Erythrocyte Adenosine Triphosphate Research Articles

Erythrocyte deformability and nitric oxide mobilization under pannexin-1 and PKC dependence

The erythrocyte adenosine triphosphate (ATP) is utilised for protein phosphorylation and exported through the pannexin 1 hemichannel (Px1) in the microcirculation. The physiological stimuli for ATP release are dependent of blood shear rate level and of the tissue oxygen content. The deoxygenated and oxygenated states of haemoglobin are respectively bound and unbound to N terminal domain of the protein band 3 of the erythrocyte membrane in dependence of its degree of phosphorylation. The protein tyrosine kinase (PTK) and protein tyrosine phosphatase (PTP) contribute to the phosphorylation degree of band 3 and are modulated by protein kinase C (PKC). Chelerythrine (Che) is a competitive inhibitor of ATP for PKC and a negative modulator of erythrocyte deformability. The aim of this study was to assess the mobilization of nitric oxide (NO) in erythrocyte in absence and presence of Che and Px1 inhibitor (carbenoxolone). Erythrocyte deformability was evaluated in presence of carbenoxolone (Carb). Regarding the effects observed in the erythrocyte by presence of Che or Carb, the values of efflux of NO and the concentration of nitrosogluthatione are similar and with no changes in relation to their absence. Px1inhibition by Carb 10 μM ameliorates the erythrocyte deformability at a shear force of 0.6 and 1.2 Pa. The PKC inhibitor shows similar effects to the Carb on the mobilization of nitric oxide in erythrocyte. The blockage of ATP release by Carb from erythrocytes suggests a possible benefit to develop in ischemia reperfusion or in inflammatory response where will be needed to rescue the excess of NO present and ameliorate the red blood cell deformability at low shear rates.

Some pathophysiologic mechanisms of cardiovascular diseases in patients with chronic prostatitis

Aim. To study the relation of autonomic disorders severity, energy and lipid metabolism parameters, immune, hormonal disorders and structural and functional changes of the myocardium in patients with chronic prostatitis. Methods. The study included 75 patients with chronic prostatitis, who were divided into two groups: the first group consisted of 48 patients with the sympathetic autonomous nervous system hyper activation, the second group - of 27 patients with autonomic balance. Echocardiography, 24-hour ECG monitoring with heart rate variability analysis were performed in all patients. The overall serum level of non-esterified fatty acids and glycerol, red blood cells levels of macroergic substances, lipid and long-chain fatty acids fractions were measured. Hormonal profile included estimation of total testosterone level, sex hormone-binding globulin, calculated free testosterone index. Serum cytokines profile was also studied. Results. In patients with sympathetic activity and prostatitis, most of heart rate variability parameters were significantly lower compared to patients with autonomic balance and controls. Patients with left ventricle diastolic dysfunction had higher serum concentrations of pro-and anti-inflammatory cytokines. Dysautonomia with prolonged sympathetic autonomous nervous system hyper activation was frequently found in patient with chronic prostatitis (64% of cases), contributing to low fatty acids utilization in myocardium and reduced levels of glycerol (by 32.3%) and adenosine triphosphate (by 49.5%) in erythrocytes. These disorders were accompanied by left ventricular diastolic dysfunction in 19.2% of patients and by arrhythmias in over than a half of patients. Conclusion. Autonomic disorders (sympathetic autonomous nervous system hyper activation associated with decreased parasympathetic control of the cardiovascular system) are quite common in patients with chronic prostatitis, leading to fatty acids utilization impairment, resulting in blood accumulation of non-esterified fatty acids, low serum glycerol levels, adenine nucleotide imbalance) accompanied by low unbound testosterone level, serum cytokines profile imbalance, reduction of cardiac hemodynamic indicators and development of cardiac arrhythmias.

