Regional hemodynamics during postexercise hypotension. II. Cutaneous circulation

2004 ◽  
Vol 97 (6) ◽  
pp. 2071-2076 ◽  
Author(s):  
Brad W. Wilkins ◽  
Christopher T. Minson ◽  
John R. Halliwill
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Local Heating ◽  
Exercise Bout ◽  
Internal Temperature ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Arterial Blood ◽  
Postexercise Hypotension ◽  
Cutaneous Circulation

After an acute bout of exercise, there is an unexplained elevation in systemic vascular conductance that is not completely offset by an increase in cardiac output, resulting in a postexercise hypotension. The contributions of the splanchnic and renal circulations are examined in a companion paper (Pricher MP, Holowatz LA, Williams JT, Lockwood JM, and Halliwill JR. J Appl Physiol 97: 2065–2070, 2004). The purpose of this study was to determine the contribution of the cutaneous circulation in postexercise hypotension under thermoneutral conditions (∼23°C). Arterial blood pressure was measured via an automated sphygmomanometer, internal temperature was measured via an ingestible pill, and skin temperature was measured with eight thermocouples. Red blood cell flux (laser-Doppler flowmetry) was monitored at four skin sites (chest, forearm, thigh, and leg), and cutaneous vascular conductance (CVC) was calculated (red blood cell flux/mean arterial pressure) and scaled as percent maximal CVC (local heating to 43°C). Ten subjects [6 men and 4 women; age 23 ± 1 yr; peak O2 uptake (V̇o2 peak) 45.8 ± 2.0 ml·kg−1·min−1] volunteered for this study. After supine rest (30 min), subjects exercised on a bicycle ergometer for 1 h at 60% of their V̇o2 peak and were then positioned supine for 90 min. Exercise elicited a postexercise hypotension reaching a nadir at 46.0 ± 4.5 min postexercise (77 ± 1 vs. 82 ± 2 mmHg preexercise; P < 0.05). Internal temperature increased (38.0 ± 0.1 vs. 36.7 ± 0.1°C preexercise; P < 0.05), remaining elevated at 90 min postexercise (36.9 ± 0.1°C vs. preexercise; P < 0.05). CVC at all four skin sites was elevated by the exercise bout ( P < 0.05), returning to preexercise values within 50 min postexercise ( P > 0.05). Therefore, although transient changes in CVC occur postexercise, they do not appear to play an obligatory role in mediating postexercise hypotension under thermoneutral conditions.

Abstract P156: Estrogen Regulation of Endothelin-B Receptor Mediated Vasodilation

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Katherine Haigh ◽  
Ronald F Feinberg ◽  
Hugh S Taylor ◽  
Megan M Wenner
Keyword(s):  
Postmenopausal Women ◽  
Young Women ◽  
Local Heating ◽  
Receptor Blockade ◽  
Ovarian Hormone ◽  
Hormone Production ◽  
Doppler Flowmetry ◽  
Arterial Blood ◽  
Etb Receptor ◽  
Endothelin B

Our laboratory has recently demonstrated that a loss of endothelin-B (ETB) receptor mediated dilation contributes to impaired vasodilatory function in postmenopausal women. It is unclear if these changes are due to aging, or alterations in ovarian hormones that occur after menopause. The purpose of this study was to test the hypothesis that in a low estradiol state, there is a loss of ETB mediated dilation, and that estradiol administration reverses these responses and mediates dilation. Methods: We tested 8 young women (YW: 24±2 years, 23±1 kg/m 2 , mean arterial BP 84±2mHg) and 6 postmenopausal women (PMW: 56±1 years, 24±1 kg/m 2 , mean arterial BP 94±2mHg). In YW, we suppressed endogenous ovarian hormone production with daily gonadotropin-releasing hormone antagonist (GnRHant; Ganirelix) administration for 10 days, adding estradiol (E2, 0.1 mg/day, Vivelle dot patch) on days 4-10. PMW were tested at baseline and after 1-week E2 administration (0.1 mg/day, Vivelle dot patch). We measured nitric-oxide mediated vasodilation in the cutaneous circulation during local heating (42°C) via laser Doppler flowmetry, followed by microdialysis perfusions of sodium nitroprusside (28mM) with local heating to 43°C to elicit maximal dilation. Cutaneous vascular conductance (CVC) was calculated as cutaneous blood flow/mean arterial blood pressure, and expressed as a percent of maximal dilation. Results: ETB receptor blockade increased vasodilation in YW during hormone suppression with GnRHant (control: 88±3 vs. BQ-788: 94±2 CVC %max, P <0.05). However, ETB receptor blockaded tended to reduce vaodilation during E2 administration (control: 88±3 vs. BQ-788: 82±2 CVC %max, P =0.12). In PMW, ETB receptor blockade had no significant effect on vasodilatory responses (control: 90±4 vs. BQ-788: 95±2 CVC %max, P =0.20). Similarly, ETB receptor blockade did not alter vasodilation after E2 administration (control: 88±7 vs. BQ-788: 88±4 CVC %max). Conclusions: These preliminary data suggest that suppression of endogenous ovarian hormone production alters ETB receptor responses in young women, which is partially mediated by E2. Additional data are needed to determine ETB receptor sensitivity to E2 after menopause.

