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Biomedical subjects

K Messmer

Publications and source records attributed to K Messmer.

At least 37 records · Page 2Linked to original sources

Impact of hyperthermic preconditioning on postischemic hepatic microcirculatory disturbances in an isolated perfusion model of the rat liver.

Sublethal hyperthermia and the following recovery from this heat exposure, referred to as hyperthermic preconditioning, elicits a transient state of tolerance to oxidative insults through an intracellular protective response: stress response. The impact of hyperthermic preconditioning on hepatic microcirculatory disturbance, which is one of the determinants of ischemia/reperfusion-induced injury of the liver, was investigated by using intravital fluorescence microscopy. Thirty minutes of ischemia and a subsequent 120 minutes of reperfusion was induced in an in situ isolated perfusion model of Sprague-Dawley rats. Heat stress was given by whole-body hyperthermia, and a subsequent recovery was allowed for 18 or 48 hours, respectively. Postischemic decrease in sinusoidal perfusion rate and sinusoidal diameter, leukocyte stagnation in sinusoids, and leukocyte adhesion in postsinusoidal venules were significantly attenuated in both hyperthermia-pretreated groups. A recovery of bile production, a reduction of liver enzyme release, and an attenuation of tissue edema and histological damage were also observed. A marked expression of heat shock protein (HSP) 70 and heme oxygenase (HO-1)/HSP32 was correlatively observed in the liver tissue coincident with the induction of these protective effects. Hyperthermic preconditioning provides a continuous long-term and constant inhibitory effect (up to 48 hours after heat exposure) on postischemic injury of the liver through the attenuation of microcirculatory disturbances. These beneficial effects might be associated with a concomitant increase in HSP70 and HO-1/HSP32 expression.

Animals↗

[Acute normovolemic hemodilutin (ANH). Effects of ANH on the diastolic function of the left ventricle].

Ischemia-induced changes of diastolic leftventricular (LV) properties commonly precede corresponding ECG-changes. In the present experimental study the consequences of acute normovolemic hemodilution (ANH) induced dilutional anemia (hematocrit, hct 20%) for LV diastolic function were investigated. A total of 22 anaesthetized, splenectomized beagle dogs breathing room air were hemodiluted with isooncotic hydroxyethylstarch solution (6% HAES 200,000/0.5) until a hct value of 20% was reached. Before and after ANH intravascular blood volume (indocyaningreen dilution technique), global and regional myocardial blood flow (radioactive microspheres technique) and the following parameters reflecting LV diastolic properties were ascertained: 1) the maximum rate of LV pressure decrease (LVdp/dtmin), 2) slope and intercept of the enddiastolic pressure-volume relationship (EDPVR, conductance technique) and 3) the time-constant of isovolumic LV pressure decline "tau". After ANH to hct 20% diastolic LV function was found unchanged. Particularly the load-independent parameters (EDPVR-slope and tau) remained constant. The decrease of LV dp/dtmin (-2724 +/- 479 vs. -2388 +/- 408 mmHg.sek-1; p < 0.05) reflects ANH induced changes of LV pre- and afterload. Signs of subendocardial perfusion mismatch were not encountered. Presumed that the coronary vascular system is intact ANH to hct 20% does not provoque changes of LV diastolic function. Moreover neither myocardial perfusion and oxygenation nor myocardial function are endangered by this degree of dilutional anemia.

Animals↗

Roundtable conference on tissue oxygenation in acute medicine, Brussels, Belgium, 14-16 March 1998.

* Nutritional tissue perfusion and tissue metabolic demand are heterogeneously distributed. * Oxygen diffusion occurs preferentially at the precapillary arteriolar level. * Determination of adequacy of tissue oxygenation requires local organ measurements. * While there remains considerable variability in individual RBC transfusion practices, a recent clinical trial questioned the efficacy of RBC transfusion to hemoglobin concentrations greater than 80 gm/l in patients without heart disease [63]. * RBC substitutes, including cell-free hemoglobin solutions and PFC solutions are efficacious, yet may exhibit a number of direct vascular effects.

Belgium↗

Role of hypotension in brain-death associated impairment of liver microcirculation and viability.

