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PubMed2002

Quantification in soil and the rhizosphere of the nematophagous fungus Verticillium chlamydosporium by competitive PCR and comparison with selective plating.

A competitive PCR (cPCR) assay was developed to quantify the nematophagous fungus Verticillium chlamydosporium in soil. A gamma-irradiated soil was seeded with different numbers of chlamydospores from V. chlamydosporium isolate 10, and samples were obtained at time intervals of up to 8 weeks. Samples were analyzed by cPCR and by plating onto a semiselective medium. The results suggested that saprophytic V. chlamydosporium growth did occur in soil and that the two methods detected different phases of growth. The first stage of growth, DNA replication, was demonstrated by the rapid increase in cPCR estimates, and the presumed carrying capacity (PCC) of the soil was reached after only 1 week of incubation. The second stage, an increase in fungal propagules presumably due to cell division, sporulation, and hyphal fragmentation, was indicated by a less rapid increase in CFU, and 3 weeks was required to reach the PCC. Experiments with field soil revealed that saprophytic fungal growth was limited, presumably due to competition from the indigenous soil microflora, and that the PCR results were less variable than the equivalent plate count results. In addition, the limit of detection of V. chlamydosporium in field soil was lower than that in gamma-irradiated soil, suggesting that there was a background population of the fungus in the field, although the level was below the limit of detection. Tomatoes were infected with the root knot nematode (RKN) or the potato cyst nematode (PCN) along with a PCN-derived isolate of the fungus (V. chlamydosporium isolate Jersey). Increases in fungal growth were observed in the rhizosphere of PCN-infested plants but not in the rhizosphere of RKN-infested plants after 14 weeks using cPCR. In this paper we describe for the first time PCR-based quantification of a fungal biological control agent for nematodes in soil and the rhizosphere, and we provide evidence for nematode host specificity that is highly relevant to the biological control efficacy of this fungus.

Animals↗
PubMed2003

Expression of heteropolymeric ferritin improves iron storage in Saccharomyces cerevisiae.

Saccharomyces cerevisiae was engineered to express different amount of heavy (H)- and light (L)-chain subunits of human ferritin by using a low-copy integrative vector (YIp) and a high-copy episomal vector (YEp). In addition to pep4::HIS3 allele, the expression host strain was bred to have the selection markers leu2(-) and ura3(-) for YIplac128 and YEp352, respectively. The heterologous expression of phytase was used to determine the expression capability of the host strain. Expression in the new host strain (2805-a7) was as high as that in the parental strain (2805), which expresses high levels of several foreign genes. Following transformation, Northern and Western blot analyses demonstrated the expression of H- and L-chain genes. The recombinant yeast was more iron tolerant, in that transformed cells formed colonies on plates containing more than 25 mM ferric citrate, whereas none of the recipient strain cells did. Prussian blue staining indicated that the expressed isoferritins were assembled in vivo into a complex that bound iron. The expressed subunits showed a clear preference for the formation of heteropolymers over homopolymers. The molar ratio of H to L chains was estimated to be 1:6.8. The gel-purified heteropolymer took up iron faster than the L homopolymer, and it took up more iron than the H homopolymer did. The iron concentrations in transformants expressing the heteropolymer, L homopolymer, and H homopolymer were 1,004, 760, and 500 micro g per g (dry weight) of recombinant yeast cells, respectively. The results indicate that heterologously expressed H and L subunits coassemble into a heteropolymer in vivo and that the iron-carrying capacity of yeast is further enhanced by the expression of heteropolymeric isoferritin.

6-Phytase↗
PubMed1998

Production and characterization of improved adenovirus vectors with the E1, E2b, and E3 genes deleted.

