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Biomedical subjects

Dirk Bruegger

Publications and source records attributed to Dirk Bruegger.

8 recordsLinked to original sources

The endothelial glycocalyx affords compatibility of Starling's principle and high cardiac interstitial albumin levels.

OBJECTIVE: To test the role of an oncotic pressure gradient across the endothelial glycocalyx with respect to extravasation of fluid and colloids and development of tissue edema in a whole organ setting. METHODS: We measured filtration in the intact coronary system of isolated guinea pig hearts, comparing colloid-free perfusion and perfusion with 1.67% albumin or 2% hydroxyethylstarch (oncotic pressures 5.30 vs. 11.10 mm Hg, respectively). Heparinase was used to alter the endothelial glycocalyx. RESULTS: Extremely high net organ hydraulic conductivity was obtained with colloid-free perfusion (9.14 microl/min/g tissue). Supplementing perfusate with albumin caused a significant decrease, also vs. hydroxyethylstarch (1.04 vs. 2.67 microl/min/g, p < 0.05). Albumin also lowered edema formation vs. the other perfusion modes (p < 0.05). Stripping the glycocalyx of heparan sulfate reduced the effect of colloids, especially that of albumin. The steady-state concentrations of hydroxyethylstarch and albumin in the mixed interstitial fluid leaving the intact coronary bed averaged about 95% of the intravascular level. Electron and light microscopy indicated that colloid extravasated mainly in the venular sections. CONCLUSION: We propose a low-filtration model for the coronary system with different barrier properties in arteriolar/capillary and venular sections. Arteriolar/capillary: very little fluid and colloid extravasation due to the endothelial surface layer formed by the glycocalyx and albumin plus the endothelial strand barrier; venular: little net extravsation of fluid and colloids despite large pores, because of low hydrostatic and oncotic pressure differences between intra- and extravascular spaces. The latter sites provide physiological access of large solutes (colloids) to the tissue.

Albumins↗

Effect of high altitude and exercise on microvascular parameters in acclimatized subjects.

The role of microvascular fluid shifts in the adaptation to hypobaric hypoxia and its contribution to the pathophysiology of AMS (acute mountain sickness) is unresolved. In a systematic prospective study, we investigated the effects of hypobaric hypoxia and physical exercise alone, and in combination, on microvascular fluid exchange and related factors. We used computer-assisted VCP (venous congestion plethysmography) on the calves of ten altitude-acclimatized volunteers. We investigated the effects of: (i) actively climbing to an altitude of 3196 m, (ii) airlifting these subjects to the same altitude, and (iii) exercise at low altitude. CFC (capillary filtration capacity), Pvi (isovolumetric venous pressure) and Qa (calf blood flow) were assessed before and after each procedure and then repeated after an overnight rest. Measurements of CFC showed no evidence of increased microvascular permeability after any of the procedures. Pvi was significantly decreased (P<0.001) from 20.3+/-4.4 to 8.9+/-4.3 mmHg after active ascent, and was still significantly lower (P=0.009) after overnight rest at high altitude (13.6+/-5.9 mmHg). No such changes were observed after the passive ascent (16.7+/-4.0 mmHg at baseline; 17.3+/-4.5 mmHg after passive ascent; and 19.9+/-5.3 mmHg after overnight rest) or after exercise at low altitude. After the active ascent, Qa was significantly increased. We also found a significant correlation between Qa, Pvi and the number of circulating white blood cells. In conclusion, we found evidence to support the hypothesis that increased microvascular permeability associated with AMS does not occur in acclimatized subjects. We also observed that the microvascular equilibrium pressure (Pvi) fell in inverse relation to the increase in Qa, especially in hypoxic exercise. We hypothesize that this inverse relationship reflects the haemodynamic changes at the microvascular interface, possibly attributable to the flow-induced increases in endothelial surface shear forces.

Acclimatization↗

Contrasting effects of colloid and crystalloid resuscitation fluids on cardiac vascular permeability.

