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P Gaehtgens

Publications and source records attributed to P Gaehtgens.

At least 19 recordsLinked to original sources
PubMed1992

Changes in haemorheology in the racing greyhound as related to oxygen delivery.

Arterial blood samples were obtained from six greyhounds during rest, immediately before, and after a 704-m (7/16th mile) race. Measurements were made of various haematological (red cell count, haemoglobin, packed cell volume, white cell count, plasma proteins) and haemorheological variables. Blood and plasma viscosity were determined at high wall shear stresses (67-200 dynes.cm-2, 670-2000 microN.cm-2) in a 20-microns glass capillary device which was designed to take the diameter dependence of blood viscosity (Fahraeus-Lindqvist effect) into account. Compared to values at rest, substantial haemoconcentration occurred before the race, mainly due to splenic discharge of red cells. Additional haemoconcentration was found after the race. The increase of effective blood viscosity caused by elevation of packed cell volume was greater than the increase in O2 binding capacity resulting from the elevated haemoglobin concentration, suggesting that the haemoconcentration observed in the exercising greyhound does not enhance O2 delivery to skeletal muscle. The main physiological effect of red cell discharge from the contracting spleen appeared to be a consequence of the volume rather than the composition of the circulating blood.

Animals↗
PubMed1992

Differential adhesion of granulocytes to five distinct phenotypes of cultured microvascular endothelial cells.

Adhesion of isolated human polymorphonuclear granulocytes (PMNs) to five different phenotypes of cultured microvascular endothelial cells derived from bovine corpora lutea was investigated by measuring the myeloperoxidase content of cell lysates. Untreated and interleukin 1 (IL-1) -pretreated confluent monolayers were overlaid with unstimulated and phorbol ester (PMA)-stimulated PMNs in the absence and presence of the monoclonal antibody IB4 recognizing and functionally blocking beta 2 (CD18) of the leukocyte integrins. Unstimulated PMN adhesion was highest on type 4, followed by type 3 and 5 endothelial cells. This adhesion was not inhibited by treatment with IB4. IL-1 pretreatment of endothelial cells resulted in a significant increase of PMN adhesion on types 1, 2, and 4, most of which was also beta 2 integrin-independent. PMA-stimulation of PMNs increased adhesion to maximal values on cell types 1 and 5, which was largely blocked by IB4. Type 2 endothelial cells supported significantly less PMA-stimulated PMN adhesion than all other types. In the presence of IB4, adhesion of PMNs to untreated and IL-1-pretreated type 3 and 4 endothelial cells was significantly reduced by PMA. This reduction of beta 2 integrin-independent adhesion by PMA stimulation is compatible with possible shedding of the lectin-like leukocyte adhesion molecule, L-selectin, from PMNs. Differential PMN adhesion may reflect distinctive expression of endothelial adhesion molecules in different phenotypes of microvascular endothelial cells. Endothelial specialization within the microcirculation may have important functional consequences for the inflammatory response in vivo.

Animals↗
PubMed1992

Haemorheology and exercise: intrinsic flow properties of blood in marathon running.

Haemorheological and haematological parameters were studied in venous blood samples taken from 8 endurance-trained athletes before and after a marathon run. Viscometry was performed in a 20 microns glass capillary and in a Couette viscometer. Apparent blood viscosity was lower in the capillary than in the rotational viscometer, but significant differences between pre- and post-run samples were not observed in either system. This is presumably due to the absence of changes of haematocrit (pre-run [mean +/- SD]: 0.453 +/- 0.016, post-run: 0.456 +/- 0.018). Although protein concentration increased significantly from 70.8 +/- 2.1 g/l (pre-run) to 76.0 +/- 3.9 g/l (post-run), the difference of plasma viscosity was not statistically significant (pre-run: 1.26 +/- 0.03 cP, post-run: 1.30 +/- 0.07 cP). In all samples, plasma viscosity showed a significant positive correlation with total protein, globulin, albumin, but not with fibrinogen concentration. Cone-plate aggregometry and a filtration technique were used to evaluate red cell aggregation and deformability, two determinants of blood rheology which also were not different between pre- and post-run samples. The absence of viscosity changes in relation to the marathon run may be due to the relative stability of blood and plasma volume, which can be deduced from haematological parameters. Alterations of plasma composition (e.g. acidosis or hyperosmolality) seem to cause only minor, if any, changes of microrheological cell properties.

