[Longitudinal oxygen gradients in cerebra micro vessels in acute anaemia in rats].

Using a fine-tip oxygen microelectrodes the longitudinal gradients of oxygen tension (pO2) have been studied in small arterioles (with lumen diameter in control of 5 +/- 20 microm) and in capillaries of the rat brain cortex during stepwise decrease of the blood haemoglobin concentration [Hb] from control [Hb]--14.4 +/- 0.3 g/dl to 10.1 +/- 0.2 g/dl (step 1), 7.0 +/- 0.2 g/dl (step 2) and 3.7 +/- 0.2 g/dl (step 3). All data are presented as "mean +/- standard error". Oxygen tension was measured in arteriolar segments in two locations distanced deltaL = 265 +/- 34 microm, n = 30. Mean diameter of studied arterioles was 10.7 +/- 0.5 microm, n = 71. Length of studied capillary segments was about deltaL = 201 +/- 45 Mm, n = 18. The measured longitudinal pO2 gradient (deltapO2/deltaL) in arterioles amounted 0.03 +/- 0.01 mmHg/microm, n = 15 in control; 0.06 +/- 0.01 mmHg/microm, n = 16 (step 1); 0.07 +/- +/- 0.01 mmHg/microm, n = 14 (step 2); 0.1 +/- 0.01 mmHg/microm, n = 30 (step 3). In the capillaries, the deltapO2/deltaL amounted to: 0.07 +/- 0.01 mmHg/microm, n = 17 (control); 0.09 +/- 0.02 mmHg/microm, n = 16 (step 1); 0.08 +/- 0.01 mmHg/microm, n = 15 (step 2); 0.1 +/- 0.02 mmHg/microm, n = 18 (step 3). An over threefold decrease in the system blood oxygen capacity did not result in significant changes (p > 0.05) of the deltapO2/deltaL in capillaries that might result in relatively homogeneous oxygen flux from blood to tissue in acute anaemia. The longitudinal gradients of blood O2 saturation (deltaSO2/deltaL) in studied arterioles and capillaries were obtained using oxygen dissociation curve (ODC) of haemoglobin in the system blood. The gradients deltaSO2/deltaL in capillaries was shown to be threefold higher than the corresponding gradients in arterioles. The data show that anatomic capillaries are the main source of oxygen to brain tissue as in control and in hypoxic conditions. Sufficient oxygen delivery to brain tissue in acute anaemia is maintained by compensatory mechanisms of cardiovascular and respiratory systems. The data presented are the first measurements of the longitudinal pO, gradients in capillaries and minute cortical arterioles at acute anaemia.

Tissue oxygen tension profiles close to brain arterioles and venules in the rat cerebral cortex during the development of acute anemia.

Acute anemia (stages 1 and 2) led to decreases in pO2 at the walls of radial venules (lumen diameter 13.1 +/- 0.5 microm) and in the tissues at distances of up to 40 mum from the walls, indicating increased extraction of oxygen from the blood by the smallest microvessels. Further decreases in the blood hemoglobin concentration (stage 3) did not produce any significant changes in the nature of tissue pO2 profiles close to the walls of these microvessels. In the intercapillary space, tissue pO2 decreased in proportion to the decrease in the systemic blood hemoglobin concentration, though tissue hypoxia (p(t)O2 < or = 8-10 mmHg) was seen only in tissue in which the microvessels had inadequate (decreased) blood flow responses.

[Profiles next to the walls of the rat cerebral arterioles and venules in acute anemia].

Acute anemia was shown to result in increase of pO2 in the wall of radial arterioles (with lumen diameter of 14.7 +/- 0.9 microm) and in the tissue near the studied arterioles, while decreasing as compared to control values at the distance 60 urn from the vessel wall. Hypoxic tissue zones were not manifested even in severe anemia near the studied arterioles. In radial venules (with lumen diameter of 13.1 +/- 0.5 microm) acute anemia (steps 1-2) resulted in decrease in pO2 in the wall and in tissue at 40 microm from the wall, indicating substantial O2 extraction from the blood of the minute microvessels. There were no significant changes in tissue pO2 profiles near the studied venules during steps 2-3 in acute normovolemic hemodilution. The intercapillary tissue pO2 fell proportionally to hemoglobin concentration in systemic blood, while tissue hypoxia (p(t)O2 < 8--10 mm Hg) was present only in tissue microzones nearest to the microvessels with impaired responses of the blood flow to the anemic stimuli.