Computational Analysis of a Microfluidic Device for Measuring Oxygen‐Dependent ATP Release from Erythrocytes

Release of adenosine triphosphate (ATP) from erythrocytes is believed to be a key component of the system for regulating microvascular blood flow. Recently, shear rate‐dependant ATP release from erythrocytes was measured using a microfluidic device (Wan et al, PNAS, 2008). These authors found ATP release occurred within 25–75ms following increased shear. The present work seeks to apply a similar approach to oxygen‐dependant ATP release, the dynamics of which are thought to be important in regulation of microvascular O2 delivery. Our computational model allows for the analysis of such a system to: i. design the optimal device to measure ATP release and ii. quantitatively interpret the resulting output signal. A computational model was constructed based on hemodynamics, convective‐diffusive transport of O2 and ATP, ATP/luciferin‐luciferase reaction kinetics, and optics. The computational model shows erythrocyte O2 levels can be altered rapidly enough to measure a delay in ATP release of 25ms. We show that this computational model is appropriate for analyzing properties associated with erythrocyte ATP release including the relationship between hemoglobin O2 saturation and magnitude of ATP release.

Effects and Mechanisms of Action of Polyene Macrolide Antibiotic Nystatin on Babesia gibsoni In Vitro

Nystatin is a membrane-active polyene macrolide antibiotic and a channel-forming ionophore. Nystatin exhibits in vitro activity against Babesia gibsoni infecting normal canine erythrocytes containing low potassium (LK) and high sodium concentrations, i.e., LK erythrocytes. The calculated IC(50) value of nystatin against B. gibsoni infecting LK erythrocytes was 31.96 µg/ml. The anti-babesial activity of nystatin disappeared when B. gibsoni in LK erythrocytes were incubated in culture media containing high potassium concentrations (HK). Moreover, when the parasites were harbored in canine HK erythrocytes, which contained high potassium and low sodium concentrations as a result of high Na-K-ATPase activity, the in vitro anti-babesial activities of nystatin also disappeared, apparently due to protection by HK erythrocytes. This suggested that nystatin could show in vitro anti-babesial activity against B. gibsoni by its ionophorous activity, the same as other ionophores such as valinomycin. Subsequently, the effects of nystatin on the host cells were observed. Nystatin could not modify the intracellular concentrations of potassium, sodium, adenosine triphosphate, or glucose in either LK or HK erythrocytes, although it caused weak hemolysis in HK erythrocytes. In addition, nystatin did not affect the survival of canine peripheral polymorphonuclear leukocytes. In conclusion, nystatin destroyed B. gibsoni by ionophorous activity but did not affect either canine erythrocytes or leukocytes in vitro.

This Month in Gastroenterology

This Month in Gastroenterology

Inosine Triphosphate Protects Against Ribavirin-Induced Adenosine Triphosphate Loss by Adenylosuccinate Synthase Function

Genetic variation of inosine triphosphatase (ITPA) causing an accumulation of inosine triphosphate (ITP) has been shown to protect patients against ribavirin (RBV)-induced anemia during treatment for chronic hepatitis C infection by genome-wide association study (GWAS). However, the biologic mechanism by which this occurs is unknown. We examined whether ITP can be used by adenosine triphosphatase (ATPase) in human erythrocytes or recombinant human adenylosuccinate synthase (ADSS). RBV-induced adenosine triphosphate (ATP) reduction in erythrocytes was compared with the genetically determined low or normal activity of ITPA, leading respectively to high or normal ITP levels. Although ITP is not used directly by human erythrocyte ATPase, it can be used for ATP biosynthesis via ADSS in place of guanosine triphosphate (GTP). With RBV challenge, erythrocyte ATP reduction was more severe in the wild-type ITPA genotype than in the hemolysis protective ITPA genotype. This difference also remains after inhibiting adenosine uptake using nitrobenzylmercaptopurine riboside (NBMPR). Interestingly, the alleviation of ATP reduction by the hemolysis protective ITPA genotype was canceled by the ADSS inhibitor 6-mercaptoethanol (6-MP). ITP confers protection against RBV-induced ATP reduction by substituting for erythrocyte GTP, which is depleted by RBV, in the biosynthesis of ATP. Because patients with excess ITP appear largely protected against anemia, these results confirm that RBV-induced anemia is due primarily to the effect of the drug on GTP and consequently ATP levels in erythrocytes.

