Search PubMed⌕ Search

Biomedical subjects

K Messmer

Publications and source records attributed to K Messmer.

At least 235 records · Page 13Linked to original sources
PubMed1995

Effects of inhaled prostacyclin as compared with inhaled nitric oxide on right ventricular performance in hypoxic pulmonary vasoconstriction.

OBJECTIVE: Recently, inhalation of prostacyclin (PGI2) has been shown to cause selective pulmonary vasodilation. However, the effects of inhaled PGI2 on right ventricular (RV) performance are still unknown and therefore were compared with those of inhaled nitric oxide (NO). DESIGN: Reported measurements design. SETTING: Animal research laboratory. ANIMALS: Six anesthetized, ventilated dogs (28 +/- 2 kg). INTERVENTIONS: Pulmonary hypertension was induced by decreasing FIO2 to 0.09-0.11 ('hypoxic pulmonary vasoconstriction', HPV). Subsequently, a single dose of either NO (50 ppm) or PGI2-aerosol (0.9 +/- 0.3 ng/kg/min) was randomly added to the inspired gas. MEASUREMENTS AND MAIN RESULTS: Measurements were performed before induction of HPV and 10 minutes after application and withdrawal of each drug. Central hemodynamics, global RV function, and local RV function (n = 5, sonomicrometry) were assessed. HPV resulted in an increase of pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), RV stroke work, right coronary artery flow, maximal rate of RV pressure increase (RV dP/dtmax), and maximal velocity of shortening of contractile elements (Vmax). In contrast, RV ejection fraction, RV end-diastolic volume, RV end-diastolic fiber length, and systolic fiber shortening were unchanged. Both PGI2-aerosol and NO attenuated the HPV-induced increase in PAP and PVR without affecting arterial pressure. NO, but not PGI2, resulted in an increase of RV ejection fraction from 42 to 46% (p < 0.05). Right coronary flow dropped from 29 to 21 mL/min during PGI2 (p < 0.05). RV stroke work, RV dP/dtmax, and Vmax decreased subsequent to both NO and PGI2, whereas local RV function was not affected. CONCLUSIONS: In pulmonary hypertension induced by HPV, PGI2-aerosol and inhaled NO reduced RV afterload and, hence, RV oxygen demand, with only minor changes of stroke volume and cardiac output, indicating an improvement of overall efficiency of RV contraction. RV ejection fraction increased on NO, but not with PGI2. This might be explained by the fact that the reduction of pulmonary vascular resistance during PGI2 amounted to only 65% of the effect of NO. In summary, both inhaled NO and PGI2-aerosol showed beneficial effects on RV performance and may prove helpful in the treatment of acute pulmonary hypertension.

Administration, Inhalation↗
PubMed1995

Hypertonic saline dextran does not increase cardiac contractile function during small volume resuscitation from hemorrhagic shock in anesthetized pigs.

Small volumes of hypertonic saline dextran (10% of shed blood volume [SBV] restore cardiac output (CO) and increase arterial pressure in hemorrhagic shock. Besides rapid expansion of plasma volume, a positive inotropic effect has been proposed as an additional mechanism for the immediate onset of the cardiovascular response. This study compares the effects of 7.2% saline/10% dextran 60 (HSDex, n = 8) and normal saline (NS; n = 6) on central hemodynamics and cardiac contractility assessed by end-systolic elastance (Ees; conductance technique) and segmental preload recruitable stroke work (sPRSW; sonomicrometry). In anesthetized open chest pigs (28 +/- 1 kg, mean +/- SEM) shock was induced by blood withdrawal (40% of blood volume) to maintain mean arterial pressure (MAP) at 45 mm Hg for 75 min. Resuscitation was started by bolus infusion (2 min) of either HSDex (10% of SBV) or the identical sodium load of NS (80% of SBV); 30 min later both groups received 6% dextran (10% of SBV). Hemorrhagic shock reduced CO (-45%) and left ventricular end-diastolic volume (Ved; -70%) while Ees increased (NS:2.2 +/- 0.4 to 7.5 +/- 1.8 mm Hg/mL, P < 0.05; HSDex: 1.9 +/- 0.2 to 9.1 +/- 2.6 mm Hg/mL, P = 0.085). Within 5 min after infusion of either solution CO returned to baseline values and MAP (NS +55%, HSDex +64%) and Ved (+100%) increased. Neither HSDex nor NS increased Ees above shock levels (NS, 8.7 +/- 4.9 mm Hg/mL; HSDex, 7.3 +/- 2.6 mm Hg/mL) and no group differences occurred in other measurements of contractility (dP/dt40,sPRSW). Plasma osmolality increased to 328 +/- 3 mOsmol/kg with HSDex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Does colloid-induced plasma hyperviscosity in haemodilution jeopardize perfusion and oxygenation of vital organs?

