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Biomedical subjects

A Koller

Publications and source records attributed to A Koller.

At least 145 records · Page 8Linked to original sources
PubMed1991

Modified arteriolar responses to ATP after impairment of endothelium by light-dye techniques in vivo.

In this study we investigated whether endothelial cells are involved in the dilation of third-order arterioles (14 to 22 microns) in response to adenosine triphosphate (ATP) in cremaster muscle of pentobarbital-anesthetized rats. Two light/dye (L/D) techniques were employed to achieve selective, local endothelial impairment. One of these techniques utilizes a mercury lamp and sodium fluorescein, the other a Helium-Neon laser and Evans blue dye. L/D treatment (illumination with the appropriate wavelengths of light in the presence of an intravascular dye) of a 20-to 100-microns segment of an arteriole resulted in a complete loss of arteriolar dilation in response to topical administration of acetylcholine (10(-6) M) and arachidonic acid (AA, 10(-5) M). These agents were applied in 100-microl aliquots without interrupting the continuous suffusion with Ringer-gelatin solution and caused a approximately 70% increase in vascular diameter before the L/D intervention. Selectivity of the impairment was assessed by arteriolar responses to the nonendothelium-dependent dilator agents adenosine (10(-5) M) and sodium nitroprusside (2 X 10(-7) M), which elicited the same degree of dilation before and after L/D treatment. Under control conditions ATP (10(-6), 10(-5), and 10(-4) M) elicited dose-dependent increases in arteriolar diameter (from 38 to 74%). After impairment of arteriolar endothelium, dilation in response to all doses of ATP was significantly reduced. Theophylline (30 microM) significantly inhibited arteriolar dilation in response to adenosine (10(-6), 10(-5), and 10(-4) M) but did not affect the responses to various doses of ATP. Moreover, impairment of endothelium enhanced constrictor responses of arterioles to norepinephrine (0.6 X 10(-8) M). These results indicate that arteriolar endothelium of skeletal muscle can mediate or modulate arteriolar responses to various vasoactive agents, suggesting that it has an important role in the regulation of blood flow.

Acetylcholine↗
PubMed1991

Endothelial regulation of wall shear stress and blood flow in skeletal muscle microcirculation.

In the presence of intact endothelium, in control conditions, calculated wall shear rate (WSR) (means +/- SE: 2,658 +/- 123 s-1; n = 21) was independent of arteriolar diameter (16.2-27.2 microns; correlation coefficient: r = 0.12, P greater than 0.05) in cremaster muscle of pentobarbital-anesthetized rats. An increase in blood flow velocity (due to parallel arteriolar occlusion) elicited a significant increase in WSR (to 4,981 +/- 253 s-1) followed by a delayed (6-15 s) increase in diameter (from: 22.5 +/- 0.6 to 29.5 +/- 0.8 microns), which consequently resulted in a significant decrease in WSR (to 3,879 +/- 203 s-1). As a result of the increased flow velocity and dilation, calculated arteriolar blood flow increased by 230%. After impairment of the endothelium of arterioles by a light-dye technique, basal WSR became significantly higher (3,604 +/- 341 s-1), and despite a greater increase in WSR (10,360 +/- 1,471 s-1) the dilation was absent. Now an inverse linear correlation was found between arteriolar diameter and WSR both before (r = 0.58, P less than 0.05) and during increased flow velocity conditions (r = 0.85, P less than 0.05). Also, arteriolar blood flow that was already less after impairment of endothelium increased by only 66% during the period of increased flow velocity due to the absence of dilation. Results suggest that an increase in wall shear stress is the stimulus for the endothelium-dependent mechanism that elicits "flow dependent" arteriolar dilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

EDRF released from microvascular endothelial cells dilates arterioles in vivo.