Adult↗
PubMed1992

Blood viscosity in tube flow: dependence on diameter and hematocrit.

Since the original publications by Martini et al. (Dtsch. Arch. Klin. Med. 169: 212-222, 1930) and Fahraeus and Lindqvist (Am. J. Physiol. 96: 562-568, 1931), it has been known that the relative apparent viscosity of blood in tube flow depends on tube diameter. Quantitative descriptions of this effect and of the dependence of blood viscosity on hematocrit in the different diameter tubes are required for the development of hydrodynamic models of blood flow through the microcirculation. The present study provides a comprehensive data base for the description of relative apparent blood viscosity as a function of tube diameter and hematocrit. Data available from the literature are compiled, and new experimental data obtained in a capillary viscometer are presented. The combined data base comprises measurements at high shear rates (u > or = 50 s-1) in tubes with diameters ranging from 3.3 to 1,978 microns at hematocrits of up to 0.9. If corrected for differences in suspending medium viscosity and temperature, the data show remarkable agreement. Empirical fitting equations predicting relative apparent blood viscosity from tube diameter and hematocrit are presented. A pronounced change in the hematocrit dependence of relative viscosity is observed in a range of tube diameters in which viscosity is minimal. While a linear hematocrit-viscosity relationship is found in tubes of < or = 6 microns, an overproportional increase of viscosity with hematocrit prevails in tubes of > or = 9 microns. This is interpreted to reflect the hematocrit-dependent transition from single- to multifile arrangement of cells in flow.

Animals↗
PubMed1992

Redistribution of red blood cell flow in microcirculatory networks by hemodilution.

The effect of isovolemic hemodilution on red blood cell flow distribution was studied in complete self-contained microvessel networks of the rat mesentery. Hematocrit, diameter, and length of all vessel segments as well as the topological structure were determined in control networks (systemic hematocrit, 0.54) and after hemodilution (systemic hematocrit, 0.30). Hemodilution was performed by exchanging blood with hydroxyethyl starch (MW 450,000; 6%) or homologous plasma. With hemodilution, the decrease of microvessel hematocrit exceeded that of systemic hematocrit. The average discharge hematocrit in capillaries was 79% of systemic hematocrit in the control group and 73% with hemodilution (p less than 0.001). The heterogeneity of capillary hematocrit within the network, expressed by the coefficient of variation, increased from 0.4 to 0.7. By using the morphological and topological data of four networks, the distribution of hematocrits was also calculated using a hydrodynamic flow model. The modeling results were found to be in close agreement with the experimental data. This indicates that the observed changes can be deduced from established rheological phenomena, most of all phase separation at arteriolar bifurcations. The changes in hematocrit distribution after hemodilution are accompanied by a redistribution of red blood cell flow within the network: relative to total red blood cell flow, red blood cell flow in the distal capillaries of the network increases by about 40% at the expense of the proximal capillaries that are close to the feeding arteriole and that exhibit the highest red blood cell flow under control conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Why networks?

The development of the network concept is prompted by the accumulated quantitative disagreement between the behaviour of single microvessels and the changes of total tissue blood flow, as well as by the ubiquitous flow heterogeneity. It is further driven by the difficulty to attach function-oriented nomenclatures to structural elements of the terminal vascular bed. So far, the efforts of mathematical network modelling have led to a reasonably coherent analysis of microcirculatory hemodynamics from available data on network geometry and blood rheology. These efforts have shown that complete data sets are important because of the non-symmetric architecture of most networks. Due to its effect on exchange efficiency, the relationship between network heterogeneity and total flow regulation remains the currently most relevant physiological problem. So far, the hypothesis of flow heterogeneity being controlled through intra-network communication and consecutive readjustment of flow and flux dispersions is intriguing, but speculative.