BACKGROUND AND METHODS: The infusion of dextran solutions is associated with haemodilution and, under some conditions, with a slight increase in plasma viscosity. To clarify the compound effects of simultaneous haemodilution and plasma viscosity increases on macro- and microhaemodynamics, we investigated the changes in arterial perfusion (radiolabelled microspheres, 15 microns ø) and oxygenation (tissue Po2) of vital organs using an animal model of plasma hyperviscosity. In nine splenectomized beagles plasma viscosity was increased step by step from 1.06 (baseline) to 2.14, and 2.99 mPa.s by infusion of small amounts (4% of total blood volume) of an ultra-high-molecular-weight dextran (50% w/v, mw: 500,000). RESULTS: Despite the significant increase in plasma viscosity, cardiac output as well as specific organ blood flows in heart, brain, liver, and muscle rose steadily with each step of viscosity, while the haematocrit declined from 0.31 to 0.24 and 0.20, respectively. Medians of tissue Po2 in liver peaked at a viscosity of 2 mPa.s and returned to baseline values at 3 mPa.s, whereas in non-working skeletal muscle Po2 values were maximal at 3 mPa.s. CONCLUSION: These results indicate that the impact of plasma viscosity on the rheological properties of whole blood is completely offset by the concomitant reduction of haematocrit. Thus, the comparatively minor changes in plasma viscosity observed after prolonged use of clinical dextrans and other colloids in no way compromise the perfusion and oxygenation of vital organs.

Animals↗
PubMed1995

Prostacyclin aerosol and inhaled nitric oxide fail to reverse pulmonary vasoconstriction induced by thromboxane analogue in dogs.

Inhalation of either prostacyclin (PGI2) as an aerosol or nitric oxide (NO) has been shown to elicit selective pulmonary vasodilation during hypoxic pulmonary vasoconstriction in dogs. Hypoxia may produce cardiovascular changes confounding interpretation of drug effects. Therefore, we investigated the effects of PGI2-aerosol and inhaled NO (50 p.p.m.) on pulmonary pressure-flow relationships (P/Q plots) during thromboxane analogue (U46619) induced pulmonary vasoconstriction. In eight anaesthetized dogs infusion of U46619 (0.33 +/- 0.18 micrograms kg-1 min-1) increased the slope (3.5 +/- 1.1 to 8.4 +/- 1.7 mmHg L-1 min-1, P < 0.001) and the intercept (4.4 +/- 2.3 to 10.2 +/- 4.6 mmHg, P < 0.01) of P/Q plots indicating pulmonary vasoconstriction. Inhalation of both aerosolized PGI2 solution (10 micrograms mL-1) and NO (50 p.p.m.) reduced neither the slope nor the intercept of the P/Q plots. Increasing the concentration of the aerosolized PGI2 solution to 50 micrograms mL-1 (n = 3) did not enhance the effect on pulmonary circulation but systemic vascular resistance fell by 23%. Oxygenation and intrapulmonary shunt remained unchanged during both PGI2-aerosol and inhaled NO. The failure of PGI2-aerosol to induce pulmonary vasodilation indicates that during aerosolization PGI2-concentrations at receptor sites on pulmonary vessels were insufficient to surmount U46619 induced vasoconstriction; this notion is supported by unchanged arterial plasma concentrations of the PGI2 degradation product 6-keto-PGF1 alpha. Considering that NO inhaled at comparable concentrations in sheep reversed U46619 induced pulmonary vasoconstriction, species differences may account for the failure of both PGI2-aerosol and NO to dilate pulmonary vessels in dogs.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1995

Microcirculatory models of ischaemia-reperfusion in skin and striated muscle.