Adenovirus (Ad)-based vectors have great potential for use in the gene therapy of multiple diseases, both genetic and nongenetic. While capable of transducing both dividing and quiescent cells efficiently, Ad vectors have been limited by a number of problems. Most Ad vectors are engineered such that a transgene replaces the Ad E1a, E1b, and E3 genes; subsequently the replication-defective vector can be propagated only in human 293 cells that supply the deleted E1 gene functions in trans. Unfortunately, the use of high titers of E1-deleted vectors has been repeatedly demonstrated to result in low-level expression of viral genes still resident in the vector. In addition, the generation of replication-competent Ad (RCA) by recombination events with the E1 sequences residing in 293 cells further limits the usefulness of E1-deleted Ad vectors. We addressed these problems by isolating new Ad vectors deleted for the E1, E3, and the E2b gene functions. The new vectors can be readily grown to high titers and have several improvements, including an increased carrying capacity and a theoretically decreased risk for generating RCA. We have also demonstrated that the further block to Ad vector replication afforded by the deletion of both the E1 and E2b genes significantly diminished Ad late gene expression in comparison to a conventional E1-deleted vector, without destabilization of the modified vector genome. The results suggested that these modified vectors may be very useful both for in vitro and in vivo gene therapy applications.

Adenoviridae↗
PubMed2005

Cobalt chloride administration in athletes: a new perspective in blood doping?

Blood doping is an illegal and unfair way of enhancing athletic performance by increasing the oxygen carrying capacity of the blood. Currently used methods usually involve stimulation of erythropoiesis. Gene therapy targeting the hypoxia inducible factor pathway may be an attractive alternative to traditional blood doping techniques. Hypoxia activates a large number of genes with essential roles in cell and tissue adaptation to low oxygen. Cobalt chloride is a well established chemical inducer of hypoxia-like responses such as erythropoiesis. Cobalt supplementation is not banned and therefore would not be detected by current anti-doping testing. Although there is as yet no direct or anecdotal evidence of cobalt chloride administration to athletes, its use should be warned against as being not only unfair but potentially dangerous.

Cell Hypoxia↗
PubMed2000

Haematocrit and red blood cell transport in preterm infants: an observational study.

AIMS: To test whether cardiac output acts as a compensatory response to changes in haematocrit. METHODS: A cohort of 38 preterm infants (27-31 weeks' gestation) was studied with repeated Doppler measurements of left ventricular output during the 1st month of life. Red blood cell transport was calculated when the duct was closed. RESULTS: Multiple regression analysis showed that left ventricular output correlated negatively with haematocrit when the duct was closed (n = 84) and when it was open (n = 59). The influence of an increase of 10% in haematocrit absolute value on mean (SD) left ventricular output was estimated at -55 (11) ml/kg/min. Mean (SD) red blood cell transport was 132 (30) ml/kg/min with a mean (SD) intra-individual variability of 20% (8.8%). Red blood cell transport was increased more frequently by left ventricular output than by haematocrit. Haematocrit and left ventricular output but not red blood cell transport were dependent on postnatal age. CONCLUSION: These results suggest that in preterm infants cardiac output adaptation is effective in attenuating the effects of red blood cell mass variations on systemic oxygen carrying capacity.

Cardiac Output↗
PubMed1962

The blood volume and plasma protein levels before and after gastrectomy.

This paper is a survey of a series of 185 plasma volume estimations carried out on 75 gastric surgical patients before and after operation at St. James's Hospital in 1958-59. In the majority of cases serum proteins were also measured. The purpose of this work was to study the effects of gastric operations, and especially of partial gastrectomy, on patients' blood volume, the oxygen-carrying capacity of the blood as measured by the total circulating red cell volume, and serum protein content.

Blood Proteins↗
PubMed1991

Induction of a reduction in haemoglobin concentration by enalapril in stable, moderate heart failure: a double blind study.