Microvascular endothelial cells (MECs) from rat epididymal fat pad were isolated and cultured in vitro on Cytodex 3 microcarrier beads. In Krebs-suffused cremaster muscle of pentobarbital-anesthetized rats arteriolar diameters (mean control diam 20.9 +/- 0.9 micron) were measured using image shearing video microscopy. Two lines of suffusate (1.5 ml/min each) were established; one contained a column of microcarrier beads only (no cells in line; NC) the other contained a 1-ml column of MECs grown on beads (through cells; TC). The muscle preparation and the MECs were first treated with indomethacin (Indo; 28 microM). Indo treatment blocked arteriolar dilation to A23187 (1 microM) and arachidonic acid (AA; 0.25 microM) administered into the NC line. A 4.0 +/- 0.6 micron increase in arteriolar diameter was observed, however, when A23187 (but not AA) was infused through the TC line containing Indotreated MECs on beads. The A23187-elicited dilation was abolished by the introduction of NG-monomethyl-L-arginine (L-NMMA; 200 microM) into the TC line. Administration of atropine (2 microM) onto the cremaster muscle via the NC line inhibited the dilations in response to acetylcholine (ACh; 2.7 microM) given through the NC line. Infusion of ACh through the TC line onto the atropine-treated cremaster muscle, however, elicited a 5.8 +/- 1.3 micron increase in arteriolar diameter, a response that was blocked by prior administration of L-NMMA into the TC line. Arteriolar dilation induced by adenosine (0.5 microM) or sodium nitroprusside (0.5 microM) applied via the NC or TC line was unaffected by L-NMMA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Active transport of proteins into the nucleus.

Nuclear proteins are actively and posttranslationally transported across the nuclear envelope. This transport is a highly selective process that can be divided into two steps, receptor-binding followed by translocation through the nuclear envelope. Receptor-binding is mediated by nuclear localization signals that have been identified in many nuclear proteins. Translocation is energy-dependent and occurs through the nuclear pore complex.

Amino Acid Sequence↗
PubMed1990

Consequences of 6 weeks of strength training on red cell O2 transport and iron status.

Effects of endurance training on O2 transport and on iron status are well documented in the literature. Only a few data are available concerning the consequences of strenuous anaerobic muscular exercise on red cell function. This study was performed to test the influence of strength training alone on parameters of red cell O2 transport and iron status. Twelve healthy untrained males participated in a strength-training programme of 2-h sessions four times a week lasting 6 weeks. After 6 weeks a small but significant reduction of haemoglobin (Hb; -5.4 g.l-1) was found (p less than 0.05). Mean red cell volume did not change, but a pronounced decrease of mean cell Hb concentration (from 329.2 g.l-1, SE 2.5 to 309.8 g.l-1, SE 1.2; p less than 0.001) and mean corpuscular Hb (from 29.6 pg, SE 0.4 to 27.7 pg, SE 0.3; p less than 0.01) was observed. Serum ferritin decreased significantly by 35% (p less than 0.01); transferrin, serum iron and iron saturation of transferrin were unaltered. Serum haptoglobin concentration was diminished significantly by 30.5% (p less than 0.01). The reticulocyte count had already increased after 3 weeks of training (p less than 0.05) and remained elevated during the following weeks. Strength training had no significant influence on the O2 partial pressure at which Hb under standard conditions was 50% saturated, red cell 2,3-diphosphoglycerate and ATP concentration as well as on erythrocytic glutamate-oxalacetate transaminase activity. The data demonstrate that mechanical stress of red cells due to the activation of large muscle masses led to increased intravascular haemolysis, accompanied by a slightly elevated erythropoiesis, which had no detectable influence on Hb-O2 affinity. Training caused an initial depletion of body iron stores (prelatent iron deficiency). Although Hb had decreased by the end of the training phase a true "sports anaemia" could not be detected.

Adult↗
PubMed1990

Endothelium regulates skeletal muscle microcirculation by a blood flow velocity-sensing mechanism.