Intravital microscopy is used for analysis of the microcirculation in various organs, e.g. mesentery, intestine, heart, liver and lung, requiring either exteriorization or in situ visualization techniques in anaesthetized animals. In contrast, the implantation of transparent chambers has been employed to allow chronic observation of the microcirculation in intact, non-anaesthetized animals. This paper reports results with two transparent chamber models: the skin-fold chamber model in the hamster and the mouse. An overview is provided of the technical development of the chamber technique and of the various experimental studies that have been performed using these models in ischaemia-reperfusion of striated muscle. Particular emphasis is given to a description of the methods used to induce ischaemia and reperfusion, namely pressure-induced or tourniquet-induced ischaemia. While the former allows simulation of the pathophysiological situation in compartment syndromes, the latter provides an appropriate simulation of the clinical situation in vascular, transplantation and reconstructive surgery. Future possibilities for these microcirculation models in research into the pathophysiology of ischemia-reperfusion are outlined, and potential therapeutic measures to preserve postischaemic tissue are discussed.

Animals↗
PubMed1995

Reduction of post-traumatic intracranial hypertension by hypertonic/hyperoncotic saline/dextran and hypertonic mannitol.

Cerebral injury is seen in one of three patients with multiple traumas; thus efficient shock treatment is a most important measure against the development of secondary brain damage. Small-volume resuscitation in severe hemorrhagic shock by hypertonic/hyperoncotic saline/dextran has been shown to instantaneously normalize cardiac output and to raise systemic blood pressure. In this study, the fluid regimen was compared with hypertonic mannitol to investigate their therapeutic efficacy in intracranial hypertension. The experiments were performed in rabbits subjected to a focal lesion of the brain to induce acute, vasogenic brain edema. The resulting intracranial hypertension was enhanced in a standard manner by inflation of an epidural balloon until an intracranial pressure (ICP) of 17 mm Hg was obtained. Intravenous administration of either 7.2% saline/10% dextran-60 or of 20% mannitol rapidly decreased the elevated ICP. After the first injection, ICP lowering was maintained longer by the mannitol than by the hypertonic saline/dextran, whereas no differences in duration of ICP lowering were found when the infusions of these solutions were repeated. The systemic blood pressure increased after injection of the saline/dextran solution, but it tended to decrease after injection of the mannitol. Transient increases in plasma osmolality, colloid-osmotic pressure, and plasma-Na+ were more pronounced after administration of the saline/dextran solution than after the administration of the mannitol. No difference in the tissue water content between the traumatized and contralateral hemisphere was observed in the animals receiving mannitol; however, after saline/dextran infusion, the water content was somewhat increased in the exposed hemisphere but decreased in the nonexposed, contralateral hemisphere (decreased to a point even below the corresponding level of animals who received the mannitol). The increase of the cerebral water content of the traumatized hemisphere was associated with a respective increase of the cerebral Na+ content and a (nonsignificant) decrease of the K+ content. The present findings demonstrate that the hypertonic/hyperoncotic saline/dextran was as efficient as the mannitol in reducing ICP that had been increased by a cerebral lesion and a space-occupying mass; the underlying mechanisms responsible for the reduction might differ. Because of the powerful hemodynamic properties of the saline/dextran in circulatory shock, administration of the solution in patients with multiple traumas and head injury might be particularly advantageous for the prevention of secondary ischemic brain damage.

Animals↗
PubMed1995

In vitro effects of oxidized low density lipoprotein on CD11b/CD18 and L-selectin presentation on neutrophils and monocytes with relevance for the in vivo situation.