scholarly journals Desensitization of Adrenaline-Induced Red Blood Cell H+ Extrusion in Vitro After Chronic Exposure of Rainbow Trout to Moderate Environmental Hypoxia

1991 ◽  
Vol 156 (1) ◽  
pp. 233-248 ◽  
Author(s):  
S. THOMAS ◽  
R. KINKEAD ◽  
P. J. WALSH ◽  
C. M. WOOD ◽  
S. F. PERRY
Keyword(s):  
Rainbow Trout ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Whole Blood ◽  
Inverse Correlation ◽  
Adrenergic Stimulation ◽  
Plasma Adrenaline ◽  
Arterial Blood Gas ◽  
Arterial Blood

The sensitivity of red blood cell Na+/H+ exchange to exogenous adrenaline was assessed in vitro using blood withdrawn from catheterized rainbow trout (Oncorhynchus mykiss) maintained under normoxic conditions [water PO2, (PwO2)=20.66 kPa] or after exposure to moderate hypoxia (PwO2=6.67-9.33 kPa) for 48 h, which chronically elevated plasma adrenaline, but not noradrenaline, levels. Peak changes in whole-blood extracellular pH over a 30 min period after adding 50–1000 nmoll−1 adrenaline were employed as an index of sensitivity; the blood was pre-equilibrated to simulate arterial blood gas tensions in severely hypoxic fish (PaO2=2.0 kPa, PaCO2=0.31 kPa). Blood pooled from normoxic fish displayed a dose-dependent reduction in whole-blood pH after addition of adrenaline. Blood pooled from three separate groups of hypoxic fish, however, displayed diminished sensitivity to adrenaline, ranging from complete desensitization to a 60%reduction of the response. Subsequent experiments performed on blood from individual (i.e. not pooled) normoxic or hypoxic fish demonstrated an inverse correlation between the intensity of H+ extrusion (induced by exogenous adrenaline addition) and endogenous plasma adrenaline levels at the time of blood withdrawal. However, acute increases in plasma adrenaline levels in vitro did not affect the responsiveness of the red blood cell to subsequent adrenergic stimulation. The intensity of H+ extrusion was inversely related to the PaO2in vivo between 2.67 and 10.66 kPa, and directly related to the logarithm of the endogenous plasma adrenaline level. The results suggest that desensitization of Na+/H+ exchange in chronically hypoxic fish is related to persistent elevation of levels of this catecholamine. This desensitization can be reversed in vitro as a function of time, but only when blood is maintained under sufficiently aerobic conditions.