Animals↗
PubMed1991

Lectin-like cell adhesion molecule 1 mediates leukocyte rolling in mesenteric venules in vivo.

During the inflammatory response, granulocytes and other leukocytes adhere to and emigrate from small venules. Before firm attachment, leukocytes are observed rolling slowly along the endothelium in venules of most tissues accessible to intravital microscopy. The molecular mechanism underlying this early type of leukocyte-endothelial interaction is unknown. Leukocyte rolling was investigated in venules (diameter, 40 microns) of the exposed rat mesentery. Micro-infusion of a recombinant soluble chimera (LEC-IgG) of the murine homing receptor lectin-like cell adhesion molecule 1 (LEC-CAM 1; gp90MEL) into individual venules reduced the number of rolling leukocytes by 89% +/- 2% (mean +/- SEM, n = 20 venules), while a similar CD4 chimera (CD4-IgG) had no effect (inhibition 14% +/- 7%, n = 25). Rolling was also greatly reduced by a polyclonal serum against LEC-CAM 1 (inhibition 84% +/- 3%, n = 35); preimmune serum was ineffective (11% +/- 13% inhibition, n = 28). These findings indicate that LEC-CAM 1 mediates the adhesive interaction underlying leukocyte rolling and thus may play an important role in inflammation and in pathologic conditions involving leukocytes.

Animals↗
PubMed1991

Heterogeneity of capillary perfusion.

Heterogeneity represents a general feature of capillary networks. All of the parameters which describe hemodynamic, geometric or functional aspects of such networks exhibit considerable spatial dispersion. This is to some extent the result of the morphological and topological design of the network, reinforced by the nonhomogeneous nature of the flowing blood. Temporal dispersions are introduced by smooth muscle activity, which may be rhythmic or just oscillatory, but also by the passage of white cells causing transient perturbations. The functional relevance of perfusion heterogeneity follows from its effect on exchange efficiency. While evidence for the existence of physiological control mechanisms of heterogeneity is uncertain, intranetwork communication between upstream and downstream vessel segments appears to support the adaptation of supply to demand under physiological conditions.

Animals↗
PubMed1991

Endothelial, not hemodynamic, differences are responsible for preferential leukocyte rolling in rat mesenteric venules.

At the onset of the inflammatory process, leukocytes roll along venular but not arteriolar walls before they firmly attach and emigrate. To test whether differences in hydrodynamic flow conditions are responsible for the preferential occurrence of leukocyte rolling in venules, we varied wall shear rate, gamma w, between 30 and 2,000 sec-1 by selective micro-occlusion of side branches in venules and arterioles (diameter, 20-37 microns) of the exposed mesentery of anesthetized rats. In venules, 39% (range, 6-77%) of all passing leukocytes were found interacting with the endothelium (rolling), whereas this fraction was only 0.6% in arterioles. The fraction of rolling leukocytes in venules decreased from 49 +/- 13% at gamma w less than 100 sec-1 (N = 12) to 24 +/- 13% at gamma w greater than 400 sec-1 (N = 12). Mean leukocyte rolling velocity in venules increased with gamma w, but the most frequent rolling velocity class was 20-40 microns/sec at all shear rates. In arterioles, even prolonged (up to 90 minutes) conditions of reduced flow (gamma w less than 150 sec-1) did not induce leukocyte rolling. Radial distribution of freely flowing leukocytes not different in arterioles and venules. The data indicate that hemodynamic factors are not responsible for the difference of leukocyte adhesion between arterioles and venules. The venular endothelium appears to be specialized to support leukocyte adhesion during inflammation. This finding correlates with reports on preferential expression of various endothelial-leukocyte adhesion molecules on venular endothelial cells.

Animals↗
PubMed1991

A new approach to intravital videomicroscopy of rat spinotrapezius muscle.