Transmural oxygen tension gradients in rat cerebral cortex arterioles.

Modified needle oxygen microelectrodes and vital microscopy were used to measure transmural oxygen tension gradients (PO2) in pial arterioles with lumen diameters of 20-90 microm. A relationship between the magnitude of the transmural PO2 gradient and arteriole wall tone was found: in control conditions, PO2 gradients were 1.17 +/- 0.06 mmHg/microm (n = 40), while in conditions of arteriolar wall dilation the transmural PO2 gradient decreased to 0.68 +/- 0.04 mmHg/microm (p < 0.001, n = 38). These data provide the first measurements of transmural PO2 gradients in pial arterioles of different calibers at different levels of vascular tone and have fundamental importance for assessing the role of arterial microvessels in tissue oxygen supply processes. The results obtained here provide evidence that oxygen consumption by the vessel wall is within the range characteristic of enveloping tissues and that oxygen consumption by the endothelial cell layer probably has no significant effect on the magnitude of the transmural PO2 gradient.

[Transmural gradients of oxygen tension on cerebral microvessels in rats].

Using modified oxygen needle microelectrodes, vital microscopy with video-recording facilities, measurements of tissue oxygen tension (PO2) profiles near the cortical arterioles and transmural PO2 gradients on pial arterioles of the rat were performed. At control transmural PO2 gradient averaged 1.17 +/- 0.06 mm Hg/microm (mean +/- SEM, n = 40). Local dilatation of the arteriolar wall (microapplication of sodium nitroprusside approximately 2 x 10(-7) M) resulted in marked drop of the transmural PO2 gradient to 0.68 +/- 0.04 mm Hg/microm (p < 0.001, n = 38). The important finding of the study is the dependence of the transmural PO2 gradient on the vascular tone of pial arterioles. The data presented allow to conclude that O2 consumption of the arteriolar wall lies within the range for surrounding tissue and O2 consumption of the endothelial layer and, apparently, has no substantial impact on transmural PO2 gradient.

Oxygen tension in rat cerebral cortex microvessels in acute anemia.

Polarigraphic microelectrodes were used to study the distribution of oxygen tension (pO(2)) in arterioles (lumen diameters 8-80 microm) and venules (lumen diameters 8-120 microm) in the rat cerebral cortex during acute reductions in blood hemoglobin ([Hb]). Isovolumic hemodilution with 5% albumin solution was performed in steps from an initial [Hb] of 14.1 +/- 0.3 g/dl (control) to 9.8 +/- 0.3 g/dl (step 1), 6.6 +/- 0.4 g/dl (step 2), and 4.6 +/- 0.3 g/dl (step 3). Mild anemia (step 1, hematocrit 30%) led to an increase in pO(2) in the arterial side of the microcirculatory bed, with virtually no change in pO(2) in the venous side. Step 2 (hematocrit 20%) was accompanied by a further insignificant increase in pO(2) in arterioles, while there was a significant reduction (on average to 32 mmHg) in venules. Step 3 (hematocrit 13-14%) led to a (statistically insignificant) increase in pO(2) in arterioles. pO(2) in venules decreased, on average, to 27 mmHg; the proportion of smallest venules with low pO(2) values (less than 20 mmHg) increased to 31% (from 3% in controls). In some capillaries, pO(2) was 5-10 mmHg, which was an indicator of the presence of hypoxic zones in brain tissues. These zones primarily arose close to the smallest capillary and venous microvessels, with slowed or impaired blood flow.

[Oxygen tension in cerebral microvessels in acute anaemia in rats].