OBJECTIVE: To study the long term effects (12 weeks) of enalapril on central haemodynamic function and on arterial oxygen content and its determinants--haemoglobin concentration and oxygen saturation--in patients with stable moderate heart failure. DESIGN: Double blind placebo controlled randomised study. PATIENTS: 17 patients with stable moderate heart failure caused by dilated cardiomyopathy which was treated with diuretics and digoxin. METHODS: Central haemodynamic function, arterial oxygen content, arterial haemoglobin concentration, and arterial oxygen saturation were measured at rest and during submaximal exercise. Plasma volume and total body haemoglobin were determined at rest. RESULTS: With enalapril treatment heart rate, pulmonary capillary wedge pressure, mean arterial pressure, and systemic vascular resistance decreased significantly both at rest and during submaximal exercise. Cardiac output did not change at rest but tended to increase (p = 0.06) during submaximal exercise. Arterial oxygen saturation remained unchanged while haemoglobin concentration and arterial oxygen content were significantly reduced. Total body haemoglobin was significantly reduced but the plasma volume remained unchanged. At rest, the reduction in arterial oxygen content resulted in a significantly reduced mixed venous oxygen content. However, during submaximal exercise the increase in cardiac output fully compensated for the reduction in arterial oxygen content and this effect was indicated by the unaltered mixed venous oxygen content. No changes were found in the placebo group after twelve weeks. CONCLUSIONS: Enalapril unloads the heart and reduces haemoglobin concentration. During submaximal exercise, the improvement in systemic blood flow was counterbalanced by this negative effect on the oxygen carrying capacity and systemic oxygen delivery was unchanged.

Adult↗
PubMed1988

Pharmacologic modulation of erythropoietin production.

A model for the regulation of erythropoietin production has been presented. This model proposes that a primary O2-sensing reaction in the kidney is initiated by a decrease in ambient PO2, a rapid decrease in gas exchange in the lung, a diminished oxygen-carrying capacity of hemoglobin, a molecular deprivation of oxygen, or a decrease in renal blood flow. It is proposed that the primary oxygen-sensing reaction may trigger the release of several mediators that stimulate adenylate cyclase through a receptor-activated stimulation of a G protein in the renal cell membrane. Some of the agents that are thought to be released during hypoxia, which may trigger this cascade, are adenosine (A2 activation), eicosanoids (PGE2, PGI2, and 6-keto PGE1), oxygen-free radicals (superoxide and H2O2), and catecholamines with beta-2 adrenergic receptor agonist properties. The activation of adenylate cyclase generates cyclic AMP, which activates protein kinase A, leading to the production of a phosphoprotein that, in turn, activates a nuclear protein involved in transcription and/or translation for erythropoietin biosynthesis and/or secretion. A second part of this model concerns the effect of hypoxia on a renal cell membrane phosphodiesterase and the generation of inositol triphosphate and diacylglycerol. Diacylglycerol may interact with diacylglycerol lipase to generate arachidonic acid, which, together with arachidonic acid generated by the interaction of phospholipase A2 on membrane phospholipids, produces eicosanoids. Eicosanoids may play a secondary role in Ep production/secretion. The model further proposes that calcium levels in both renal and liver cells may be important in regulating erythropoietin biosynthesis and/or secretion. It is proposed that an increase in intracellular calcium leads to the inhibition of erythropoietin biosynthesis and/or secretion and a decrease in intracellular calcium increases erythropoietin production. The specific mechanism by which calcium regulates erythropoietin biosynthesis and secretion is not well understood. However, a good correlation is seen with several agents that decrease intracellular calcium and increase erythropoietin production as well as with other agents that increase intracellular calcium and decrease erythropoietin production. When inositol triphosphate levels are increased, an increase in the mobilization of intracellular calcium from the endoplasmic reticulum or another intracellular pool occurs. This increased intracellular calcium probably activates a calcium calmodulin kinase and produces a phosphoprotein that inhibits erythropoietin production/secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

Effects of hematocrit on oxygenation of the isolated perfused rat liver.