In rat cremaster muscle, utilizing parallel arteriolar occlusion, we found that an increase in red blood cell (RBC) velocity (3.5-26.5 mm/s) per se induced an increase in diameter (1.5-9.4 microns) of arterioles (mean control diam 21.5 +/- 0.6 microns; n = 25). The dilation of arterioles appeared only when RBC velocity increased and started always with a delay (mean 8.4 +/- 0.5 s) after the increase in flow velocity. A positive linear correlation was found between peak changes in RBC velocity and diameter (r = 0.87, P less than 0.05). The velocity sensor as well as the mechanism(s) that mediates this response is likely to be located in endothelial cells, because the dilation to increased RBC velocity was completely eliminated after impairment of arteriolar endothelium with light-dye (L-D) treatment. The in vivo demonstration of this phenomenon in arterioles suggests the existence of a new endothelium-dependent, flow velocity-sensitive mechanism for the regulation of blood flow in the microcirculation.

Animals↗
PubMed1990

Role of endothelium in reactive dilation of skeletal muscle arterioles.

In cremaster muscle of pentobarbital-anesthetized rats, the role of endothelium in the reactive dilation of an arteriole (mean control diameter: 18.2 +/- 0.5 microns) during and after short (approximately 20 s) or long (approximately 80 s) occlusion of a parent arteriole was investigated. Distal to the occluder, arteriolar diameter increased during the occlusion (mean peak increase: 6.9 +/- 0.4 and 6.7 +/- 1.1 microns, respectively) and increased even further after the release of the occlusion as blood flow was reestablished (additional mean increase: 6.5 +/- 0.7 and 5.8 +/- 0.8 microns, respectively). The duration of arteriolar dilation after the release of the occlusion was dependent on the duration of occlusion (252.2 +/- 37 vs. 411.3 +/- 57 s; P less than 0.05). After impairment of the arteriolar endothelium by light/dye treatment, a dilation was still present during both the shorter and longer occlusions (mean increase: 4.73 +/- 1.4 and 4.73 +/- 1.3 microns, respectively); however, in both cases the additional dilation after release of the occlusion was greatly diminished. The duration of reactive arteriolar responses following impairment of the endothelium was significantly reduced only on release of the shorter occlusions. The results suggest that reactive dilation (hyperemia) of arterioles is the result of multiple, endothelium-dependent and endothelium-independent vasoactive factors.

Animals↗
PubMed1990

Prostaglandins mediate arteriolar dilation to increased blood flow velocity in skeletal muscle microcirculation.

In cremaster muscle of pentobarbital-anesthetized rats, temporary occlusion of an arteriole increased red blood cell velocity (mean increase, 8.2 +/- 1.0 mm/sec from a control velocity of 7.9 +/- 0.7 mm/sec) in proximal parallel arteriolar branches (mean control diameter, 19.4 +/- 0.6 microns). Increases in flow velocity were consistently followed by proportional delayed (6-15 seconds) increases in arteriolar diameter (5.8 +/- 0.7 microns). Administration of NG-monomethyl-L-arginine (200 microM), an inhibitor of the synthesis of endothelium-derived relaxing factor that blocked the arteriolar responses to acetylcholine (1 microM) but not to arachidonic acid (10 microM), did not affect the dilation (mean increase, 8.9 +/- 1.1 microns) due to increases in red blood cell velocity (13.4 +/- 1.5 mm/sec). However, the cyclooxygenase inhibitor indomethacin (or meclofenamate), which completely blocked the dilator response to arachidonic acid but did not change the response to acetylcholine, inhibited the arteriolar dilation (mean increase, 0.3 +/- 0.2 micron) due to increases in red blood cell velocity (9.3 +/- 1.0 mm/sec). Inhibition of prostaglandin synthesis also reduced the increase in calculated blood flow by 57% during occlusion. These results suggest that the arterioles are sensitive to increases in blood flow velocity (wall shear stress), in response to which they release prostaglandins, eliciting vasodilation. The existence of this phenomenon in the skeletal muscle microcirculation suggests a new regulatory mechanism that, by modulation of vascular resistance in the microvascular network, has the role of normalizing wall shear stress and providing for substantial increases in tissue blood flow.

Acetylcholine↗
PubMed1989

The cost of departure from optimal radii in microvascular networks.