Using polarographic oxygen microelectrodes, distribution of oxygen tension (pO2) in the rat cerebral arterioles (with a lumen diameter of 8-80 microm) and venules (with a lumen diameter of 8-120 microm) has been studied in acute reduction of haemoglobin concentration in the blood. Isovolumic haemodilution with 5 % albumin solution has been performed stepwise from 14 g/dl (control) to 10 g/dl (step 1), 7 g/dl (step 2) and to 4.6 g/dl (step 3). It was shown that step 1 of haemodilution led to no impairment of oxygen supply to the brain cortex. Step 2 resulted in moderate increase of pO2 in arterioles, whereas in venules oxygen tension fell down substantially (on the average, to 32 mm Hg). Step 3 resulted insignificant increase of pO2 in arterioles. A further fall of pO2 (to 27 mm Hg) in studied venules was recorded. The portion of venules with low pO2 grew to 31% (only 3 % in control). Microregions with a near-to-zero pO2 were recorded in some capillaries. This indicates presence of hypoxic zones in brain tissue. Hypoxic and anoxic microregions originate at this stage of anemia in locations with relatively low and/or impaired blood supply.

[Oxygen diffusion through the venule walls in the rat cerebral cortex during breathing with pure oxygen]. / Diffuziia kisloroda cherez stenku venul kory golovnogo mozga krys pri dykhanii chistym kislorodom.

Using oxygen microelectrodes, distribution of oxygen tension (pO2) has been studied in venules of the rat brain cortex at normobaric hyperoxia (spontaneous breathing with pure oxygen). It has been shown that inhalation of oxygen results in sharp increase of pO2 in majority of the venules under study. The pO2 distribution along the length of venous microvessels of 7-280 microns in diameter is best approximated by equation: pO2 = 76.44 e-0.0008D, n = 407. The pO2 distribution was characterised by extremely high pO2 values (180-240 mm Hg) in some minute venules. Heterogeneity of pO2 distribution in venous microvessels at hyperoxia was shown to be significantly increased. Profiles of pO2 between neighbouring arterioles and venules were for the first time measured. The data clearly evidenced that O2 diffusional shunting took place between cortical arterioles and venules, provided they were distanced from each other for not over 80-100 microns. Distribution of pO2 in venules has been shown to be dependent on the blood flow in the brain cortical microvessels.

Oxygen transport in the rat brain cortex at normobaric hyperoxia.

The distribution of oxygen tension (PO(2)) in microvessels and in the tissues of the rat brain cortex on inhaling air (normoxia) and pure oxygen at atmospheric pressure (normobaric hyperoxia) was studied with the aid of oxygen microelectrodes (diameter = 3-6 microm), under visual control using a contact optic system. At normoxia, the PO(2) of arterial blood was shown to decrease from [mean (SE)] 84.1 (1.3) mmHg in the aorta to about 60.9 (3.3) mmHg in the smallest arterioles, due to the permeability of the arteriole walls to oxygen. At normobaric hyperoxia, the PO(2) of the arterial blood decreased from 345 (6) mmHg in the aorta to 154 (11) mmHg in the smallest arterioles. In the blood of the smallest venules at normoxia and at normobaric hyperoxia, the differences between PO(2) values were smoothed out. Considerable differences between PO(2) values at normoxia and at normobaric hyperoxia were found in tissues at a distance of 10-50 microm from the arteriole walls (diameter = 10-30 microm). At hyperbaric hyperoxia these values were greater than at normoxia, by 100-150 mmHg. In the long-run, thorough measurements of PO(2) in the blood of the brain microvessels and in the tissues near to the microvessels allowed the elucidation of quantitative changes in the process of oxygen transport from the blood to the tissues after changing over from the inhalation of air to inhaling oxygen. The physiological, and possibly pathological significance of these changes requires further analysis.

[Oxygen transport in the cerebral cortex of rats breathing a hyperoxic gas mixture]. / Transport kisloroda v kore golovnogo mozga krys pri dykhanii giperoksicheskoi gazovoi smes'iu.