The isolated perfused rat liver is used ubiquitously for metabolic and endocrine studies of hepatic function, yet few data are available regarding the inadequacy of the oxygenation of such preparations. Moreover, the isolated rat liver is usually deprived of its arterial supply and perfused via the hepatic portal vein with low-hematocrit or cell-free solutions. To investigate the efficacy of the oxygen supply, we determined the effect of hematocrit on the relation between oxygen consumption and perfusate flow. We then attempted to define a hematocrit at which hepatic oxygenation was maximal. Livers of male rats anesthesized with pentobarbital sodium were perfused via the portal vein with fresh canine red blood cells suspended in Krebs-Ringer-bicarbonate buffer. Perfusions were carried out at various flow rates, and the relation between perfusate flow and oxygen uptake was determined. At flow rates above 100 ml X min-1 X 100 g liver-1, oxygen uptake was independent of flow but below that value was flow limited, regardless of whether the hematocrit was 10, 20, or 40%. To determine the optimal hematocrit for hepatic oxygen uptake, hepatic portal venous and hepatic venous pressures were held at 10 and 0 mmHg, respectively. The hematocrit was lowered in steps from 80 to 10%. Blood flow increased exponentially as hematocrit fell while oxygen uptake increased to a maximum at approximately 20%. It is concluded that an hematocrit of approximately 20% provides the optimal combination of blood flow and oxygen-carrying capacity while maintaining physiological perfusion pressures, e.g., 10 mmHg.

Animals↗
PubMed2003

Microcirculatory changes during chronic adaptation to hypoxia.

Microcirculatory changes in the window chamber preparation in Syrian golden hamsters, secondary to chronic hypoxia adaptation, are presented herein. Adaptation was attained by keeping animals in a 10% oxygen environment for 1 wk and 5% the following week. The following groups were studied: group 1, adapted to chronic hypoxia and kept in a 5% oxygen environment throughout the experiment; group 2, adapted to chronic hypoxia and kept in a 21% oxygen environment 24 h before and during the experiment; and group 3, control. Adaptation caused venule enlargement and hematocrit increase (68.6 +/- 2.44 in group 1, 70 +/- 2.66 in group 2, and 43.27 +/- 2.30 in group 3; P < 0.05). Whereas heart rate decreased in adapted animals, blood pressure remained constant. Group 1 presented alkalosis, hypocapnia, and hypoxemia. The adapted groups had decreased blood flow velocity in arterioles and veins. We found no difference in microvasculature oxygen tension between groups 2 and 3; however, the number of capillaries with flow was markedly reduced in group 1 but significantly increased in group 2. Our findings suggest that, as an adaptation to hypoxia, erythropoiesis may prove beneficial by increasing blood viscosity and shear stress, leading to vasodilatation, in addition to the increase in oxygen-carrying capacity. Calculations show that oxygen extraction in the tissue of the window chamber model was significantly lowered in adapted animals breathing 5% oxygen, but was unchanged from the control when breathing 21% oxygen, even though blood hemoglobin content was increased from 14.5 +/- 0.07 g/dl at control to 21.04 +/- 1.24 g/dl in the adapted animals (P < 0.05).

Adaptation, Physiological↗
PubMed2005

Effects of extreme hemodilution with hemoglobin-based O2 carriers on microvascular pressure.

A surface-modified polyethylene glycol-conjugated human hemoglobin (MP4) and alpha alpha-cross-linked human hemoglobin (alpha alpha Hb) were used to restore oxygen carrying capacity in conditions of extreme hemodilution (hematocrit 11%) in the hamster window model preparation. Changes in microvascular function were analyzed in terms of effects on capillary pressure and functional capillary density (FCD). MP4, at 1.0 +/- 0.2 g/dl blood concentration, significantly lowered mean arterial pressure (MAP) below baseline (99.6 +/- 7.6 mmHg) to 82.4 +/- 6.9 mmHg (P < 0.05) and decreased of FCD to 70 +/- 9%. alpha alpha Hb caused a greater recovery in MAP to 94.4 +/- 6.2 mmHg and lowered FCD to 62 +/- 8%. However, differences between alpha alpha Hb and MP4 in FCD were not statistically significant. Capillary pressures were in the ranges of 17-21 mmHg for MP4 and 15-19 mmHg for alpha alpha Hb, with both significantly lower than baseline (P < 0.05). Pressure in 80-microm-diameter arterioles was significantly increased with alpha alpha Hb relative to MP4 (P < 0.05). These results were compared with previous findings on the relation between capillary pressure and FCD; they supported the concept of a relationship between FCD and capillary pressure. Measurement of changes in arteriolar diameter, microvascular blood flow, and FCD show that there was no statistical difference between using alpha alpha Hb and MP4 in extreme hemodilution. Microvascular resistance in arterioles with a diameter range of 70-80 microm showed an increase relative to control with alpha alpha Hb, whereas MP4 caused a decrease.