In the Murray optimality model of branching vasculatures, the radii of vessels are related to blood viscosity, vascular metabolic rate, and blood flow rate, in such a way as to minimize the total work (hydraulic and metabolic) of the system. The model predicts that flow is proportional to the cube of a vessel radius, and that at junctions the cube of the radius of the parent vessel equals the sum of the cubes of the daughter radii. In comparing real vasculatures to the Murray model, we have previously had no expressions for evaluating the apparent energy cost for departures from the optimal junction exponent of 3. Such expressions are derived here. They show that junction exponents, from about 1.5 to large positive values, are within 5% of the energy minimum. With the new equations, observed individual junctions or entire vascular trees can be compared, energy-wise, with the Murray optimum. Junctions in the transverse arteriolar trees of cat sartorius muscle were compared to the Murray optimality model, using these new expressions. The junction exponents for these small pre-capillary vessels had a broad range, with a median value greater than the Murray optimum of 3. The exponents were restricted, however, to values requiring, at individual junctions, little increase in energy. The majority of junctions had energy costs less than 1% above the Murray minimum. For entire trees involving many junctions the departures from optimality averaged less than 10%. Thus, while the branching geometry for these microvascular trees deviates significantly from the Murray optimum in the direction of larger daughter to parent ratios, the departures are small in energy terms.

Animals↗
PubMed1989

Effects of endothelial impairment on arteriolar dilator responses in vivo.

In pentobarbital-anesthetized rats we investigated the role of the endothelium in the dilation of third-order arterioles of cremaster muscle to acetylcholine, adenosine, and sodium nitroprusside in vivo. Responses to the topical administration of these agents were measured with image shearing and recorded with video microscopy before and after light-dye (L-D) treatment of a 50- to 100-microns segment of the arteriole under study. L-D treatment consisted of intravascular administration of sodium fluorescein and the illumination of a discrete area of the arteriole under study with its excitation light from a mercury lamp. Before L-D treatment, acetylcholine (10(-7) to 10(-5) M) and adenosine (10(-6) to 10(-4) M) produced dose-dependent increases in arteriolar diameter (vasodilation). After L-D treatment of the arteriolar segment, administration of 10(-7) M acetylcholine evoked a vasoconstriction (-19% from control), and the dilator responses to 10(-6) and 10(-5) M were inhibited by 91 and 77%, respectively. In contrast, the arteriolar dilator responses to all doses of adenosine and sodium nitroprusside (2 x 10(-7) M) were not altered by this treatment. In addition, the dilator responses to acetylcholine were not changed in the nonilluminated, distal, and proximal segments of the arterioles. These findings suggest that L-D treatment selectively alters the function of the endothelium resulting in the loss of vasodilation to acetylcholine, whereas arteriolar smooth muscle function does not appear to be affected.

Acetylcholine↗
PubMed1989

Endothelial impairment inhibits prostaglandin and EDRF-mediated arteriolar dilation in vivo.

The role of endothelium in the vasodilation of third order arterioles of cremaster muscle to a variety of vasoactive agents was investigated in pentobarbital-anesthetized rats. Changes in diameter to topical administration of agents were measured with image shearing, before and after mercury light/sodium fluorescein (light/dye) treatment of a 50- to 100-microns segment of the arteriole under study and were recorded with video microscopy. Before light/dye treatment, arachidonic acid (10(-5) M), prostaglandin E2 (5 x 10(-6) M), A23187 (2 x 10(-6) M), acetylcholine (10(-5) M), and adenosine (10(-4) M) elicited dilation between 75 and 106% of basal diameter. After light/dye treatment, dilations to arachidonic acid, A23187, and acetylcholine were completely eliminated; however, the responses to prostaglandin E2 and adenosine were not altered. These results indicate that light/dye treatment interferes with the production of or response to prostaglandins as well as other endothelial mediators, like endothelium-derived relaxing factor (EDRF). In a second series of experiments, bradykinin, in concentrations of 10(-9), 10(-8), and 10(-7) M elicited dose-dependent dilations, which were partially inhibited by indomethacin and completely abolished after additional light/dye treatment. Dilation of arterioles to adenosine was maintained throughout these experiments. These data suggest that vasodilation to bradykinin is mediated partly via prostaglandin production and partly via other endothelium-derived factor(s).