Modulation of endothelial nitric oxide synthase expression by red blood cell aggregation

2004 ◽  
Vol 286 (1) ◽  
pp. H222-H229 ◽  
Author(s):  
Oguz K. Baskurt ◽  
Ozlem Yalcin ◽  
Sadi Ozdem ◽  
Jonathan K. Armstrong ◽  
Herbert J. Meiselman
Keyword(s):  
Nitric Oxide ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Cell Aggregation ◽  
Shear Stresses ◽  
Control Mechanisms ◽  
Vascular Control ◽  
Arterial Blood ◽  
Rbc Aggregation ◽  
Endothelial Nitric Oxide

The effects of enhanced red blood cell (RBC) aggregation on nitric oxide (NO)-dependent vascular control mechanisms have been investigated in a rat exchange transfusion model. RBC aggregation for cells in native plasma was increased via a novel method using RBCs covalently coated with a 13-kDa poloxamer copolymer (Pluronic F-98); control experiments used RBCs coated with a nonaggregating 8.4-kDa poloxamer (Pluronic F-68). Rats exchange transfused with aggregating RBC suspensions demonstrated significantly enhanced RBC aggregation throughout the 5-day follow-up period, with mean arterial blood pressure increasing gradually over this period. Arterial segments (≈300 μm in diameter) were isolated from gracilis muscle on the fifth day and mounted between two glass micropipettes in a special chamber equipped with pressure servo-control system. Dose-dependent dilation by ACh and flow-mediated dilation of arterial segments pressurized to 30 mmHg and preconstricted to 45–55% of the original diameter by phenylephrine were significantly blunted in rats with enhanced RBC aggregation. Both responses were totally abolished by nonspecific NO synthase (NOS) inhibitor ( Nω-nitro-l-arginine methyl ester) treatment of arterial segments, indicating that the responses were NO related. Additionally, expression of endothelial NOS protein was found to be decreased in muscle samples obtained from rats exchanged with aggregating cell suspensions. These results imply that enhanced RBC aggregation results in suppressed expression of NO synthesizing mechanisms, thereby leading to altered vasomotor tonus; the mechanisms involved most likely relate to decreased wall shear stresses due to decreased blood flow and/or increased axial accumulation of RBCs.

Actively circulating blood volume in endotoxin shock measured by indicator dilution

1979 ◽  
Vol 236 (2) ◽  
pp. H291-H300 ◽  
Author(s):  
C. F. Rothe ◽  
R. H. Murray ◽  
T. D. Bennett
Keyword(s):  
Blood Cell ◽  
Blood Volume ◽  
Red Blood Cell ◽  
Mixing Time ◽  
Volume Of Distribution ◽  
Endotoxin Shock ◽  
Circulating Blood Volume ◽  
Arterial Blood ◽  
Concentration Changes ◽  
Volumes Of Distribution

To estimate the size of the actively circulating blood volume of splenectomized dogs during control conditions and after endotoxin infusion, the pattern of concentration changes of 51Cr-labeled erythrocytes and 125I-labeled albumin was monitored. A dual exponential equation was fitted to the data. The total red blood cell and albumin volumes of distribution were determined from the slow exponential disappearance curves. The active red blood cell and albumin volumes were 89.8 +/- 5.3% and 92.0 +/- 2.0% of the total volumes, respectively. After endotoxin shock (mean arterial blood pressure 49.1 +/- 17.8 mmHg) the active volumes fell to only 60.0 +/- 10.3% and 56.2 +/- 20.0% of the total volumes, respectively. The fast-mixing time constants were similar (3.1 +/- 1.4 min and 2.5 +/- 2.7 min, respectively) and did not change significantly during the endotoxin shock, indicating that the albumin tag mixed into its larger volume of distribution as rapidly as the cells mixed into their indicated volume. We conclude that 1) an active blood volume can be distinguished, 2) it decreases for both red blood cells and albumin in endotoxin shock, and 3) a major part of the "extravascular plasma volume," as estimated by albumin dilution, is in the actively circulating circulation.