Animals↗
PubMed2006

Increased cardiac output and microvascular blood flow during mild hemoconcentration in hamster window model.

The effect of small hematocrit (Hct) increases on cardiac index (cardiac output/body wt) and oxygen release to the microcirculation was investigated in the awake hamster window chamber model by means of exchange transfusions of homologous packed red blood cells. Increasing Hct between 8 and 13% from baseline increased cardiac index by 5-31% from baseline (P < 0.05) and significantly lowered systemic blood pressure (P < 0.05). The relationship between Hct and cardiac index is described by a second-order polynomial (R2 = 0.84; P < 0.05) showing that Hct increases up to 20% from baseline increase cardiac index, whereas increases over 20% from baseline decrease cardiac index. Combining this data with measurements of blood pressure allowed to determine total peripheral vascular resistance, which was a minimum at 8-13% Hct increase and was described by a second-order polynomial (R2 = 0.83; P < 0.05). Oxygen measurements in arterioles, venules, and the tissue at 8-13% Hct increase were identical to control; thus, as a consequence of increased flow and oxygen-carrying capacity, oxygen delivery and extraction increased, but the change was not statistically significant. Previous results with the same model showed that the observed effects are related to shear stress-mediated release of nitric oxide, an effect that should be also present in the heart microcirculation, leading to increased blood flow, myocardial oxygen consumption, and contractility. We conclude that a minimum viscosity level is necessary for generating the shear stress required for maintaining normal cardiovascular function.

Animals↗
PubMed1985

Crystalloid and perfluorochemical perfusates in an isolated working rabbit heart preparation.

Krebs-Henseleit buffer (KH) and a perfluorochemical (FC-43) were compared as perfusates in an isolated working rabbit heart preparation. Both perfusates were oxygenated in an identical manner using an infant bubble oxygenator. After 60 min of perfusion, no difference could be detected in the ratio of wet to dry heart weight between KH- and FC-43-perfused hearts (KH, 6.25 +/- 0.3; FC-43, 5.99 +/- 0.20). Left ventricular systolic pressure, maximal rate of left ventricular pressure rise, mean aortic systolic pressure, cardiac output, aortic flow, left ventricular power, and myocardial O2 consumption (MVO2) were significantly higher in FC-43-perfused hearts throughout the time of perfusion. However, there were no differences in resistance to cardiac output and heart rate. In KH- and FC-43-perfused hearts, MVO2 and left ventricular power were closely correlated (KH, r = 0.793; FC-43, r = 0.831). Significantly higher coronary flow of KH-perfused hearts could be attributed to the lower viscosity of KH (1.05 Pa . s) compared with FC-43 (1.91 Pa . s). Increased O2 extraction during KH perfusion could not compensate for low O2-carrying capacity of KH buffer (345 compared with 705 nmol O2 X ml-1 in FC-43 emulsion). A postischemic increase of coronary flow was observed only in FC-43-perfused hearts (28%). These results demonstrate a different response of perfused heart preparations to FC-43 and KH buffer.

Animals↗
PubMed1987

Microvascular hematocrit and red cell flux in rat cremaster muscle.