Oxidized LDL (oxLDL) has been identified as a potent stimulus of leukocyte adhesion to endothelium, a hallmark of early atherogenesis. A cytofluorometric study was performed to further characterize the mechanisms by which oxLDL stimulates the rapid adhesion of leukocytes to endothelium in vitro and in vivo. Incubation (30 minutes at 37 C) of whole blood (diluted with buffered saline to 1 x 10(6) leukocytes/ml) with oxLDL (0.85 mg LDL cholesterol/ml; oxidized by 7.5 mumol/L Cu2+ for 18 hours) but not native LDL stimulated the upregulation of CD11b/CD18 adhesion receptors on neutrophils (anti-leu-15 binding: 178 +/- 16% of baseline, P < 0.01, means +/- SD of n = 10 experiments) and on monocytes (169 +/- 34% of baseline, P < 0.01). This phenomenon was almost entirely inhibited by n-butanol or the vasoactive drug pentoxifylline (PTX), which also significantly reduced oxLDL-induced leukocyte adhesion to venular and arteriolar endothelium, as assessed by intravital microscopy on the dorsal skinfold chamber in hamsters (venules: 49 +/- 19 versus 120 +/- 34 cells/mm2, P < 0.05; arterioles: 9 +/- 4 versus 52 +/- 7 cells/mm2, P < 0.01) 30 minutes after intravenous injection of oxLDL (4 mg/kg body weight; means +/- SD of n = 7 hamsters per group). Butanol and PTX also significantly reduced the upregulation of CD11b/CD18 by f-methionyl-leucyl-phenylalanine (fMLP) and platelet-activating factor (PAF) but not by phorbol myristate acetate (PMA). Whereas fMLP and PAF stimulate leukocytes via binding to specific cell surface receptors and triggering complex signal transduction pathways, PMA bypasses these pathways and directly activates intracellular protein kinase C. By analogy, we propose that oxLDL upregulates CD11b/CD18 through its previously documented ability to stimulate the generation of second messengers. The effect of n-butanol and PTX on receptor presentation cannot be explained by changes in plasma membrane fluidity, as both agents failed to reverse the decrease in plasma membrane fluidity of neutrophils after stimulation with oxLDL, as assessed by fluorescence anisotropy measurement of the membrane marker diphenylhexatriene. Incubation of isolated neutrophils but not of whole blood with oxLDL resulted in a significant loss of L-selectin from the neutrophil surface (anti-TQ-1 binding: 40 +/- 13% of baseline, P < 0.01). A significant loss of this adhesion receptor on neutrophils and monocytes was also observed after stimulation of isolated neutrophils and whole blood with fMLP, PAF, and PMA.(ABSTRACT TRUNCATED AT 400 WORDS)

1-Butanol↗
PubMed1994

7.2% NaCl/10% dextran 60 versus 20% mannitol for treatment of intracranial hypertension.

Severe head injury is frequently associated with extracranial injuries causing hemorrhagic hypotension. Volume replacement with isotonic fluids not only is therapeutically of limited efficacy but may aggravate posttraumatic brain edema. On the other side, hypertonic/hyperoncotic saline/dextran solution (HHS) shown to restore cardiovascular function in hemorrhagic shock instantaneously, was found to decrease intracranial pressure in experimental head injury. Currently the therapeutic efficacy of HHS and mannitol on ICP was compared at 24 hrs after a focal cerebral lesion and inflation of an epidural balloon in rabbits. Both solutions given at an equimolar dose rapidly lowered the ICP. After the first injection, ICP reduction was longer maintained with mannitol (189 +/- 27 min) as compared to HHS (98 +/- 14 min), while no difference in duration of lowering ICP was found after the second injection. Due to its blood pressure effects, HHS afforded a higher cerebral perfusion pressure than mannitol. In animals with HHS, the water content of the traumatized hemisphere was increased while the contralateral hemisphere was dehydrated. With mannitol, no differences in water content were found between the injured and uninjured hemisphere. The efficiency of HHS in hemorrhagic shock and intracranial hypertension render the fluid mixture particularly promising in patients with polytrauma in combination with head injury.

Animals↗
PubMed1994

Impact of microcirculatory flow pattern changes on the development of acute edematous and necrotizing pancreatitis in rabbit pancreas.

Impairment of pancreatic microcirculation has often been advocated as one pathogenic mechanism in necrotizing pancreatitis. In contrast, data on pancreatic capillary perfusion in edematous pancreatitis are scarce. It was the aim of this experimental study to compare changes in pancreatic microcirculation in edematous and necrotizing pancreatitis. Twelve rabbits were allocated to two groups. Two different models of acute pancreatitis were used. Edematous pancreatitis was elicited by intravenous administration of cerulein (25 micrograms/kg/hr) (N = 6). Necrotizing pancreatitis of the biliary type was induced by pressure-controlled intraductal infusion of a mixture of taurocholate, trypsin, and blood (N = 6). Pancreatic microcirculation was quantified by means of intravital microscopy assessing functional capillary density, blood cell velocity, and distribution of the plasma marker FITC-dextran 70. Systemic hemodynamics were maintained at baseline values by fluid administration. Regardless of edema or necrosis, pronounced extravasation of FITC-dextran was recorded in the early stage of pancreatitis. In cerulein-induced pancreatitis, hyperemia developed as indicated by an increase in blood cell velocity in the presence of homogeneous capillary perfusion. In contrast, a progressive reduction of the number of perfused capillaries was detected in necrotizing pancreatitis. In conclusion, pancreatic microvascular perfusion may be regarded as an important pathogenetic factor for the determination of acute pancreatitis.