Hypotension in brain-dead organ donors is considered a determinant factor of graft viability. The aim of this study was to elucidate the role of hypotension in brain-death associated impairment of hepatic microcirculation and function. Male Sprague-Dawley rats with an intracranial balloon were used. Group I (n = 7) served as sham controls. In group II (n = 7) brain death was induced through inflation of an intracranial balloon. In group III (n = 7) hypotension without brain death was induced by means of pentobarbital. In group II, a steep rise of arterial pressure was followed by a fall to a lower level (P < 0.01, vs. group I). Also in group III arterial pressure was lower (P < 0.01, vs. group I). In group II, bile production was diminished (P < 0.05). Impaired sinusoidal perfusion (P < 0.01) and enhanced leukocyte endothelium interaction (P < 0.05) were documented in hepatic microvasculature. Electron microscopic analysis revealed vacuolization of hepatocytes; these changes were not observed in group III. Brain death induces specific changes of liver microcirculation, function and histomorphology. Independent of associated hypotension, brain death per se impairs donor liver graft quality.

Alanine Transaminase↗

Acceleration of wound healing by topical drug delivery via liposomes.

BACKGROUND: Despite intensive research, impaired wound healing remains a considerable complication. Therefore, topically applied liposome-encapsulated buflomedil hydrochloride was investigated for its ability to improve wound repair in normal (n=16) and ischemic (n=16) skin tissue. METHODS: Experiments were performed using the wound healing model of the ear of hairless mice. Standardized skin wounds (4.25 mm(2)) were created by circular excision of the epidermal layer and the subcutaneous tissue. Liposomes were applied daily until complete neovascularization of the wound occurred. Tissue regeneration by complete epithelialization and neovascularization of the wound area, microcirculatory parameters, and leukocyte-endothelium interaction were investigated by means of intravital microscopy. Microvascular perfusion was assessed by laser-Doppler flowmetry. RESULTS: Topical application of buflomedil liposomes led to a significantly (P<0.05) accelerated wound closure in both normal (9.6+/-0.7 days) and ischemic (13.4+/-0.1 days) skin tissue compared with animals that were treated with unloaded liposomes (controls; 13.1+/-0.8 days; 15.3+/-0.6 days). Complete neovascularization of the wound was also enhanced (P<0.05) in buflomedil-treated animals (normal tissue 18.8+/-0.4 days; ischemic tissue 19.6+/-0.7 days) compared with controls (20.6+/-0.6 days; 22. 6+/-1.2 days). CONCLUSION: These data suggest that buflomedil-loaded liposomes might be of beneficial use for clinical wound care.

Administration, Cutaneous↗

Characterization and prevention of phototoxic effects in intravital fluorescence microscopy in the hamster dorsal skinfold model.

Intravital microscopy is widely used to study the microcirculation. However, the use of fluorescent dyes can induce phototoxic effects which may affect the measurements, particularly in tissue exposed to oxidative stress. The aim of the study was to determine the threshold light dose at which fluorescent microscopy is associated with phototoxic effects in the hamster dorsal skinfold chamber under normal and pathological conditions. The extent of phototoxicity in the microcirculation in the hamster skinfold chamber was investigated using intravital fluorescent microscopy during 60 min of illumination (1048 mW/cm2) applying two different concentrations of fluorescein isothiocyanate dextran under baseline conditions (groups A and B) and following 4 h of ischemia (groups C and D). In the second part of the study the microvasculature was analyzed regarding phototoxic effects during a standardized intravital microscopic examination after 4 h of pressure induced ischemia. Groups I and II (n=7) were studied using epiillumination after injection of fluorescein isothiocyanate dextran plus rhodamine 6G or rhodamine 6G only. In group III (n=7) only transillumination was used. Arteriolar vasospasm, microvascular perfusion failure, thrombus formation, and enhanced leukocyte endothelium interaction were observed as signs of a phototoxic effect in normal tissue. However, the light doses needed to induce these effects clearly exceeded those during standard examinations. The induction of a 4-h ischemia and reperfusion further enhanced these effects. Despite the predamage by ischemia/reperfusion the comparison of epiillumination and transillumination microscopy using a standard protocol showed no differences regarding the parameters analyzed at any time. This indicates that epiillumination and the fluorescent dyes per se did not affect the experimental results. These results show that ischemia/reperfusion studies in the dorsal skinfold chamber of the Syrian golden hamster can be carried out safely without the risk of inducing phototoxic effects by fluorescent microscopy. Nevertheless every laboratory using epiillumination and fluorescent dyes should take precautions to avoid these effects by the use of sensitive cameras to lower the light dose.