Transient erythrocyte changes caused by infiltration of liver by plasma cell leukemia

Marked erythrocyte anisopoikilocytosis was noted in a 52-year-old man with relapsed IgD multiple myeloma. Complete blood count showed a white cell count of 14,100/mm3 with 40% circulating plasma cells. Most of the red blood cells (RBCs) were either target cells or microspherocytes, with occasional acanthocytes, stomatocytes, and knizocytes ( Images 1 and 2a). The direct antiglobulin test was negative. He had no history of a hemoglobinopathy or an RBC membrane disorder and had normal erythrocyte morphology during remission. He had renal impairment and grossly deranged liver function with elevated alanine aminotransferase of 128 u/l (normal <40 u/l), gamma glutamyltransferase of 591 u/l (normal <50 u/l) and bilirubin of 174 umol/l (normal <17 umol/l). An ultrasound scan (USS) of liver showed hepatomegaly with diffusely abnormal coarse echogenicity, consistent with infiltration by myeloma. He had hypercalcemia and hypophosphatemia at presentation, which resolved with treatment over the next 3 weeks. Severe anisopoikilocytosis with microspherocytes (solid arrows), acanthocytes (dotted arrows), and a knizocyte (dashed arrow) on the initial blood film at plasma cell leukemic relapse phase of myeloma. Two abnormal plasma cells, one binucleate and the other bilobed, are seen (×100 oil; MGG). (a) Initial blood film at relapse showing a bilobed plasma cell and widespread red cell changes including numerous target cells, microspherocytes (solid arrows), occasional acanthocytes and stomatocytes. A single knizocyte (dashed arrow) is also seen. Plasma cells constituted 40% of circulating white cells at this stage (×40; MGG). (b) Less marked red cells changes a week after initiation of treatment. Plasma cells have reduced in number, but circulating forms are still present. Most of the target cells have disappeared but microspherocytosis (solid arrows) remains conspicuous. A single nucleated RBC is seen at the bottom, most likely due to marrow infiltration by myeloma (×40; MGG). (c) Complete clearance of plasma cells from circulation during the 3rd week of treatment. Most of the red cells are now normal, though a few microspherocytes (solid arrows) persist (×40; MGG). (d) Normal blood film at 4th week of treatment (×40; MGG). He was treated with a combination of bortezomib, doxorubicin, and dexamethasone, to which he responded rapidly with clearance of plasma cells, normalization of liver function, improvement in renal function and reduction of paraprotein level. All the red cell changes disappeared serially over a period of 4 weeks ( Image 2b–d). USS of liver was repeated at this stage and showed normal size and echo pattern of liver. In retrospect, this patient had hepatic infiltration by plasma cell leukemia, which reversed completely with chemotherapy. The RBC changes were secondary to this and all abnormalities resolved with return of normal liver function. Target cells and acanthocytes are well described changes with hepatic dysfunction and are believed to be the result of net membrane accumulation of cholesterol, alteration in phospholipids and decreased lecithin cholesterol acyltransferase (LCAT) activity [1, 2]. Knizocytes are triconcave red cells with a band of hemoglobin in the center with an area of pallor on either side and are known to occur in hemolytic states or liver dysfunction. The prominent acquired microspherocytosis noted in this patient is more difficult to explain. In the absence of autoimmune hemolysis, the most likely reason for spherocytosis was the hypophosphatemia which persisted until the 3rd week of treatment. Depletion of phosphate can cause low erythrocyte adenosine triphosphate levels, which in turn can result in spherocytosis [3]. Reversible erythrocyte anisopoikilocytosis of such severity has not been reported so far in conjunction with hepatic infiltration by plasma cell leukemia.