Decreased active vasodilator sensitivity in aged skin

1997 ◽  
Vol 272 (4) ◽  
pp. H1609-H1614 ◽  
Author(s):  
W. L. Kenney ◽  
A. L. Morgan ◽  
W. B. Farquhar ◽  
E. M. Brooks ◽  
J. M. Pierzga ◽  
...  
Keyword(s):  
Heat Stress ◽  
Local Heating ◽  
Interactive Effect ◽  
Older Men ◽  
Whole Body ◽  
Age Difference ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Age Related ◽  
The Right

Older men and women respond to local and reflex-mediated heat stress with an attenuated increase in cutaneous vascular conductance (CVC). This study was performed to test the hypothesis that an augmented or sustained noradrenergic vasoconstriction (VC) may play a role in this age-related difference. Fifteen young (22 +/- 1 yr) and 15 older (66 +/- 1 yr) men exercised at 50% peak oxygen uptake in a 36 degrees C environment. Skin perfusion was monitored at two sites on the right forearm by laser-Doppler flowmetry: one site pretreated with bretylium tosylate (BT) to block the local release of norepinephrine and thus VC and an adjacent control site. Blockade of reflex VC was verified during whole body cooling using a water-perfused suit. CVC (perfusion divided by mean arterial pressure) at each site was reported as a percentage of the maximal CVC (%CVCmax) induced at the end of each experiment by prolonged local heating at 42 degrees C. Neither age nor BT affected the %CVCmax (75-86%) attained at high core temperatures. During the early rise phase of CVC, the %CVCmax-change in esophageal temperature (delta T(es)) curve was shifted to the right in the older men (effective delta T(es) associated with 50% CVC response for young, 0.22 +/- 0.04 and 0.39 +/- 0.04 degrees C and for older, 0.73 +/- 0.04 and 0.85 +/- 0.04 degrees C at control and BT sites, respectively). BT had no interactive effect on this age difference, suggesting a lack of involvement of the VC system in the attenuated CVC response of individuals over the age of 60 yr. Additionally, increases in skin vascular conductance were quantitatively compared by measuring increases in total forearm vascular conductance (FVC, restricted to the forearm skin under these conditions). After the initial approximately 0.2 degrees C increase in T(es), FVC was 40-50% lower in the older men (P < 0.01) for the remainder of the exercise. Decreased active vasodilator sensitivity to increasing core temperature, coupled with structural limitations to vasodilation, appears to limit the cutaneous vascular response to exertional heat stress in older subjects.

scholarly journals To the Question about the Methods Used in Combustiology Practice to Assess the Condition of Patients and Predict General and Local Complications

2021 ◽  
Vol 6 (6) ◽  
pp. 33-43
Author(s):  
О. V. Shapoval ◽  
◽  
N. А. Komaromi ◽  
M. M. Patsatsyia
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Thermal Damage ◽  
Glycosylated Hemoglobin ◽  
Abdominal Pressure ◽  
Burn Wound ◽  
Doppler Flowmetry ◽  
Hematological Indices ◽  
Local Complications ◽  
Burn Disease

The aim. The article is devoted to the methods used in combustiology practice to assess the condition of patients and predict general and local complications. Results. With severe thermal trauma, there is a risk of developing life-threatening conditions in the victims, in particular, sepsis and multiple organ failure. Informative for assessing the course of burn disease is a modified scale of physiological disorders, which takes into account the syndrome of systemic inflammatory response, endogenous intoxication during periods of toxemia and septicotoxemia, and concomitant pathology. The development of intoxication in severe burn injuries requires determining the degree of severity of the process and its assessment in dynamics. The toxicity of blood plasma is studied by the resistance of red blood cell membranes in the acid hemolysis reaction, indicators of the red blood cell intoxication index, and the content of universal markers of intoxication, in particular, medium-weight molecules. Methods for biosensor indication of cytotoxic factors have also been developed. Assessment of the severity of the condition of victims with burns and monitoring the effectiveness of therapy is carried out taking into account the level of procalcitonin and presepsin. To determine the effect of the wound process on the formation of early sepsis in patients with burns in the capillary zone of thermal damage, the content of homocysteine, endothelin and nitric oxide is studied. To assess the severity of the condition of burn patients and predict the development of complications, the values of integral hematological indices are informative. Reliable data on the depth of a burn wound are obtained using thermotopometry and pH measurement of burn wounds, the method of magnetic resonance imaging. In order to assess violations and dynamics of blood supply restoration in the area of thermal damage, the method of laser Doppler flowmetry and optical tissue oximetry is used. Determination of interstitial pressure in burns of the extremities and intra-abdominal pressure in common burns is a way to predict the development of compartment syndrome. To monitor the patient's glycemic status, it is proposed to determine the level of glycosylated hemoglobin. Microbiological research data is used to predict the risk of developing general complications of burn disease, as well as – together with cytological data and methods for determining the maturity of granulation tissue – to assess the readiness of granulating wounds for autodermoplasty. Conclusion. The development of new effective ways to predict and prevent the development of complications in burns is promising