Animals↗

Anti-ICAM-1 blockade reduces postsinusoidal WBC adherence following cold ischemia and reperfusion, but does not improve early graft function in rat liver transplantation.

BACKGROUND/AIM: The present in vivo study investigated the impact of a monoclonal antibody directed against the intercellular adhesion molecule-1 (ICAM-1) on initial microvascular reperfusion injury after liver transplantation. METHODS: Orthotopic, syngeneic liver transplantation including arterial reconstruction was performed in male Lewis rats after 24 h graft storage in University of Wisconsin (UW) solution at 4 degrees C. Animals received either an anti-ICAM-1 antibody (n=7), an IgG1 control antibody (n=8) or saline only (n=7). Hepatic microvascular alterations during the initial 90 min of reperfusion were assessed using intravital fluorescence microscopy. Early graft dysfunction was determined by analysis of bile flow. RESULTS: After treatment with anti-ICAM-1 mAb, hepatic microvascular perfusion was found improved when compared with that of IgG1- and saline-treated controls. In addition, anti-ICAM-1 mAb effectively reduced the number of permanently adherent white blood cells in postsinusoidal venules (284.4+/-59.1 mm(-2) vs IgG1: 371.9+/-26.7 mm(-2) and saline: 431.8+/-46.4 mm(-2); p<0.05). In contrast, the number of stagnant white blood cells in sinusoids was higher (p<0.05) in liver grafts with blocked ICAM-1 (320.6+/-17.2 mm(-2)) compared with that of IgG1- (215.2+/-11.1 mm(-2)) and saline-treated controls (226.4+/-14.0 mm(-2)). Measurement of hepatic uptake of fluorescent-labeled latex particles did not reveal significant differences in phagocytic activity. Finally, bile flow also did not differ between the three groups studied. CONCLUSION: Together these results indicate that ICAM-1 is involved in the process that mediates white blood cells adherence in postsinusoidal venules, whereas in hepatic sinusoids other mechanisms apart from ICAM-1-mediated white blood cells adherence seem to be fundamental for posttransplant white blood cells accumulation. Our data further suggest that white blood cells adherence in postsinusoidal venules via ICAM-1 does not make a major contribution to the pathogenesis of early cold ischemia/reperfusion injury after liver transplantation.

Animals↗

Automation of the use of fluorescent microspheres for the determination of blood flow.

Fluorescent-labeled microspheres (FM) are a new tool for the determination of organ blood flow. However, the FM-method is labor intensive, because of the necessity to recover the microspheres from the tissue samples. The aim of this study was to automate the FM-method. A Zymate-Robotic System (Zymark, Idstein, Germany) was modified to handle a novel filtration device. The robot is surrounded by 12 different stations which are necessary to process the samples. It performs the sequential steps which are needed to recover the microspheres from the samples. The dyes are finally released from the FM with a solvent and their fluorescent intensity is measured online using a spectrophotometer (Perkin Elmer, Uberlingen, Germany). The robotic system is able to recover the FM through digestion and filtration of the tissue samples using the new filter, to dissolve the FM and to release the dyes so that their fluorescent intensities can be measured for the calculation of organ blood flow.

Animals↗

Compatibility of different colloid plasma expanders with perflubron emulsion: an intravital microscopic study in the hamster.

BACKGROUND: Perfluorocarbon-based oxygen carriers have been proposed as an adjunct to autologous blood conservation techniques during elective surgery. To date, the effects of perfluorocarbon emulsions at the microcirculatory level have not been studied extensively. In this study the effects of perflubron emulsion on the microcirculation after acute normovolemic hemodilution (ANH) were investigated using different colloid plasma expanders. METHODS: The dorsal skin fold chamber model and intravital fluorescence microscopy were used for analysis of the microcirculation in the thin striated skin muscle of conscious hamsters (body weight, 40-60 g). Measurements of microvascular perfusion and leukocyte adhesion (n = 6 animals per experimental group) were made before and at 10, 30, and 60 min after ANH (to hematocrit 0.3) with either 6% hydroxyethyl starch 200/0.6 (HES), 3.5% gelatin, 5% human serum albumin (HSA), or 6% dextran 60 (DX-60) followed by intravenous injection of 3 ml/kg body weight of a 60% weight/volume perfluorocarbon emulsion based on perflubron (perfluorooctyl bromide) emulsified with egg yolk lecithin. RESULTS: Acute normovolemic hemodilution with HES, gelatin, or HSA followed by injection of perflubron emulsion elicited no alterations of local microvascular perfusion or leukocyte-endothelium interaction as assessed in arterioles and postcapillary venules. However, ANH with DX-60 followed by injection of perflubron emulsion led to a significant reduction of erythrocyte velocity in postcapillary venules and an increase in venular leukocyte sticking that was never observed with DX-60 alone. CONCLUSIONS: Hydroxyethyl starch, gelatin, and HSA are compatible with perflubron emulsion in the setting of ANH. Only DX-60 appeared to be incompatible with perflubron emulsion, as evidenced by impairment of capillary perfusion.