Acetylcholine↗
PubMed1989

[Effect of stress ulcer prevention on the incidence of ventilation pneumonia at a pulmologic intensive care unit].

In a retrospective analysis, the influence of stress ulcer prophylaxis on the incidence of ventilation pneumonia (VP) was investigated. In VP, we were able to isolate enterobacteria from the tracheal aspirate or bronchial secretion significantly (p = 0.015) more frequently than in the case of environmentally acquired and nosocomial pneumonia which were treated in the intensive care unit but did not comply with the criteria for VP. The detection of intestinal bacteria in the respiratory tract in VP patients supports the hypothesis that the "gastro-pulmonary" colonisation pathway represents a decisive factor in the development of VP. Patients undergoing long-term ventilation who had received ranitidine for prophylaxis of stress ulcer, developed VP statistically significantly more frequently (p = 0.044) than did patients with sucralfat cover. The non-physiologically high acid juice pH associated with the use of H2-antagonists leads to an increase in intestinal organisms within the stomach. By ascending the upper GI tract, the bacteria finally colonise the respiratory tract. Through the application of sucralfat, whose ulcerprotective action is not achieved by the inhibition of acid in the stomach, the incidence of VP in a pulmological intensive care unit was reduced.

Adolescent↗
PubMed1989

Flow velocity-dependent regulation of microvascular resistance in vivo.

In skeletal (cremaster) muscle of pentobarbital anesthetized rats we tested the hypothesis that blood flow-dependent regulation of vascular resistance exists in the microcirculation. During occlusion of an arteriole we found that the consequent increase in red blood cell (RBC) velocity in a proximal parallel arteriole was followed by a mean increase in diameter of 32 percent (mean control diameter: 21.5 +/- 0.5 microns) of the arteriole under study. The increase in arteriolar diameter always appeared with a delay (mean: 8.4 +/- 0.5 s) following the onset of changes in RBC velocity. Upon release of the occlusion RBC velocity decreased followed by a decline in diameter of the arteriole under study. Since the changes in arteriolar diameter during this experimental intervention cannot be explained on the basis of previously described blood flow-regulatory mechanisms in the microcirculation we conclude that changes in blood flow velocity (wall shear stress) per se induced the changes in arteriolar diameter. The existence of this phenomenon suggests a new, flow velocity-sensitive mechanism which can regulate - via changes in diameter - the supply and distribution of blood flow in the microcirculation in vivo.

Animals↗
PubMed1988

Distribution of vascular resistance in terminal arteriolar networks of cat sartorius muscle.

Morphometric information on the terminal arteriolar networks (n = 10) in cat sartorius muscle [Koller et al., Am. J. Physiol. 253 (Heart Circ. Physiol. 22): H154-H164, 1987] is utilized in the calculations of distribution of vascular hindrance throughout the networks. These networks have tree-type geometry, i.e., they do not contain closed loops. The results are discussed in terms of simulated flow distribution. The flow calculations are based on the exact geometry of the arteriolar networks (the control and dilated diameter and the length of each vascular segment) and on assumed values of postarteriolar resistances. Three cases of postarteriolar resistances are considered: zero, constant, and randomly distributed. With zero postarteriolar resistances, the distribution of flow in the terminal arteriolar segments would be highly heterogenous. The simulated flow in each terminal segment is determined primarily by the number of bifurcations on the pathway leading to the terminal segment, with a slight compensation for the length of the pathways. The coefficient of variation of flow in the control state, CV(Qc), would be close to the value in the dilated state, CV(Qd). When each of the terminal segments is connected to a constant postarteriolar resistance, the CV's in both states decrease. The coefficient of variation in the dilated state becomes significantly smaller than in the control state. When postarteriolar resistances are randomly distributed, both CV's increase, and their values become closer to each other. These results suggest that postarteriolar resistances may play a very important role in distribution of flow in the microvascular network. This study formulates a framework for the quantification of the effect of arteriolar dilation on flow redistribution in the network.

Animals↗