BACKGROUND: Fluid extravasation may lead to myocardial edema and consequent reduction in ventricular function. Albumin is presumed to interact with the endothelial glycocalyx. The authors' objective was to compare the impact of different resuscitation fluids (human albumin, hydroxyethyl starch, saline) on vascular integrity. METHODS: In an isolated perfused heart model (guinea pig), Krebs-Henseleit buffer was augmented with colloids (one third volume 5% albumin or 6% hydroxyethyl starch 130/0.4) or crystalloid (0.9% saline). Perfusion pressure and vascular fluid filtration (epicardial transudate formation) were assessed at different flow rates. After global, stopped-flow ischemia (37 degrees C, 20 min), hearts were reperfused with the same resuscitation fluid additives. In a second series, the authors applied the respective perfusates after enzymatic digestion of the endothelial glycocalyx (heparinase, 10 U over 15 min). RESULTS: Both 5% albumin and 6% hydroxyethyl starch decreased fluid extravasation versus saline (68.4 +/- 5.9, 134.8 +/- 20.5, and 436.8 +/- 14.7 microl/min, respectively, at 60 cm H(2)O perfusion pressure; P < 0.05), the corresponding colloid osmotic pressures being 2.95, 5.45, and 0.00 mmHg. Digestion of the endothelial glycocalyx decreased coronary integrity in both colloid groups. After ischemia, a transient increase in vascular leak occurred with Krebs-Henseleit buffer containing hydroxyethyl starch and saline, but not with albumin. The authors observed no difference between intravascular and bulk interstitial colloid concentration in the steady state. Notwithstanding, electron microscopy revealed an intact endothelial glycocalyx and no interstitial edema in the albumin group. CONCLUSION: Ex vivo, albumin more effectively prevented fluid extravasation in the heart than crystalloid or artificial colloid. This effect was partly independent of colloid osmotic pressure and may be attributable to an interaction of albumin with the endothelial glycocalyx.

Albumins↗

Changes in acid-base balance following bolus infusion of 20% albumin solution in humans.

OBJECTIVE: To evaluate changes in acid-base balance following bolus infusions of a 20% albumin solution. DESIGN AND SETTING: Randomized prospective study in a university hospital. PATIENTS AND PARTICIPANTS: Two groups of eight patients each undergoing gynecological surgery. INTERVENTIONS: Patients were randomly assigned to receive either 0.9% saline or lactated Ringer's solution. At the end of surgery two boluses of 0.5 g/kg body weight of a 20% albumin solution were administered. Arterial blood gases, electrolytes, and total protein were measured. The strong ion difference and the amount of weak plasma acid were calculated. pH and titratable acidity of the 20% albumin solution were determined. MEASUREMENTS AND RESULTS: The infusion of a 20% albumin solution resulted in a significant decrease in pH from 7.284 to 7.262 in the saline group and from 7.422 to 7.394 in the Ringer's group. In both groups the 20% albumin solution caused an increase in strong ion difference and an increase in the amount of weak plasma acid. The observed changes in serum bicarbonate concentration were in good agreement with the changes in strong ion difference and the amount of weak plasma acid. The 20% albumin solution possessed a pH of 6.95 and a titratable acidity of 8.5 [corrected] mEq/l. CONCLUSIONS: According to the Stewart approach, the observed changes in acid-base balance are the net result of the two opposing effects of the strong ion difference and the amount of weak plasma acid. Alternatively, the acidifying effect of the 20% albumin solution may stem from the titratable acid content of the solution.

Acid-Base Equilibrium↗

Atrial natriuretic peptide induces shedding of endothelial glycocalyx in coronary vascular bed of guinea pig hearts.

Atrial natriuretic peptide (ANP) is reported to enhance vascular permeability in vivo. Our aim was to evaluate the impact of ANP on coronary extravasation of fluids and macromolecules and on the integrity of the endothelial glycocalyx. Isolated guinea pig hearts (n = 6/group) were perfused with Krebs-Henseleit buffer in a Langendorff mode. A 6% hydroxyethyl starch (HES) solution was infused into the coronary system for 20 min without (Control group) and simultaneously with (ANP group) ANP at 10(-9) M. In two further series, the glycocalyx was enzymatically degraded by means of heparinase (Hep) application (10 IU over 15 min), followed again by the infusion of HES in the absence (Hep group) and presence (ANP+Hep group) of ANP. Net fluid filtration, extravasation of HES, electron microscopic visualization of the glycocalyx, and quantification of shedding of syndecan-1, a component of the glycocalyx, were determined. An increase in fluid leak was observed in ANP, ANP+Hep, and Hep hearts [+29%, +31%, +14%, respectively; a decrease was observed in Control hearts (-13%)]. Similarly, an accelerated extravasation of colloid was observed in these three groups. Coronary release of syndecan-1 increased 9- to 18-fold during infusion of ANP. Electron microscopy revealed a dramatic degradation of the glycocalyx after ANP. These results indicate that the endothelial glycocalyx serves as a barrier to transmural exchange of fluid and colloid in the coronary vascular system. ANP causes rapid shedding of individual components of the glycocalyx and histologically detectable degradation. Thus the permeability-increasing effect of ANP may be at least partially related to changes in the integrity of the endothelial glycocalyx.