Animals↗

Diaspirin-crosslinked hemoglobin reduces mortality of severe hemorrhagic shock in pigs with critical coronary stenosis.

OBJECTIVE: To evaluate the effects of resuscitation with a 10% diaspirin-crosslinked hemoglobin (DCLHb) solution on global hemodynamic variables, systemic and myocardial oxygen transport and tissue oxygenation, and contractile function of the left ventricle in an experimental model of severe hemorrhagic shock and critical stenosis of the left anterior descending coronary artery (LAD). DESIGN: Prospective, placebo-controlled, randomized study. SETTING: Experimental animal laboratory. SUBJECTS: A total of 20 anesthetized pigs. INTERVENTIONS: After implementation of a permanent critical LAD stenosis (ie, maintenance of basal blood flow but absence of reactive hyperemia after a 10-sec complete vessel occlusion), hemorrhagic shock (target mean aortic pressure, 45 mm Hg) was induced within 15 mins by programmed withdrawal of blood and maintained for 60 mins. Subsequently, the volume of plasma lost during hemorrhage was replaced by either a balanced electrolyte solution containing 10 g/dL DCLHb (DCLHb group; n = 10) or an 8 g/dL human albumin solution (HSA) oncotically matched to DCLHb (HSA group; n = 10). Data were collected immediately after the infusion of the different solutions and again after 60 mins had elapsed. MEASUREMENTS AND MAIN RESULTS: Although five of ten HSA-treated animals died of acute left ventricular failure within the first 20 mins after complete fluid resuscitation, all of the DCLHb-treated animals survived the 60-min observation period after resuscitation (p < .05). This significant difference in mortality is explained by higher coronary perfusion pressure in DCLHb-treated animals (75 +/- 17 vs. 27 +/- 17 torr DCLHb vs. HSA group; p < .05) and persistence of subendocardial ischemia and hypoxia (radioactive microspheres method) in HSA-treated animals on resuscitation particularly affecting the LAD-supported myocardium (subendocardial oxygen delivery: 20 +/- 11 vs. 3 +/- 1 mL oxygen x g(-1) x min(-1), DCLHb vs. HSA group; p < .05). Except for enhanced myocardial contractility immediately on infusion of DCLHb (maximal left ventricular pressure increase: 2373 +/- 782 vs. 1730 +/- 543 torr x sec(-1) DCLHb vs. HSA group; p < .05), no differences were detected between groups concerning the variables of systemic oxygen transport, tissue oxygenation, and regional contractile function of the myocardium (determined with microsonometry). CONCLUSIONS: Fluid resuscitation with 10% DCLHb solution completely reverses hemorrhagic shock-induced subendocardial ischemia and hypoxia in the presence of compromised coronary circulation and thereby prevents early death after resuscitation.

Animals↗

A new chamber technique for intravital microscopic observations in the different soft tissue layers of mouse hindleg.

