a patient with a precipitous drop in blood pressure following oral antihypertensive medications. Case Presentation. A 75-year-old Sri Lankan male presented following a generalized tonic-clonic seizure to a tertiary care hospital. Upon recovery, he was noted to have severe brachia diplegia affecting shoulder movements with preserved hand muscle power and motor functions of the lower limb. The previous day, he was newly diagnosed with markedly elevated blood pressure without acute end organ involvement. Treatment with three antihypertensives had been initiated. Noncontrast CT of the brain revealed watershed infarctions affecting both cerebral hemispheres.ConclusionIt is generally unwise to lower blood pressure very rapidly, as ischemic damage can occur in vascular beds that are habituated to high levels of blood pressure in the brain. Ischemic damage caused by rapid lowering of blood pressure may rarely result in "man-in-the-barrel syndrome" leading to severe functional disability.
| S-EPMC7532409 | biostudies-literature
Project description:IntroductionSpontaneous blood pressure drop within the first 24 h has been reported following arterial recanalisation in ischaemic stroke patients. We aimed to assess if spontaneous blood pressure drop within the first hour after mechanical thrombectomy is a marker of early neurological recovery.Patients and methodsRetrospective observational single-centre study including ischaemic stroke patients treated with mechanical thrombectomy. Blood pressure parameters from admission, mechanical thrombectomy start, mechanical thrombectomy end and hourly within 24 h after mechanical thrombectomy were reviewed. Primary outcome was early dramatic neurological recovery (8-point-reduction in NIHSS or NIHSS ≤ 2 at 24 h). Secondary outcome was functional independence at 90 days (mRankin 0-2).ResultsWe included 458 patients in our analysis. Two-hundred (43.7%) patients achieved dramatic neurological recovery following mechanical thrombectomy. One hour after mechanical thrombectomy end, median systolic blood pressure was significantly different between outcome groups (129 vs. 138 mmHg, p = 0.005) and a higher drop in median systolic blood pressure was seen in the dramatic neurological recovery group (15 vs. 9 mmHg). Optimal cut-off for predicting dramatic neurological recovery was a systolic blood pressure drop of 10.5 mmHg (sensitivity 0.54, specificity 0.55, AUC 0.55). On multivariate analysis, spontaneous systolic blood pressure drop was associated with higher odds of achieving dramatic neurological recovery (OR for 10 mmHg blood pressure drop 1.14, 95% CI 1.01-1.29, p = 0.04). No significative association between any blood pressure parameter drop and functional independence at 90 days was found.DiscussionWe hypothesised that spontaneous systolic blood pressure drop is a marker of successful reperfusion and, therefore, a marker of improvement of cerebral autoregulation due to the reduced final ischaemic core.ConclusionSpontaneous systolic blood pressure drop after mechanical thrombectomy is an early predictor of dramatic neurological recovery.
| S-EPMC7856584 | biostudies-literature
Project description:OBJECTIVE:This study applied a new external ventricular catheter, which allows intracranial pressure (ICP) monitoring and cerebral spinal fluid (CSF) drainage simultaneously, to study cerebral vascular responses during acute CSF drainage. METHODS:Six patients with 34 external ventricular drain (EVD) opening sessions were retrospectively analyzed. A published algorithm was used to extract morphological features of ICP recordings, and a template-matching algorithm was applied to calculate the likelihood of cerebral vasodilation index (VDI) and cerebral vasoconstriction index (VCI) based on the changes of ICP waveforms during CSF drainage. Power change (?P) of ICP B-waves after EVD opening was also calculated. Cerebral autoregulation (CA) was assessed through phase difference between arterial blood pressure (ABP) and ICP using a previously published wavelet-based algorithm. RESULTS:The result showed that acute CSF drainage reduced mean ICP (P?=?0.016) increased VCI (P?=?0.02) and reduced ICP B-wave power (P?=?0.016) significantly. VCI reacted to ICP changes negatively when ICP was between 10 and 25 mmHg, and VCI remained unchanged when ICP was outside the 10-25 mmHg range. VCI negatively (r?=?-?0.44) and VDI positively (r?=?0.82) correlated with ?P of ICP B-waves, indicating that stronger vasoconstriction resulted in bigger power drop in ICP B-waves. Better CA prior to EVD opening triggered bigger drop in the power of ICP B-waves (r?=?-?0.612). CONCLUSIONS:This study demonstrates that acute CSF drainage reduces mean ICP, and results in vasoconstriction which can be detected through an index, VCI. Cerebral vessels actively respond to ICP changes or cerebral perfusion pressure (CPP) changes in a certain range; beyond which, the vessels are insensitive to the changes in ICP and CPP.