Targeted O2 delivery by low-P50 hemoglobin: a new basis for O2 therapeutics

2003 ◽  
Vol 285 (4) ◽  
pp. H1411-H1419 ◽  
Author(s):  
Amy G. Tsai ◽  
Kim D. Vandegriff ◽  
Marcos Intaglietta ◽  
Robert M. Winslow
Keyword(s):  
Blood Cell ◽  
Red Blood Cells ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Capillary Density ◽  
Bovine Hemoglobin ◽  
Free Hemoglobin ◽  
Plasma Hemoglobin ◽  
Arterial Blood ◽  
Surface Modified

To assess O2 delivery to tissue by a new surface-modified, polyethylene glycol-conjugated human hemoglobin [MP4; Po2 at 50% saturation of hemoglobin (P50); 5.4 mmHg], we studied microcirculatory hemodynamics and O2 release in golden Syrian hamsters hemodiluted with MP4 or polymerized bovine hemoglobin (PolyBvHb; P50 54.2 mmHg). Comparisons were made with the animals' hemodiluted blood with a non-O2 carrying plasma expander with similar solution properties (Dextran-70). Systemic hemodynamics (arterial blood pressure and heart rate) and acid-base parameters were not correlated with microhemodynamics (arteriolar and venular diameter, red blood cell velocity, and flow). Microscopic measurements of Po2 and the O2 equilibrium curves permitted analysis of O2 release in precapillary and capillary vessels by red blood cells and plasma hemoglobin separately. No significant differences between the groups of animals with respect to arteriolar diameter, flow, or flow velocity were observed, but the functional capillary density was significantly higher in the MP4-treated animals (67%) compared with PolyBvHb-treated animals (37%; P < 0.05) or dextran-treated animals (53%). In the PolyBvHb-treated animals, predominant O2 release (both red blood cells and plasma hemoglobin) occurred in precapillary vessels, whereas in MP4 animals most of the O2 was released from both red blood cells and plasma hemoglobin in capillaries. Base excess correlated directly with capillary O2 release but not systemic O2 content or total O2 release. Higher O2 extraction of both red blood cell and plasma hemoglobin in capillaries represents a new mechanism of action of cell-free hemoglobin. High O2 affinity appears to be an important property for cell-free hemoglobin solutions.

Noteworthy Literature Published in 2018 for Cardiothoracic Anesthesiologists

2019 ◽  
Vol 23 (2) ◽  
pp. 148-155 ◽  
Author(s):  
Elizabeth Landry ◽  
Jochen Daniel Muehlschlegel
Keyword(s):  
Cardiopulmonary Bypass ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Red Blood Cell Transfusion ◽  
Left Ventricular Assist Devices ◽  
Transfusion Strategy ◽  
Stroke Incidence ◽  
Arterial Blood

The year 2018 was marked by high-quality, impactful articles spanning the basic, translational, and clinical spectrum in the field of cardiothoracic anesthesia. In this article, we present several hand-picked articles from the past year that we feel were the most significant in shaping our specialty. Large multicenter, randomized controlled trials presenting clinical outcome data dominated the publishing arena: is a restrictive red blood cell transfusion strategy superior to a liberal red blood cell transfusion strategy during cardiopulmonary bypass? Does a low mean arterial blood pressure strategy during cardiopulmonary bypass increase stroke incidence? Does the obesity paradox apply to cardiac surgery? Advancing technology continues to revolutionize our field: can the MitraClip be used to effectively treat secondary mitral regurgitation? Can stem cells improve cardiac function in patients with left ventricular assist devices? These studies allow us to shape our practice in an evidence-based manner, so that we may evolve as a specialty and deliver the best care to our patients.

scholarly journals The Role of Red Blood Cell Distribution Width for Predicting 1-year Mortality in Patients Admitted to the Emergency Department with Severe Dyspnoea