Acute Disease↗
PubMed1994

Photodynamic therapy-induced alterations in interstitial fluid pressure, volume and water content of an amelanotic melanoma in the hamster.

The effect of photodynamic therapy (PDT) on interstitial fluid pressure (IFP), tumour volume and water content was measured in melanomas grown in hamsters. Unlike control tumours, treated tumours exhibited a 40-60% increase in volume at 1, 3 and 6 h post PDT. IFP also increased at 1 and 3 h after PDT, but decreased to 50% of control value after 24 h, presumably as a result of PDT-induced microcirculatory impairment.

Animals↗
PubMed1994

Improvement of skin flap perfusion by subdermal injection of recombinant human basic fibroblast growth factor.

The effect of subcutaneously injected recombinant human basic fibroblast growth factor (bFGF) was studied in an arterial skin flap model on the ear of the hairless mouse. Fifty-three male, hairless mice were randomly assigned to 4 groups and pretreated in two different time intervals with different doses of human bFGF. Microvascular perfusion of the skin flaps was determined over a 5-day period by means of intravital microscopy after intravenous injection of the fluorescence marker fluorescein isothiocyanate-dextran (M(r) 150,000). Human bFGF (2,700 ng) injected 6 days before flap creation could not improve perfusion of the flap (n = 10) when compared with controls. However, when applied 18 days before flap creation (n = 13), the same dose resulted in a significant reduction of nonperfused tissue at day 5 after flap creation (12.3% vs 26.8%, p < 0.01). Eighteen-day pretreatment with 1,200 ng (n = 10) and 480 ng (n = 10) had no significant effect on skin flap perfusion. We conclude, therefore, that successful pretreatment with bFGF for prevention of skin flap necrosis is time and dose dependent.

Animals↗
PubMed1994

Visualization of nutritive perfusion following tourniquet ischemia in arterial pattern skin flaps: effect of vasoactive medication.

We present an experimental model that makes it possible to investigate the effects of global ischemia and reperfusion on microvascular perfusion and viability of ill-proportioned (poorly designed) arterial pattern skin flaps in hairless mice. Skin flaps were created on the ears of hairless mice by dissecting two of three nutritional vessel bundles at the ear base. Under these nonischemic conditions, 19 percent of the total flap area went on to necrose (as a result of poor flap design). Global ischemia was induced to the flap tissue for 6 hours with a tourniquet clamp directly after flap incision. The extension of perfused tissue area and flap viability were assessed at the microcirculatory level by intravital video microscopy at 1, 3, 6, and 18 hours and 7 days after reperfusion in animals treated with either normal saline (control) or the vasoactive drug buflomedil hydrochloride (3 mg/kg of body weight per day, i.v., starting 4 hours prior to flap creation and continued at daily intervals until the end of the experiments). In untreated animals (n = 18), 1 hour after clamp release we observed reperfusion of 39.55 percent (38.5/44.9) of total flap area. Reperfusion remained unchanged within the following 5 hours. Within the next 12 hours, reperfused flap area was dramatically reduced to 21.9 percent (15.1/58.4). Seven days thereafter, only 18.8 percent (10.9/42.2) of total flap area remained viable. In contrast, we found in buflomedil-treated animals (n = 18) that 57.3 percent (53.5/62.9) of the total flap tissue was reperfused within the first hour after clamp release (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The beneficial effect of human recombinant superoxide dismutase on acute and chronic rejection events in recipients of cadaveric renal transplants.