Animals↗

Effect of hypertonic saline dextran on acid-base balance in patients undergoing surgery of abdominal aortic aneurysm.

OBJECTIVE: To evaluate the magnitude and cause of metabolic acidosis after infusion of 7.5% sodium chloride 6% dextran 70. DESIGN: Randomized, prospective clinical study. SETTING: University hospital. PATIENTS: Two groups of 14 patients each, undergoing repair of abdominal aortic aneurysm. INTERVENTIONS: Patients were randomly assigned to receive either 250 mL of hypertonic saline dextran (HSD) or a conventional fluid regimen with 250 mL of hydroxyethyl starch in normal saline solution (H-NS) during the period of aortic clamping. Additionally, normal saline was used in both groups to reach a target pulmonary artery occlusion pressure of 15-18 mmHg. pH, Paco2, and serum concentrations of sodium, potassium, magnesium, calcium, chloride, lactate, albumin, and phosphate were measured. Strong ion difference was calculated as (sodium + potassium + magnesium + calcium) - (chloride + lactate). The amount of weak plasma acid was calculated. MEASUREMENTS AND MAIN RESULTS: The infusion of HSD resulted in an immediate large increase in serum sodium (19 mmol/L) and chloride (22 mmol/L), whereas the infusion of H-NS led only to mild increases in serum sodium (3 mmol/L) and chloride (6 mmol/L). Both HSD and H-NS caused concomitant and equal decreases in the amount of weak plasma acid, strong ion difference, and pH (7.28-7.30). The reduction of bicarbonate was also identical and proportional to the extent of dilution due to infusion of HSD and H-NS. This induced metabolic acidosis was corrected spontaneously in both groups 24 hrs after surgery. CONCLUSION: Both the intravenous administration of 7.5% sodium chloride and the conventional fluid regimen with saline-based 6% hydroxyethyl starch solution resulted in a metabolic acidosis of equal extent. This suggests dilution of plasma buffers or a decrease in strong ion difference to be the primary cause of metabolic acidosis.

Acid-Base Equilibrium↗

Development and validation of a mathematical algorithm for quantifying preoperative blood volume by means of the decrease in hematocrit resulting from acute normovolemic hemodilution.

BACKGROUND: The interindividual variability of blood volume (BV) is high. The aim of this work was to use the decrease in large-vessel hematocrit (HK(LV)) during acute normovolemic hemodilution (ANH) as an instrument for estimating preoperative BV. STUDY DESIGN AND METHODS: In 39 patients, (Group 1) preoperative ANH was performed. Plasma volume, red cell volume, and HK(LV) were measured before and 30 minutes after ANH, respectively. In a retrospective analysis, a mathematical algorithm was developed for estimating BV before ANH by means of the measured changes in HK(LV) and the amount of blood removed during ANH. To validate the method prospectively, ANH was performed in an additional 10 patients (Group 2). Preoperative BV was estimated and measured in the same way as in Group 1. RESULTS: In Group 1, the mean difference between estimated and measured BV before ANH was 200 +/- 403 mL (5.14 +/- 10.12%; p > 0.05; r = 0.8). In Group 2, the estimated BV before ANH was 41 +/- 348 mL (-0.53 +/- 7.84%) lower than the measured BV (p > 0.05; r = 0.94). In this group, however, two patients with an extraordinarily small (2691 mL) and large (6172 mL) preoperative BV, respectively, were identified correctly by means of the algorithm. CONCLUSIONS: The changes in HK(LV) determined during ANH provide a good "bedside" estimation of preoperative BV.

Algorithms↗

Severe metabolic acidosis resulting from a dislocated gastric band.

A 32-year-old morbidly obese woman with an obstructing dislocated gastric band is presented. Because of prolonged vomiting, a metabolic alkalosis would be expected, but instead an impressive high anion gap acidosis was observed. Because of a highly positive urine ketone test and a high serum concentration of beta-hydroxybutyrate, a ketoacidosis caused by starvation appears to be the primary cause of this metabolic acidosis. This type of acidosis was treated successfully with intravenous administration of glucose and insulin as well as sodium bicarbonate, with urgent removal of the band.

Acidosis↗