A modified preparation of the rat spinotrapezius muscle is described in which optimal conditions for intravital microscopy can be achieved while the supplying blood vessels are left fully intact, and mechanical stress to the muscle during preparation is reduced to an unavoidable minimum. The viability of the preparation is demonstrated using the response of arterial microvessels to endothelium-dependent and -independent dilators and to changes of ambient PO2, the presence of spontaneous vasomotion, and histochemical analysis of pertinent enzyme systems. The preparation is viable for much longer experimental time periods (up to 10 hours) than reported previously, provided the intensity of illumination is kept at a very low level. If the latter prerequisite is met, tissue edema, maximal vasodilation, and the associated loss of responsiveness to vasoactive stimuli of arterioles is reliably avoided.

Animals↗
PubMed1990

Blood flow in microvascular networks. Experiments and simulation.

A theoretical model has been developed to simulate blood flow through large microcirculatory networks. The model takes into account the dependence of apparent viscosity of blood on vessel diameter and hematocrit (the Fahraeus-Lindqvist effect), the reduction of intravascular hematocrit relative to the inflow hematocrit of a vessel (the Fahraeus effect), and the disproportionate distribution of red blood cells and plasma at arteriolar bifurcations (phase separation). The model was used to simulate flow in three microvascular networks in the rat mesentery with 436,583, and 913 vessel segments, respectively, using experimental data (length, diameter, and topological organization) obtained from the same networks. Measurements of hematocrit and flow direction in all vessel segments of these networks tested the validity of model results. These tests demonstrate that the prediction of parameters for individual vessel segments in large networks exhibits a high degree of uncertainty; for example, the squared coefficient of correlation between predicted and measured hematocrit of single vessel segments ranges only between 0.15 and 0.33. In contrast, the simulation of integrated characteristics of the network hemodynamics, such as the mean segment hematocrit or the distribution of blood flow velocities, is very precise. In addition, the following conclusions were derived from the comparison of predicted and measured values: 1) The low capillary hematocrits found in mesenteric microcirculatory networks as well as their heterogeneity can be explained on the basis of the Fahraeus effect and phase-separation phenomena. 2) The apparent viscosity of blood in vessels of the investigated tissue with diameters less than 15 microns is substantially higher than expected compared with measurements in glass tubes with the same diameter.

Animals↗
PubMed1990

Rheological properties and blood flow behavior in tube flow and vascular networks.

Improvement of hemorheological methodology in recent years has led to increased knowledge about rheological properties of blood. By contrast, however, the concepts underlying interpretation of rheological behavior in the cardiovascular system are less well developed. Recent rheological measurements during blood flow in small tubes show that predictions of microcirculatory hemodynamics on the basis of viscometric measurements remain uncertain. The rheological consequence of cell sedimentation as well as flow fractionation effects at microvessel bifurcations need to be taken into account.

Blood Vessels↗
PubMed1989

Venulo-arteriolar communication and propagated response. A possible mechanism for local control of blood flow.

The effect of microinjection of norepinephrine (10(-5) M) into precapillary microvessels of the rat mesentery was studied using intravital microscopy. Upon application, in 29 out of 40 cases (73%) flow ceased at the site of drug application, although in most cases the precapillary microvessels themselves did not show a diameter change due to a lack of smooth muscle cells as confirmed by transmission electron microscopy. In 17 out of the 29 cases with flow cessation (59%), an intimate contact between the venule draining the site of application and the supplying arteriole was found. Initial constriction was seen at the site where the venule crossed the arteriole. Constriction propagated both up- and downstream along the arteriole, and also across arteriolo-arteriolar arcades. Arteriolar constriction could be abolished by intentionally occluding the venule draining the norepinephrine solution. It is proposed that venuloarteriolar contacts and propagated vasomotor response may contribute to local blood flow regulation by providing a feedback loop between tissue capillaries and resistance arterioles. In three complete mesenteric microvessel networks, the arterioles (n = 34) supplying 273 out of 401 capillaries (68%) were in close proximity to venules draining these same capillaries. Each of these arterioles served, on average, 43 capillaries, showing a bimodal distribution with peaks at 4 to 16 and at 64 to 256 capillaries. On average, 62% of all capillaries drained by a given venule crossing an arteriole originated from this very arteriole, indicating a reasonably effective feedback.