In a prospective randomized double-blind placebo-controlled trial, the effect of rh-SOD, given in a dose of 200 mg intravenously during surgery to cyclosporine-treated recipients of cadaveric renal allografts, on both acute and chronic rejection events as well as patient and graft survival was investigated by analyzing the patients' charts retrospectively. The results obtained show that rh-SOD exerts a beneficial effect on acute rejection events as indicated by a significant reduction of (1) first acute rejection episodes from 33.3% in controls to 18.5%, as well as (2) early irreversible acute rejection from 12.5% in controls to 3.7%. With regard to long-term results, there was a significant improvement of the actual 4-year graft survival rate in rh-SOD-treated patients to 74% (with a projected half-life of 15 years) compared with 52% in controls (with an extrapolated half-life of 5 years). The beneficial effect of rh-SOD observed in this trial is not fully understood, although one can assume that the effect is related to its antioxidant action on ischemia/reperfusion injury of the renal allograft, thereby potentially reducing the immunogenicity of the graft. In addition and in accordance with the "response-to-injury hypothesis" in the pathogenesis of general atherosclerosis, rh-SOD has the potential to mitigate free radical-mediated reperfusion injury-induced acute endothelial cell damage that potentially may contribute to the process of chronic obliterative rejection arteriosclerosis.

Acute Disease↗
PubMed1994

Impact of leukocyte-endothelial cell interaction in hepatic ischemia-reperfusion injury.

To clarify the in vivo relevance of leukocyte-endothelial cell interactions in the manifestation of hepatic ischemia-reperfusion (I/R) injury, we studied leukocyte flow behavior in sinusoids and postsinusoidal venules of postischemic hepatic tissue in rats using intravital microscopy. Reperfusion following either 20 min (n = 9) or 60 min (n = 9) of left hepatic lobar ischemia resulted in a significant increase of the number of stagnant leukocytes in sinusoids and adherent cells in postsinusoidal venules compared with sham-operated controls (n = 10). Transmission electron microscopy revealed the extravasation of leukocytes from both sinusoids (into the space of Disse) and postsinusoidal venules. In parallel, hepatic I/R was associated with increased serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and reduced bile flow. Linear regression estimates revealed significant (P < 0.01) correlations between serum ALT (r = 0.76) and AST (r = 0.65) activities, bile flow (r = -0.62), and the number of adherent leukocytes in postsinusoidal venules. In contrast, parameters of hepatocellular integrity and function did not directly correlate with the number of stagnant leukocytes in liver sinusoids. We conclude that hepatic I/R induces accumulation, adherence, and extravasation of leukocytes in both hepatic sinusoids and postsinusoidal venules. However, the adherence of leukocytes to the endothelial lining of venules, rather than of sinusoids, may determine the manifestation of hepatocellular damage and liver dysfunction.

Alanine Transaminase↗
PubMed1994

Hypertonic hydroxyethyl starch restores hepatic microvascular perfusion in hemorrhagic shock.

The influence of small-volume resuscitation (hypertonic saline-10% hydroxyethyl starch, HS/HES) on liver microcirculation (intravital fluorescence microscopy) was studied in a nonheparinized hemorrhagic shock model [mean arterial pressure (MAP) 40 mmHg for 1 h] in rats. Resuscitation was performed with Ringer lactate (RL, 4-fold shed volume/20 min; n = 7), 10% hydroxyethyl starch 200/0.6 (HES, shed volume/5 min; n = 6), or 7.2% NaCl-10% hydroxyethyl starch 200/0.6 (HS/HES, 10% shed volume/2 min; n = 7). One hour after resuscitation, MAP increased in all groups, but it did not return to preshock values (P < 0.05). HES (16 +/- 2% nonperfused sinusoids) and HS/HES (14 +/- 2% nonperfused sinusoids), but not RL (24 +/- 2% nonperfused sinusoids), reduced (P < 0.05) shock-induced sinusoidal perfusion failure (28 +/- 3%) with restoration of leukocyte velocity in sinusoids (S) and postsinusoidal venules (V). Shock-induced stasis/adherence of leukocytes was further increased (P < 0.05) after resuscitation with RL (S, 38 +/- 6%; V, 55 +/- 20%) and HES (S, 31 +/- 8%; V, 23 +/- 14%). In contrast, resuscitation with HS/HES prevented increased leukocyte stasis in sinusoids (-4 +/- 4%) as well as adherence to endothelial lining of postsinusoidal venules (-5 +/- 10%). We conclude that replacement of only 10% of actual blood loss by means of small-volume resuscitation (HS/HES) can restore hepatic microvascular perfusion and prevent reperfusion-induced leukocyte stasis/adherence.

Animals↗