The arteriovenous distributions of volumetric flow (Q), microvessel hematocrit (Hctmicro), and estimates of red cell volumetric flux (QRBC) were obtained under control conditions in rat cremaster muscle. The results demonstrate a monotonic fall in the ratio of Hctmicro/Hctsystemic from 0.86 in 70-microns arterioles to 0.48 in capillaries followed by a subsequent rise to 0.79 in 98-microns venules. To assess the roles of Hctmicro and Q in red blood cell delivery following a period of reduced oxygen transport, tissue ischemia was produced by occluding the first order arteriole. During the occlusion, arteriolar and large venular hematocrits fell 15-30%, whereas small venular hematocrits increased 24%. After release of the occlusion, a reactive hyperemia ensued with Q, QRBC, and QHctmicro increasing significantly above control values in arterioles, capillaries, and venules. All Hctmicro returned to their control values within 10 s following resumption of flow. Based on the relationship between blood viscosity and Hctmicro, at low shear rate, these transient alterations in Hctmicro were estimated to have a profound effect on blood viscosity, and hence the resistance to blood flow. Such changes may affect recovery from an ischemic episode, although not adversely affecting the oxygen-carrying capacity of blood and convective transport of oxygen.

Animals↗
PubMed1987

Prolonged support of working rabbit hearts using Fluosol-43 or erythrocyte media.

We compared the perfluorochemical emulsion Fluosol-43 and an erythrocyte-based solution as support media for ex vivo working rabbit hearts functioning with a physiological workload. Both groups of hearts (n = 5/group) exhibited stable function (left ventricular peak systolic pressure, peak rates of left ventricular pressure rise and relaxation, aortic flow, peak aortic flow rate, stroke work, and peak power) for the first 6 h of perfusion. Coronary flow, coronary venous O2 content, and O2 supply-to-demand ratio declined similarly in both groups during the first 6 h. Both groups of hearts preferentially utilized pyruvate to glucose. The Fluosol-43-perfused hearts had higher heart rate, left ventricular peak systolic pressure, peak rate of left ventricular pressure rise, aortic flow, coronary flow, and myocardial O2 consumption compared with the erythrocyte-perfused hearts. The Fluosol-43 hearts produced more lactate and released more creatine phosphokinase than did the erythrocyte-perfused hearts, but the rates were low and constant throughout perfusion, indicating that the hearts were not progressively ischemic. After the first 6 h, function of the Fluosol-43 hearts declined, resulting in their earlier failure compared with the erythrocyte-perfused hearts. The data indicate that Fluosol-43 had sufficient O2- carrying capacity to support stable function of a rabbit heart at a physiological workload for 6 h, and differences in function and ex vivo longevity of the two groups of hearts suggested that a component or contaminant of Fluosol-43 altered sarcolemmal function and/or that a component needed for membrane integrity was lacking in the Fluosol-43 perfusate.

Animals↗
PubMed1989

Effects of hemodilution on gastric and intestinal oxygenation.

To determine the effects of hemodilution on gastric and intestinal oxygenation, isolated segments of canine stomach and small bowel were perfused by a pressurized reservoir with blood at hematocrits of 40 and 20%. Arteriovenous O2 difference, blood flow, and arterial and venous pressures were monitored continuously as perfusion pressure was reduced in 30-mmHg steps from 180 to 30 mmHg. O2 consumption was calculated as the product of the steady-state arteriovenous O2 difference and blood flow at each perfusion pressure. Gastric and intestinal O2 uptake were relatively well maintained over most of the pressure range when the hematocrit was set at 40%. After hemodilution, gastric O2 uptake decreased significantly only at 90 and 60 mmHg, but intestinal O2 uptake was significantly reduced except at 30 mmHg. When gastric and intestinal O2 uptake were plotted as a function of blood flow, the O2 uptake vs. blood flow relationship were shifted down and to the right by hemodilution. Hemodilution also linearized the O2 uptake vs. blood flow relationship in the intestine. However, when O2 uptake was plotted as function of O2 delivery, the gastric O2 uptake vs. delivery curves at the two hematocrits were superimposed on each other, but the O2 uptake vs. delivery curves for the intestine diverged except at low rates of O2 delivery. We conclude that by reducing the O2-carrying capacity of the blood, hemodilution adversely affects gastric and intestinal oxygenation. Our results also indicate that hemodilution lowers gastric O2 uptake by reducing O2 delivery; however, hemodilution lowers intestinal O2 uptake not only by reducing O2 delivery but also by impairing O2 extraction.