2017 ◽  
Vol 36 (1) ◽  
pp. 32-38
Author(s):  
Gianni Turcato ◽  
Gianfranco Cervellin ◽  
Gian Luca Salvagno ◽  
Eleonora Zaccaria ◽  
Giuseppe Bartucci ◽  
...  
Keyword(s):  
Emergency Department ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Cell Distribution ◽  
Distribution Width ◽  
Arterial Blood ◽  
Increased Risk ◽  
Red Blood Cell Distribution ◽  
Severe Dyspnoea

Summary Background: Universally accepted and validated instruments for predicting the outcome of patients presenting to the emergency department (ED) with severe dyspnoea do not exist so far, nor are they regularly used by the emergency physicians. This study hence aimed to establish whether red blood cell distribution width (RDW) may be a predictive parameter of 1-year mortality in a population of patients admitted to the ED with severe dyspnoea attributable to different underlying disorders. Methods: We retrospectively evaluated all the patients undergoing arterial blood gas analysis for severe dyspnoea (irrespective of the cause) during admission to ED of University Hospital of Verona from September 1, 2014 to November 31, 2014. Results: The final study population consisted of 287 patients for whom complete clinical and laboratory information was available. Overall, 36 patients (12.5%) died after a 1-year follow-up. The RDW value was found to be considerably increased in patients who deceased during the follow-up compared to those who survived (17.2% versus 14.8%; p<0.001). In both univariate and multivariate analyses, the RDW value was found to be a significant predictor of 1-year mortality. In particular, patients with RDW ≥ 15.0% displayed a 72% increased risk of 1-year mortality after multiple adjustments. Conclusions: The measurement of RDW, a very simple and inexpensive laboratory parameter, may represent an important factor for predicting medium-term mortality in patients presenting to the ED with severe dyspnoea.

Postexercise hypotension is not explained by a prostaglandin-dependent peripheral vasodilation

2005 ◽  
Vol 98 (2) ◽  
pp. 447-453 ◽  
Author(s):  
Jennifer M. Lockwood ◽  
Mollie P. Pricher ◽  
Brad W. Wilkins ◽  
Lacy A. Holowatz ◽  
John R. Halliwill
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Potential Contribution ◽  
Vascular Conductance ◽  
Cyclooxygenase Inhibition ◽  
Peripheral Vasodilation ◽  
Arterial Blood ◽  
Single Bout ◽  
Oral Ibuprofen ◽  
Postexercise Hypotension

In normally active individuals, postexercise hypotension after a single bout of aerobic exercise occurs due to an unexplained peripheral vasodilation. Prostaglandin production has been suggested to contribute to the increases in blood flow during and after exercise; however, its potential contribution to postexercise hypotension has not been assessed. The purpose of this study was to determine the potential contribution of a prostaglandin-dependent vasodilation to changes in systemic vascular conductance underlying postexercise hypotension; this was done by inhibiting production of prostaglandins with the cyclooxygenase inhibitor ibuprofen. We studied 11 healthy normotensive men (aged 23.7 ± 4.2 yr) before and during the 90 min after a 60-min bout of cycling at 60% peak O2 uptake on a control and a cyclooxygenase inhibition day (randomized). Subjects received 10 mg/kg of oral ibuprofen on the cyclooxygenase inhibition day. On both study days, arterial blood pressure (automated auscultation) and cardiac output (acetylene uptake) were measured, and systemic vascular conductance was calculated. Inhibition of cyclooxygenase had no effect on baseline values of mean arterial pressure or systemic vascular conductance ( P > 0.2). After exercise on both days, mean arterial pressure was reduced (−2.2 ± 1.0 mmHg change with the control condition and −3.8 ± 1.5 mmHg change with the ibuprofen condition, both P < 0.05 vs. preexercise) and systemic vascular conductance was increased (5.2 ± 5.0% change with the control condition and 8.7 ± 4.1% change with the ibuprofen condition, both P < 0.05 vs. preexercise). There were no differences between study days ( P > 0.6). These data suggest that prostaglandin-dependent vasodilation does not contribute to the increased systemic vascular conductance underlying postexercise hypotension.

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