BACKGROUND: A newly developed observation chamber has been designed for comfortable limb immobilization during intravital microscopic analysis, which permits direct, repeated, long-lasting observations of the microcirculation in the various hindleg soft tissues. METHODS: Experiments were performed under inhalation isoflurane/nitrous oxide anesthesia. Intravenously injected fluorescein isothiocyanate (FITC)-dextran (M, 150,000) and Rhodamine 6G (Sigma, St. Louis, MO) allowed for visualization of both microcirculatory phenomena in arterioles, capillaries, and venules and macrocirculatory structures as superficial saphenous artery and vein. Skin microcirculation analysis was performed from the epidermal side (group A, n = 7), whereas observation of deeper situated tissues was performed after oval skin excision on the medial surface of the tibial area (group B, n = 7). FITC-dextran (M, 150,000; group C, n = 8) injected into the foot pad permitted visualization of venous, arterial, and accompanying lymphatic vessels. With the aid of a computer-assisted microcirculation analysis system, functional capillary density, vessel diameter, edema formation, and leukocyte-endothelial cell interactions were evaluated. The ratio of rolling leukocytes, given as percentage of all leukocytes passing the vessel segment during a 30-second observation interval, and the number of sticking leukocytes per square millimeter of endothelial surface were determined. RESULTS: This new model allows the analysis of the complex in vivo changes of macro- and microcirculatory parameters in the different (venous, arterial, lymphatic) vessels of the covering tissues (skin and muscle) of the mouse hindleg. CONCLUSION: The potential applications of this technique include the study of mechanical trauma, ischemia-reperfusion injury, and tissue compression mimicking both acute and prolonged venous stasis on both the microcirculatory and macrocirculatory levels in the different tissue compartments.

Adipose Tissue↗

Effects of primary resuscitation from shock on distribution of myocardial blood flow.

Hemorrhagic shock alters heterogeneity of regional myocardial perfusion (RMP) in the presence of critical coronary stenosis in pigs. Conventional resuscitation has failed to reverse these effects. We hypothesized that improvement of the resuscitation regime would lead to restoration of RMP heterogeneity. Diaspirin-cross-linked hemoglobin (10 g/dl; DCLHb) and human serum albumin (8.0 g/dl; HSA) were used. After baseline, a branch of the left coronary artery was stenosed; thereafter, hemorrhagic shock was induced. Resuscitation was performed with either DCLHb or HSA. At baseline, the fractcal dimension (D) of subendocardial myocardium was 1.31 +/- 0.083 (HSA) and 1.35 +/- 0.106 (DCLHb) (mean +/- SD). Coronary stenosis increased subendocardial D slightly but consistently only in the DCLHb group (1.39 +/- 0.104; P < 0.05). Shock reduced subendocardial D: 1.21 +/- 0.093 (HSA; P = 0.10), 1.25 +/- 0.092 (DCLHb; P < 0.05). Administration of DCLHb increased subendocardial D in 7 of 10 animals (1.31 +/- 0.097; P = 0.066). HSA was ineffective in this respect. DCLHb infusion restored arterial pressure and increased cardiac index (CI) to 80% of baseline values. Administration of HSA left animals hypotensive (69 mmHg) and increased CI to 122% of the average baseline value. Shock-induced disturbances of the distribution of RMP were improved by administration of DCLHb but not by HSA.

Animals↗

Role of L-selectin in leukocyte sequestration in lung capillaries in a rabbit model of endotoxemia.

After a variety of pathophysiologic stimuli, neutrophils accumulate in lung capillaries and contribute to the pathogenesis of acute lung injury. Lung neutrophil sequestration has previously been attributed to mechanical retention of stiffened neutrophils, but L-selectin-mediated leukocyte/endothelial interaction may be an essential step. We investigated the effect of the anti-L-selectin antibody HuDreg 200 on leukocyte sequestration and microhemodynamics in alveolar capillaries in a model of acute endotoxemia. We used in vivo fluorescence microscopy to analyze kinetics of fluorescently labeled red and white blood cells in alveolar capillary networks of the rabbit lung. Investigations were performed over 2 h after an intravenous infusion of 0.2 ml/kg body weight (bw) NaCl, 2 mg/kg bw HuDreg 200, 20 microg/kg bw lipopolysaccharide (LPS) of Escherichia coli 0111:B4, or the combination of HuDreg 200 and LPS, respectively. Infusion of LPS induced leukocyte sequestration in alveolar capillaries, which was accompanied by a reduction of alveolar capillary perfusion and functional capillary density. These effects could be completely blocked by pretreatment of animals with HuDreg 200. We conclude that L-selectin-mediated leukocyte/endothelial interaction is a necessary prerequisite for leukocyte sequestration in alveolar capillaries in this model. Impaired alveolar capillary perfusion appeared to result directly from capillary leukocyte sequestration.

Acute Disease↗

Fibrinogen deposition at the postischemic vessel wall promotes platelet adhesion during ischemia-reperfusion in vivo.