Analysis of Variance↗
PubMed1992

Systemic and regional O2 delivery and uptake in bled dogs given hypertonic saline, whole blood, or dextran.

The mechanisms by which small volumes of hypertonic saline in dextran (HSD) resuscitate bled dogs are incompletely understood but may include a pulmonary osmolar reflex. A known negative effect of HSD is hemodilution that reduces O2-carrying capacity. Our goals in this study were to ascertain whether the putative osmotic reflex redistributed blood flow between muscle and gut and whether O2 delivery (DO2) was adequate at systemic and regional levels. Left hindlimb muscle and a segment of ileum were vascularly isolated in three groups (n = 8) of anesthetized dogs that were then bled to mean arterial pressure (MAP) of 40 mmHg for 30 min. At that point, all shed blood (approximately 40 ml/kg) was returned in the blood group (BLD); 20 ml/kg of Dextran 70 was given to the dextran group (DEX); and 5 ml/kg of 7.5% NaCl in dextran was given to the HSD group. MAP and cardiac output were restored to acceptable levels in all but was poorly maintained in HSD. The fall in hematocrit (41 to 25%) in HSD was matched by that in DEX (42 to 22%), so that DO2 only reached approximately 55% of that in BLD. Nevertheless, systemic and regional O2 uptakes were similar; O2 debt and repayment did not differ; and lactate metabolism was alike in all groups. O2 extraction did have to increase to near maximum in HSD, however. Other than a transient increase to muscle, HSD had no special effect on distribution of cardiac output. HSD was efficacious as a short-term resuscitative measure but did encroach markedly on O2 transport reserves.

Animals↗
PubMed1998

Cerebral blood flow during hypoxic hypoxia with plasma-based hemoglobin at reduced hematocrit.

We determined whether cerebral blood flow (CBF) remained related to arterial O2 content (CaO2) during hypoxic hypoxia when hematocrit and hemoglobin concentration were independently varied with cell-free, tetramerically stabilized hemoglobin transfusion. Three groups of pentobarbital sodium-anesthetized cats were studied with graded reductions in arterial O2 saturation to 50%: 1) a control group with a hematocrit of 31 +/- 1% (mean +/- SE; n = 7); 2) an anemia group with a hematocrit of 21 +/- 1% that underwent an isovolumic exchange transfusion with an albumin solution (n = 8); and 3) a group transfused with an intramolecularly cross-linked hemoglobin solution to decrease hematocrit to 21 +/- 1% (n = 10). Total arterial hemoglobin concentration (g/dl) after hemoglobin transfusion (8.8 +/- 0.2) was intermediate between that of the control (10.3 +/- 0.3) and albumin (7.2 +/- 0.4) groups. Forebrain CBF increased after albumin and hemoglobin transfusion at normoxic O2 tensions to levels attained at equivalent reductions in CaO2 in the control group during graded hypoxia. Over a wide range of arterial O2 saturation and sagittal sinus PO2, CBF remained greater in the albumin group. When CBF was plotted against CaO2 for all three groups, a single relationship was formed. Cerebral O2 transport, O2 consumption, and fractional O2 extraction were constant during hypoxia and equivalent among groups. We conclude that CBF remains related to CaO2 during hypoxemia when hematocrit is reduced with and without proportional reductions in O2-carrying capacity. Thus O2 transport to the brain is well regulated at a constant level independently of alterations in hematocrit, hemoglobin concentration, and O2 saturation.

Adjuvants, Anesthesia↗