Animals↗
PubMed1989

Red cell distribution at microvascular bifurcations.

The distribution of red cell and blood volume flow was studied at 65 arteriolar bifurcations in the rat mesentery. Hematocrit and flow velocity were measured simultaneously in all three vessel segments constituting a bifurcation. Blood flow distribution was manipulated by irreversibly occluding downstream side branches of one of the daughter vessels. The dependence of fractional red cell volume flow on fractional blood flow was described using a three-parameter (X0, B, A) logit function. The critical volume flow fraction below which only plasma enters a downstream branch (X0), the nonlinearity of the relation between red cell and blood volume flow (B), and the asymmetry of that relation which is described by the parameter A decrease with increasing diameter of the vessel feeding the bifurcation. At diameters above 30 microns, phase separation is very limited. In addition, the nonlinearity parameter B decreases with decreasing hematocrit in the feeding vessel. The asymmetry parameter A strongly depends on the diameter ratio between the two daughter branches: For a given fractional blood flow, the smaller branch receives more red cells than the larger branch. Using a model for plasma skimming based on the assumption of a planar separating surface, the shape of the radial hematocrit profile in the feeding vessel has been calculated. The model predicts a decrease in local hematocrit from the vessel axis toward the wall with a distinct marginal zone free from cell centers. With increasing vessel diameter the hematocrit profile becomes more blunted while the width of the marginal zone increases.

Animals↗
PubMed1989

Robin Fåhraeus: evolution of his concepts in cardiovascular physiology.

We give an account of the work of Robin Fåhraeus over the years 1917-1938, his contribution to our understanding of blood rheology, and its relevance to circulatory physiology. Fåhraeus published few original papers on this subject, yet he clearly understood the phenomena occurring in the tube flow of mammalian blood. 1) The concentration of cells in a tube less than 0.3 mm in diameter differs from that in the larger feed tube or reservoir, the Fåhraeus effect. This is due to a difference in the mean velocity of cells and plasma in the smaller vessel associated with a nonuniform distribution of the cells. 2) In tubes less than 0.3 mm in diameter, the resistance to blood flow decreases with decreasing tube diameter, the Fåhraeus-Lindqvist effect. We define and generalize the two effects and describe how red cell aggregation at low shear rates affects cell vessel concentration and resistance to flow. The fluid mechanical principles underlying blood cell lateral migration in tube flow and its application to Fåhraeus' work are discussed. Experimental data on the Fåhraeus and Fåhraeus-Lindqvist effects are given for red cells, white cells, and platelets. Finally, the extension of the classical Fåhraeus effect to microcirculatory beds, the Fåhraeus Network effect, is described. One of the explanations for the observed, very low average capillary hematocrits is that the low values are due to a combination of the repeated phase separation of red cells and plasma at capillary bifurcations (network effect) and the single-vessel Fåhraeus effect.

Cardiovascular Physiological Phenomena↗
PubMed1989

Time-dependent rheological behaviour of blood flow at low shear in narrow horizontal tubes.

Magnitude and time-dependence of the effects of red cell aggregation and sedimentation on the rheology of human blood were studied during low shear (tau W 2.5 to 92 mPa) flow through horizontal tubes (ID 25 to 105 microns). Immediately following reduction of perfusion pressure to a low value the red cell concentration near the tube walls decreases as a result of red cell aggregation. This is associated with a transient increase of centerline velocity. Simultaneously, sedimentation begins to occur and eventually leads to the formation of a cell-free supernatant plasma layer. Time-course and extent of this sedimentation process are strongly affected by wall shear stress variation, particularly in the larger tubes. At the lower shear stresses, centerline velocity decreases (flow resistance increases) with time following the initial acceleration period, due to sedimentation of red cells. This is followed by a further increase of resistance caused by the elevation of hematocrit occurring because of the reduction of cell/plasma velocity ratio. The time dependence of blood rheological behaviour under these flow conditions is interpreted to reflect the net effect of the partially counteracting phenomena of sedimentation and red cell aggregation.

Blood Flow Velocity↗