Insulin inhibits human erythrocyte cAMP accumulation and ATP release: role of phosphodiesterase 3 and phosphoinositide 3-kinase

In non-erythroid cells, insulin stimulates a signal transduction pathway that results in the activation of phosphoinositide 3-kinase (PI3K) and subsequent phosphorylation of phosphodiesterase 3 (PDE3). Erythrocytes possess insulin receptors, PI3K and PDE3B. These cells release adenosine triphosphate (ATP) when exposed to reduced O(2) tension via a signaling pathway that requires activation of the G protein, Gi, as well as increases in cAMP. Although insulin inhibits ATP release from human erythrocytes in response to Gi activation by mastoparan 7 (Mas 7), no effect on cAMP was described. Here, we investigated the hypothesis that insulin activates PDE3 in human erythrocytes via a PI3K-mediated mechanism resulting in cAMP hydrolysis and inhibition of ATP release. Incubation of human erythrocytes with Mas 7 resulted in a 62 +/- 7% increase in cAMP (n = 9, P < 0.05) and a 306 +/- 69% increase in ATP release (n = 9, P < 0.05), both of which were attenuated by pre-treatment with insulin. Selective inhibitors of PDE3 (cilostazol) or PI3K (LY294002) rescued these effects of insulin. These results support the hypothesis that insulin activates PDE3 in erythrocytes via a PI3K-dependent mechanism. Once activated, PDE3 limits Mas 7-induced increases in intracellular cAMP. This effect of insulin leads, ultimately, to decreased ATP release in response to Mas 7. Activation of Gi is required for reduced O(2) tension-induced ATP release from erythrocytes and this ATP release has been shown to participate in the matching of O(2) supply with demand in skeletal muscle. Thus, pathological increases in circulating insulin could, via activation of PDE3 in erythrocytes, inhibit ATP release from these cells, depriving the peripheral circulation of one mechanism that could aid in the regulation of the delivery of O(2) to meet tissue metabolic need.

Adenosine Triphosphate Depletion of Erythrocytes Simulates the Phenotype Associated with Pyruvate Kinase Deficiency and Confers Protection againstPlasmodium falciparumIn Vitro

Erythrocytes from individuals with pyruvate kinase deficiency (PKD) are resistant to invasion by Plasmodium falciparum parasites, and erythrocytes infected with ring-stage parasites are preferentially cleared by macrophages in vitro. However, the underlying molecular basis of protection is unknown. In the present study, we examined adenosine triphosphate (ATP) levels in PKD erythrocytes (ie, erythrocytes from individuals with PKD) and determined whether depletion of ATP in normal erythrocytes would recapitulate the phenotype observed with PKD. We examined ATP levels in homozygous PKLR(-/-) and heterozygous PKLR(+/-) human erythrocytes and used sodium fluoride treatment to inhibit ATP generation in normal human erythrocytes. We demonstrated that ATP levels are reduced in PKLR(-/-) (percentage of control erythrocytes, 26%; interquartile range [IQR], 21%-48%) and PKLR(+/-) erythrocytes (percentage of control erythrocytes, 64%; IQR, 60%-73%) and that there is a correlation between ATP levels in erythrocytes and both inhibition of parasite invasion and enhancement of phagocytosis of erythrocytes infected with ring-stage parasites. Analysis of ATP distribution in parasitized erythrocytes demonstrated that parasites invading PKD erythrocytes respond to low intraerythrocytic ATP levels by means of a parallel increase in parasite-derived ATP via up-regulation of P. falciparum-specific pyruvate kinase. These data suggest that reduced erythrocyte ATP levels may contribute to the protection displayed by PKD erythrocytes in vitro and may provide a model system with which to define the molecular basis of protection in inherited PKD.

Trauma-hemorrhagic shock-induced red blood cell damage leads to decreased microcirculatory blood flow*