Oxygen dissolved in the arterial blood plasma at a high pressure was shown to pass into the brain tissue from the finest arterioles. Therefore only a thin layer of the tissue immediately adjacent to these vessels is affected by the increased oxygen tension pO2. Permeability of the arteriole walls for oxygen protects the neurones against the high pO2. A special physiological feature of the oxygen transport during normobaric hyperoxia in the brain tissue involves very "steep" gradients of the pO2 in tissues and of the transferring the oxygen fraction from arterioles to venules through the tissues. The findings allow to compare distribution of the pO2 over the whole brain vessel network with that during inhalation of air or pure oxygen.

[Oxygen tension in the brain cortex arterioles during spontaneous respiration with the hypoxic gas mixture in rats]. / Napriazhenie kisloroda na arteriolakh kory golovnogo mozga krysy pri spontannom dykhanii gipoksicheskoi gazovoi smes'iu.

Hypoxic exposure of Wistar rats resulted in sharp fall of the blood oxygen saturation on 1st-5th branching order arterioles. The increased oxygen extraction at hypoxia is due to an intensive diffusion of the oxygen through the walls of the arterioles and a lowered blood flow in the brain microvessels. Permeability of the arterioles' walls for oxygen plays a negative role as it lowers the oxygen tension in the blood entering the capillaries.

[Blood carbon dioxide tension and its effect on the oxygen transport in the rat brain during normobaric hyperoxia]. / Napriazhenie uglekislogo gaza v krovi i ego vliianie na transport kisloroda v mozgu krys pri normobaricheskoi giperoksii.

Spontaneous breathing with hyperoxic gas mixture enhanced the PCO2 values both in systemic arterial blood and in the blood of sagittal ninus in rats. Transition from normoxia to normobaric hyperoxia is accompanied by an increase in the cerebral blood flow rate.

[Quantitative characteristics of oxygen tension distribution in arterioles, capillaries, and venules of the rat brain cortex in normoxemia]. / Kolichestvennye kharakteristiki raspredeleniia napriazheniia kisloroda na arteriolakh, kapilliarakh i venulakh kory golovnogo mozga krysy pri normoksemii.

Distribution of the oxygen tension in the rat brain venules in normoxemia was characteristic by its obvious heterogeneity. The data obtained suggest a tissue diffuse shunting of oxygen in the brain cortex of rats in normoxenia.

[The distribution of oxygen pressure in the pial arterioles of the rat under normobaric hyperoxia]. / Raspredelenie napriazheniia kisloroda na pial'nykh arteriolakh krysy pri normobaricheskoi giperoksii.

Breathing with air revealed that oxygen tension in arterioles practically does not depend on the diameter of vessels under study in rats. Whereas in breathing with oxygen, oxygen tension sharply decreased along the course of the microvessel bed. The above decrease seems to be due to exclusion of hemoglobin's dumping function and the effect of such factors as the ratio of arterioles surface's extension to the volume of their blood and the velocity of blood flow in pial arterioles.

[Oxygen tension in cardiac tissue and its consumption by the myocardium]. / Napriazhenie kisloroda v tkani serdtsa i ego potreblenie miokardom.

In the rat isolated and perfused heart, the rate of the oxygen consumption by the myocardium at an increased rate of perfusion increased much faster than the volume of the tissue hyperoxic areas. No correlation of average tissue pO2 in separate experiments and the oxygen consumption, was found. The increased oxygen consumption by arrested heart at increased perfusion rate seems to be due to physical conditions of the perfusion rather than to excessive oxygenation of the tissue.

[Separate flows of erythrocytes with different degrees of oxygenation in the venous vessels]. / Razdel'nye potoki éritrotsitov s raznoi stepen'iu oksigenatsii v venoznykh sosudakh.

Having studied the structure of the blood flow in pial microvessels of the rat brain, the blood flow in venules was shown to consist of separate erythrocyte flows divided by the plasma layers Visualisation of these flows is facilitated after isovolume hemodilution until the 20-25% hematocrit. The blood flows in the same microvessel were found to differ from each other essentially by the oxygen tension level and by the velocity of their transition.