[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.

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.

[Recovery of the gas exchange and oxygen transport after long-term hypothermia in rats]. / Vosstanovlenie gazoobmena i transporta kisloroda u krys posle prolongirovannoi gipotermii.

After a deep prolonged hypothermia, fast warming up of experimental rats (0.26 degree C/min) to the body temperature 35-36 degrees C entailed recovery of the heart rate, blood pressure, 1-min blood volume, oxygen consumption in rats. However, in the process of warming up, cardiac output, function of the left ventricle, oxygen consumption and the CO2 production were decreased. Acidosis and haemoconcentration following a 3 hr prolonged hypothermia were reversible.

[Recovery of the oxygen consumption, oxygen transport, and cardiac activity after hypothermia followed by respiration and cardiac arrest in rats]. / Vosstanovlenie potrebleniia kisloroda, transporta kisloroda i serdechnoi deiatel'nosti u krys posle gipotermii, soprovozhdaiushcheisia ostanovkoi dykhaniia i serdechnykh sokrashchenii.

After a 1 hr deep prolonged immersion hypothermia, warming up of experimental rats in water (the temperature increase 0.25 degree C/min) entailed a complete recovery of all the parameters of gas exchange, haemodynamics, external respiration, and the blood. After a 3 hr hypothermia, under the same conditions of warming up, oxygen consumption, CO2 production, and 1 min blood volume were obviously decreased, and the animals died within 0.5-1.0 hr.

[Gas exchange and oxygen transport during long term hypothermia following a hypothermal apnea in rats]. / Gazoobmen i transport kisloroda u krys v usloviiakh prolongirovannoí gipotermii posle gipotermicheskoi ostanovki dykhaniia.

The data obtained show that, at the initial stages of hypothermia, a decrease in the oxygen consumption and carbon dioxide production, cardiac output, and heart rate occurred in accordance with the temperature coefficient. Suppression of the tissue gas exchange was unrelated to disorders in the lung gas exchange but determined rather by a progressing weakening of heart activity, decrease in the cardiac output, and increase in the general vascular peripheral resistance.

[Gas exchange and gas transport in deeply cooled rats during slow and rapid warming using artificial pulmonary ventilation]. / Gazoobmen i transport gazov u gluboko okhlazhdennykh krys v protsesse medlennogo i bystrogo otogrevaniia s primeneniem iskusstvennoi ventiliatsii legkikh.

Artificial lung ventilation (ALV) was shown to restore the gas exchange in rats following their cooling to brain temperature 17.0-17.6 degrees C. However, the ALV proved ineffective if applied in 22.1 +/- 2.1 min after cessation of breathing. Fast warming up of the animals increased oxygen consumption and carbon dioxide production, and caused a less obvious metabolic acidosis in the rats in the course of recovering from hypothermia.

[Gas exchange and gas transport in rats during warming after deep immersion hypothermia]. / Gazoobmen i transport gazov u krys v protsesse otogrevaniia posle glubokoi immersionnoi gipotermii.

Gas exchange, oxygen transport and utilisation were shown to be limited at body temperature 17.5 degrees C in rats. Disturbances in the cardio-vascular system seem to be the main limiting factors telling on the above parameters in the course of spontaneous rewarming.

[Gas exchange and transport in the body during acute anemia correction by modified hemoglobin solution or attributed to inhalation of a hyperoxic gas mixture]. / Gazoobmen i transport gazov v organizme pri korrektsii ostroi anemii rastvorom modifitsirovannogo gemoglobina ili za schet dykhaniia giperoksicheskoi gazovoi smes'iu.

Total and specific characteristics of changes in gas exchange and transport, tissue oxygenation, circulatory and respiratory compensatory reactions were examined in three groups of necrotized Wistar rats during acute anemia correction by two methods, replacement of red cell mass loss with modified hemoglobin solution (Hb 4.4 g/dl, P50 21.5 mm Hg) or respiration with a hyperoxic mixture (90% of oxygen in nitrogen). In control animals anemia was induced with blood replacement with 6% albumin solution during atmospheric air inhalation. The studied methods for anemia correction were found to increase oxygen levels in arterial blood and similarly effective in total gas exchange maintenance; however the mechanisms of oxygen delivery from arterial blood to tissues being quite different, use of hemoglobin solution was associated with a number of adverse features in gas transport system, acid-base balance, reactions of minute volumes of circulation and respiration which were caused by changed oxygen-binding characteristics of modified hemoglobin and the presence of high concentrations of free hemoglobin in blood plasma.