To test the hypothesis that trauma-hemorrhagic shock (T/HS)-induced changes in red blood cells (RBC) contribute to the reduction of blood flow in distant organs. Laboratory study. Academic medical center laboratory. Specific pathogen-free male Sprague-Dawley rats weighing between 250 and 350 g. Rats were transfused with trauma-sham shock (T/SS), or T/HS whole blood, or RBC-depleted blood (blood with the RBC removed and consisting of white blood cells and plasma). Cardiac output and organ blood flow were measured by the radioactive microsphere technique. RBC tissue trapping, deformability, and RBC aggregation and adhesion were studied. Measurements of RBC adenosine triphosphate (ATP) and plasma fibrinogen were performed. Exchange transfusion with T/SS blood did not alter cardiac output or organ blood flow. However, cardiac output and blood flow in several organs were decreased when T/HS whole blood was used and RBCs were trapped in the organs that evidenced decreased blood flow. T/HS also increased RBC aggregation and adhesion, and decreased deformability. The ability of T/HS exchange transfusion to decrease microcirculatory blood flow did not appear to be due to plasma factors or non-RBC elements (i.e., white blood cell), because organ blood flow was not reduced after exchange transfusion with T/HS RBC-depleted blood. Likewise, neither decreased RBC ATP nor increased plasma fibrinogen explained the T/HS-induced changes that were observed. There was no change in fibrinogen levels during or after shock. Although there was a transient decrease in T/HS erythrocyte ATP levels during the early shock period, in contrast to RBC function, the ATP levels had returned to normal with resuscitation. T/HS induces significant changes in RBC functions and the injection of T/HS, but not T/SS, RBC leads to decreased organ blood flow. These findings confirm the hypothesis that T/HS-induced RBC alterations will directly cause organ hypoperfusion and suggest that T/HS-induced RBC damage contributes to this process. Thus, T/HS-induced changes in RBC function may contribute to the development of shock-induced multiple organ failure.

Disturbances of purine nucleotide metabolism in uremia

The increased concentration of adenosine triphosphate (ATP) in erythrocytes from patients with chronic renal failure (CRF) has been observed in many studies but the mechanism leading to these abnormalities still is controversial. It is believed that hyperphosphatemia and metabolic acidosis triggering enhanced reutilization of purine bases are the factors responsible for changes in erythrocyte nucleotide concentration. During the past decade we have performed several studies. A summary of the obtained results is presented. A high-performance liquid chromatography technique was used for the determination of plasma and intraerythrocyte nucleotide concentrations. Labeled adenine and adenosine were used for measuring adenine incorporation. In CRF patients treated conservatively increased concentrations of ATP levels and other nucleotides such as adenosine diphosphate were found. Adenosine monophosphate and hypoxanthine levels were lower than in controls. In hemodialyzed patients both ATP and adenosine monophosphate intraerythrocyte concentrations were higher than in controls. At the same time, adenosine monophosphate and hypoxantine level were comparable with levels in healthy people. The main pattern of nucleotides during hemodialysis remained unchanged, independent from the mode of therapy. The only exception was a decreased level of hypoxantine. Results of a consecutive study have suggested that the increased rate of adenine incorporation into the adenine nucleotide pool could be partially responsible for the increased ATP concentration in uremic erythrocytes. Last but not least, trying to elucidate the pathomechanism of adenine nucleotide disturbances in uremia, we have found that the concentration of N-methyl-2-pyridone-5-carboxamide (2PY), one of the end products of nicotinamide-adenine dinucleotide degradation, were enhanced in CRF patients to values that are potentially toxic. Our findings suggest that 2PY could be a novel uremic toxin. Disturbances of nucleotide metabolism are one of the important components of uremic syndrome.

Correlation between the physicochemical property of some nonsteroidal anti-inflammatory drugs and changes in adenosine triphosphate, glutathione and hemoglobin in rat erythrocytes.

This study was conducted to explore the relationship between physicochemical property and toxic effectiveness using rat red blood cells (RBCs). The toxic effectiveness of acid nonsteroidal anti-inflammatory drugs (NSAIDs) was systemically examined by the depletion of intracorpuscular adenosine triphosphate (ATP), glutathione (GSH), and hemoglobin (Hb) at various doses, increased every 5 fmol/RBC. When the RBCs were incubated with NSAIDs, the drugs attained maximum levels within RBC, and the levels were then reduced. The ATP depletion seemed to be observed on the excretion of the drugs prior to the depletions of GSH and Hb. The physicochemical properties of NSAIDs were obtained from QMPRPlus, SMILES code, and CS ChemRaw Ultra. Correlation between their physicochemical properties and their doses for the depletions of ATP, GSH and Hb was performed in comparison with those of the membrane bound enzyme (MBE) inhibiting- and methemoglobin (MHb)-generating drugs. The ATP depletion by NSAIDs was correlated with the GSH depletion and intracorpuscular levels of the drugs, but not with the Hb depletion. The GSH depletion was correlated with the Hb depletion and participated in the lipophilicity of the drugs.