Following ischemia-reperfusion (I/R), platelet adhesion is thought to represent the initial event leading to remodeling and reocclusion of the vasculature. The mechanisms underlying platelet adhesion to the endothelium have not been completely established. Endothelial cells rendered ischemic acquire a procoagulant phenotype, characterized by fibrinogen accumulation. Therefore, we evaluated whether fibrinogen deposition during I/R mediates platelet adhesion. Using fluorescence microscopy, fibrinogen deposition and the accumulation of platelets were assessed in vivo in a model of intestinal I/R (1.5 hours/60 minutes). Fibrinogen accumulated in arterioles and venules early after the onset of reperfusion. The deposition of fibrinogen colocalized with large numbers of adherent platelets (520 +/- 65 and 347 +/- 81 platelets/mm(2) in arterioles and venules). Pretreatment with an antifibrinogen antibody attenuated platelet adhesion. Intracellular adhesion molecule (ICAM)-1 served as a major receptor for fibrinogen, since fibrinogen deposition and platelet adhesion to the endothelial cell surface were markedly decreased in ICAM-1-deficient mice. The platelet alpha(IIb)/beta(3) integrin plays a key role in fibrinogen-dependent platelet accumulation, because (1) platelet adhesion involved RGD-recognition sequences, and (2) platelets isolated from a patient with Glanzmann's disease showed decreased interaction with the postischemic endothelium. Since platelets are demonstrated here to induce tyrosine phosphorylation in endothelial cells, platelet recruitment might contribute to the development of an inflammatory reaction during I/R.

Animals↗

Microvascular fluid filtration capacity (Kf) assessed with cumulative small venous pressure steps and with various degrees of tilt.

UNLABELLED: Orthostatic dysregulation is a frequent phenomenon in pilots experiencing extreme G forces and after prolonged exposures to microgravity in cosmonauts. We used non-invasive venous congestion plethysmography (VCP) to study microcirculatory changes and the ability to activate peripheral and centrally mediated protective mechanisms during various degrees of tilt, which we used as an orthostatic challenge. METHOD: The study, which was approved by the local ethical committee of the Institute of Biomedical Problems, was performed on six healthy 20 - 26 years old male volunteers. We applied 6 - 8 cumulative small venous congestion pressure steps (8 mmHg) to the thigh and determined the fluid filtration capacity (Kf), the linear relationship between cuff pressure (Pcuff) and measured fluid filtration (Jv). We then measured the fluid filtration (Jv) response to varying cumulative degrees of tilt, starting at 0 degrees followed by head down -8 degrees -15 degrees, -30 degrees -15 degrees, -8 degrees, 0 degrees, and then head up 15 degrees, 30 degrees, 70 degrees, 30 degrees, 15 degrees and 0 degrees. Each tilt stage was sustained for 15 minutes. The change in hydrostatic load, at the level of the strain gauge, was determined by measuring the difference in vertical height between the right atrium and mid calf at the level of the gauge. Limb arterial blood flow was measured and lung function tests were performed before and after the small cumulative pressure step protocol, as well as at the end of each tilt step. RESULTS: No significant changes in blood pressure (BP) and heart rate (HR) occurred during the cumulative pressure step protocol. However, an increase in HR was observed during the tilt, but only reached significance at 30 degrees and 70 degrees. The mean Kf value measured with small cumulative pressure steps was 3.25 +/- 0.5 (10(-3) ml.100 ml tissue(-1) mmHg(-1) = KfU), which was significantly (p < 0.005) higher than the value obtained using tilt to increase the hydrostatic load (0.98 +/- 0.2 KfU). One subject had an unchanged Kf value and experienced vaso - vagal syncope following the imposition of 70 degrees tilt, with a heart rate < 35 / min and a systolic blood pressure of 60 mmHg. The measurement of blood flow in the limb showed no significant change during the tilt procedure. The lung function measurements revealed, that only expiratory reserve volume (ERV) did significantly increase during 35 degrees and 70 degrees head up tilt. All other parameters were unchanged. We suggest that the differences in these Kf values can be explained by the activation of both central and peripheral mediated changes in pre- capillary resistance in response to the tilt. We suspect, that the vaso - vagal syncope, experienced by one subject, reflected his inability to activate these protective reflex mechanisms, a situation that could be exacerbated by sub-clinical venous insufficiency. We believe that these results show that VCP is a useful tool for the determination of intolerance to orthostatic stress.

Adult↗