[Oxygen transport and gas exchange in rats under immersion hypothermia]. / Transport kisloroda i gazoobmen u krys v usloviiakh immersionnoi gipotermii.

Changes of the oxygen consumption and the main parameters of the blood respiratory function as well as oxygen transport, were studied in Wistar rats under conditions of immersion hypothermia (with rectal temperature 15-13 degrees C). From the viewpoint of the oxygen exchange, the rectal temperature 20 degrees C was found to be the critical level of the hypothermia.

[The dependence of the blood pH, PCO2 and PO2 values measured on the microanalyzer on the hematocrit index during hemodilution and hemoconcentration]. / Zavisimost' izmeriaemykh na mikroanalizatore velichin pH, PCO2 i PO2 krovi ot pokazatelia gematokrita pri gemodiliutsii i gemokontsentratsii.

The arterial blood's pH, PCO2 and PO2 were shown to depend on the value of hematocrit in erythrocyte suspension in rats. The dependence can be described by the equation of linear regression except the oxygen tension value within its physiological range. A table of corrections is presented for the values of the blood's pH, PCO2 and PO2 for taking into consideration the factor of altered hematocrit in studies of acute anemias.

[Hemoglobin affinity for oxygen and the reaction of the gas-transport system in rats with acute anemia]. / Srodstvo gemoglobina k kislorodu i reaktsiia gazotransportnoi sistemy krys pri ostroi anemii.

A population of Wistar rats was studied for a few years. The findings revealed a considerable variability of the hemoglobin affinity to oxygen: P50 (oxygen tension at hemoglobin satiation with oxygen for 50 per cent). Two groups of the rats were studied: with P50 = 31.9 +/- 1.0 mm Hg and P50 = 42.3 +/- 1.1 mm Hg. The 2nd group rats (with reduced affinity of hemoglobin to oxygen), in acute profound anemia, revealed an enhanced resistance of gas exchange against anemia, an augmented response of the circulation minute volume, a less obvious metabolic acidosis and a lesser degree of the brain tissue hypoxia.

[The external respiratory reaction and its significance for oxygen transport in rats in acute anemic hypoxia]. / Reaktsiia vneshnego dykhaniia i ee znachenie dlia transporta kisloroda u krys v usloviiakh ostroi anemicheskoi gipoksii.

In anesthetized Wistar rats, the external respiration response, changes of the oxygen transport system's parameters and of total gas exchange, were studied in discrete acute anemia (isovolemic hemodilution with the 6.5% albumin solution). In 3 groups of rats (I--spontaneous breathing and intact pulmonary circulation; II--artificial ventilation of the lungs with a fixed volume; III--embolism of pulmonary vessels), an increase in the lung ventilation was an important compensatory response to acute anemia maintaining a high degree of arterial blood oxygenation in increased perfusion of the lungs. The conjugation of respiratory and circulatory responses plays a major role in the maintenance of gas exchange and gas transport in the organism: separate switching off of compensatory response in one of these systems leads a weakening of compensatory responses in another system.

[The role of hemoglobin affinity for oxygen in the efficiency of the respiratory function of the blood]. / O roli srodstva gemoglobina k kislorodu v éffektivnosti dykahtel'noi funktsii krovi.

In acute experiments the oxygen transport properties of two solutions of modified stroma-purified hemoglobin were investigated using anesthetized Wistar rats. The solutions were: solution 1 (Hb = 8.0 g per 100 g, P50 = 12.5 mm Hg) and solution 2 (Hb = 4.4 g per 100 g, P50 = 21.5 mm Hg). The solutions were used in stage-by-stage isovolumic substitution in rats of two groups. The modified hemoglobin solution with a lower hemoglobin oxygen affinity was found to be a more efficient blood substitute. In spite of its low oxygen capacity, it could sustain life activity at very low hematocrit values. When the oxygen capacity of blood is moderate or low, hemoglobin oxygen affinity plays a very important part in oxygen supply to different tissues, specifically to the heart. The latter determines the crucial compensatory physiological reaction to acute anemia, i. e. increase of cardiac output.