Postoperative blood salvage and reinfusion in spinal surgery: blood quality, effectiveness and impact on patient blood parameters.

Although reinfusion of salvaged shed blood has become popular in major orthopaedic procedures, this blood saving technique is still controversial. In an effort to assess the functional and metabolic status of shed blood erythrocytes and the impact of postoperative shed blood reinfusion on allogenic blood requirements and patient's blood parameters, analyses of perioperative blood samples were performed in 28 consecutive orthopaedic patients undergoing spinal fusion, in which postoperative shed blood was collected and reinfused with the ConstaVac CBC II device. In comparison with a previous series of 31 patients, this procedure reduced allogenic blood requirements by almost 30% (P < 0.05), without any increase in postoperative complications. Postoperative shed blood presented lower haematological values and higher plasma-free haemoglobin (PFHB) levels than preoperative blood, without any disturbance in morphology, median corpuscular fragility (MCF) or erythrocyte adenosine triphosphate (ATP) and diphosphoglycerate (DPG) content. Serum concentrations of enzymes--glutamate-oxalacetate aminotransferase (GOT), glutamate-piruvate aminotransferase (GPT), creatine kinase (CK), lactate dehydrogenase (LDH)--and inflammatory cytokines (IL-1beta, IL-6) were elevated in shed blood. After reinfusion, there was no alteration in coagulation parameters or cytokine levels. Serum levels of some enzymes increased at the end of surgery and remained elevated at postoperative day 2 (CK) or 7 (GOT, LDH), with a higher increase if postoperative autotransfusion was used as a blood saving method. Therefore, caution should be taken when these serum enzyme levels are used for diagnosis. In conclusion, salvaged shed blood in orthopaedic procedures of the spine seems to be an excellent source of red cells which are not significantly damaged, keeping a normal functional and metabolic status, and reduces allogenic blood requirements without significant side effects.

Low power laser protects human erythrocytes In an In vitro model of artificial heart-lung machines.

The protective effect of the low power helium-neon (He-Ne) laser against the damage of human erythrocytes in whole blood was examined in a perfusion model using an artificial heart-lung machine. Preserved human whole blood was diluted and perfused in 2 closed circuits with a double roller pump. The laser irradiated one of the circuits (laser group), and none the other (control group). In the laser group, erythrocyte deformability and erythrocyte adenosine triphosphate (ATP) levels were significantly higher, and free hemoglobin levels were significantly lower than those in the control group. Subsequent morphological findings by means of scanning electron microscope were consistent with these results. Low power He-Ne laser protected human erythrocytes in the preserved diluted whole blood from the damage caused by experimental artificial heart-lung machines. The clinical application of low power laser treatment for extracorporeal circulation is suggested.

Leukocyte-reduced blood transfusions: perioperative indications, adverse effects, and cost analysis.

Leukocyte-reduced blood transfusions: perioperative indications, adverse effects, and cost analysis.

Hemolytic anemia induced by ribavirin therapy in patients with chronic hepatitis C virus infection: role of membrane oxidative damage.

The antiviral drug ribavirin (RBV) is widely used in combination with interferon (IFN) in the treatment of chronic hepatitis C virus (HCV) infection. A major side effect of RBV is a reversible hemolytic anemia. We have evaluated the in vitro effects of RBV on erythrocyte adenosine triphosphate (ATP) content and on hexosemonophosphate shunt (HMS). The ATP levels were significantly decreased in the presence of RBV and the HMS was increased, suggesting the presence of red cell susceptibility to oxidation. In vivo, we have studied the hematologic effects of treatment with RBV alone or in combination with IFN in 11 patients with chronic hepatitis C: 6 were treated with RBV (1,000-1,200 mg/d) and 5 were treated with a combination of RBV and IFN (5 million U thrice weekly). Patients were studied at semi-monthly intervals from 0 to day 60 of therapy. Both treatments were associated with a significant reduction in hemoglobin levels (steady state level at day 45) and a marked increase in absolute reticulocyte counts. Erythrocyte Na-K pump activity was significantly diminished, whereas K-Cl cotransport and its dithiotreitol-sensitive fraction, malondialdehyde and methemoglobin levels were significantly increased. RBV-treated patients showed an increase in aggregated band 3, which was associated with a significantly increased binding of autologous antibodies and complement C3 fragments indicating an erithrophagocytic removal by reticuloendothelial system.