| S-EPMC7229699 | biostudies-literature
Project description:Background The relationship between orthostatic hypotension and clinical outcome in older adults is poorly understood. Blood pressure drop rate (ie, speed of blood pressure drop) may particularly reflect the imposed challenge to the baroreflex and the associated clinical outcome (ie, frailty and number of falls). This study aimed to compare orthostatic blood pressure drop rate and drop magnitude with regard to their association with frailty and number of falls. Methods and Results Blood pressure was measured continuously during a standardized active stand task in 168 patients (mean age 81.4±7.0; 55.4% female) who visited a geriatric outpatient clinic for cognitive or mobility problems. The association of orthostatic blood pressure drop rate, blood pressure drop magnitude, and baroreflex sensitivity (ie, increase in heart rate divided by systolic blood pressure drop magnitude) with frailty (Fried criteria and 4 frailty markers) and self-reported number of falls was assessed using linear regression models, adjusting for age and sex. Systolic blood pressure drop rate had the strongest association with frailty according to the 4 frailty markers (β 0.30; 95% CI, 0.11-0.49; P=0.003) and number of falls (β 1.09; 95% CI, 0.19-1.20; P=0.018); diastolic blood pressure drop magnitude was most strongly associated with frailty according to the Fried criteria (β 0.37; 95% CI, 0.15-0.60; P<0.001). Baroreflex sensitivity was associated with neither frailty nor number of falls. Conclusions Orthostatic blood pressure drop rate was associated with frailty and falls and may reflect the challenge to the baroreflex rather than drop magnitude.
| S-EPMC7428630 | biostudies-literature
Project description:BackgroundTransvalvular pressure drops are assessed using Doppler echocardiography for the diagnosis of heart valve disease. However, this method is highly user-dependent and may overestimate transvalvular pressure drops by up to 54%. This work aimed to assess transvalvular pressure drops using velocity fields derived from blood speckle imaging (BSI), as a potential alternative to Doppler. METHODS: A silicone 3D-printed aortic valve model, segmented from a healthy CT scan, was placed within a silicone tube. A CardioFlow 5000MR flow pump was used to circulate blood mimicking fluid to create eight different stenotic conditions. Eight PendoTech pressure sensors were embedded along the tube wall to record ground-truth pressures (10 kHz). The simplified Bernoulli equation with measured probe angle correction was used to estimate pressure drop from maximum velocity values acquired across the valve using Doppler and BSI with a GE Vivid E95 ultrasound machine and 6S-D cardiac phased array transducer.ResultsThere were no significant differences between pressure drops estimated by Doppler, BSI and ground-truth at the lowest stenotic condition (10.4 ± 1.76, 10.3 ± 1.63 vs. 10.5 ± 1.00 mmHg, respectively; p > 0.05). Significant differences were observed between the pressure drops estimated by the three methods at the greatest stenotic condition (26.4 ± 1.52, 14.5 ± 2.14 vs. 20.9 ± 1.92 mmHg for Doppler, BSI and ground-truth, respectively; p < 0.05). Across all conditions, Doppler overestimated pressure drop (Bias = 3.92 mmHg), while BSI underestimated pressure drop (Bias = -3.31 mmHg).ConclusionsBSI accurately estimated pressure drops only up to 10.5 mmHg in controlled phantom conditions of low stenotic burden. Doppler overestimated pressure drops of 20.9 mmHg. Although BSI offers a number of theoretical advantages to conventional Doppler echocardiography, further refinements and clinical studies are required with BSI before it can be used to improve transvalvular pressure drop estimation in the clinical evaluation of aortic stenosis.
| S-EPMC9287947 | biostudies-literature