Blood oxygen transport, rheology and haematological responses to confinement stress in diploid and triploid Atlantic salmon, Salmo salar

Diploid and triploid all-female Atlantic salmon ( Salmo salar) smolts were challenged with 2.5 h of confinement stress in aerated seawater. Subsequent stress responses were quantified by plasma cortisol, glucose, and lactate, and by the haematological parameters haematocrit (Hct), red blood cell count (RBCC), mean cell volume (MCV), blood haemoglobin concentration (Hb), mean cell haemoglobin (MCH), mean cell haemoglobin concentration (MCHC), total protein and erythrocyte adenosine triphosphate (ATP). The magnitude of stress responses was similar between diploid and triploid smolts. Triploid smolts displayed a higher MCH, but lower Hb than diploid smolts. The blood oxygen affinity of diploid and triploid fish was similar at 15°C over the pH range 6.76–7.99 and the isohaemoglobin components were identical. The enlarged triploid erythrocytes showed reduced shear-dependence on blood viscosity at constant Hct and are therefore unlikely to contribute to greater peripheral vascular resistance. The results show that despite having fewer, larger erythrocytes, triploids have very similar oxygen carrying capacity and haematological response to stress as diploids. This suggests that the higher farm mortality reported for triploids in response to stress is not generated by their failure to show respiratory homeostasis in the face of stress.

Changes in erythrocyte deformability after liver resection for hepatocellular carcinoma associated with chronic liver disease.

Erythrocyte deformability is an important factor in the microcirculation. The deformability in patients with chronic liver disease is less than normal. We studied changes in erythrocyte deformability in 32 patients undergoing liver resection for hepatocellular carcinoma with underlying chronic liver disease to investigate whether the measurement of deformability gives information useful for postoperative management. We measured erythrocyte deformability as erythrocyte transit time (ETT) before and after resection, as well as the erythrocyte adenosine triphosphate level, mean corpuscular volume, mean corpuscular hemoglobin concentration, and indices of liver function. The 15-minute indocyanine green retention rate (ICGR15) was measured before resection. Correlations between the change in deformability and these values were evaluated, as was correlation with the scale of the operation and with the occurrence of postoperative complications. Mean ETT was higher in the patients before resection than in healthy volunteers. ETT was correlated with serum high density lipoprotein-cholesterol (p < 0.05). The incidence of postoperative complications was higher (p = 0.001) in the patients (group A) with ETT increased during the first 3 postoperative days by >/=1 SD of the mean of the preoperative value than in patients (group B) with less change. Of the 12 patients whose ICGR15 value was >/=20%, all 9 patients in group A had postoperative complications. The increase in ETT (decrease in erythrocyte deformability) is associated with the development of postoperative complications. The measurement of erythrocyte deformability gives information useful for postoperative management, and special monitoring for postoperative complications is necessary in patients with the increase soon after liver resection.

Content of 2,3-diphosphoglycerate and adenosine triphosphate in erythrocytes and the acid-base balance in adult and newborn rats during acute hypoxia

It is shown that in deep acute hypoxic hypoxia the 2,3-diphosphoglycerate content is reduced and the adenosine triphosphate content unchanged in the erythrocytes of newborn rats. Under the same conditions adult animals show an increase of 2,3-diphosphoglycerate and a drop in the adenosine triphosphate content in the erythrocytes. The importance of these changes is discussed in terms of the mechanisms regulating the oxygen-transporting function of erythrocytes during acute hypoxic hypoxia in newborn and adult animals.

Anomalies de la glycolyse au cours des fibromyalgies

Whole blood pyruvate is significantly increased (n = 20) in fibromyalgia whereas erythrocyte adenosine triphosphate (ATP) is decreased (n = 18). The serum lactate increase induced by forearm ischemic exercise (n = 7) and lacticodehydrogenase iso-enzyme IV (n = 11) are significantly reduced.