Decrease In Erythrocyte Deformability Research Articles

Red blood cell deformability in multiple myeloma1.

The aim of this study was the evaluation of the erythrocyte deformability in multiple myeloma (MM). We enrolled 29 MM patients and we evaluated, on fasting venous blood, the erythrocyte deformability, expressed as elongation index, and examined using the diffractometric method. By comparing normal controls and MM patients, a significant decrease in erythrocyte deformability, especially at low shear stresses, was found. In this research paper we evaluated all the hypothesis for a possible explanation of the behaviour of red blood cell deformability in MM, even considering how the alteration of erythrocyte deformability worsens the microcirculatory flow in these patients in association with the marked increase in plasma viscosity.

Erythrocyte deformability and hemorheological profile in multiple myeloma.

The hemorheological profile in multiple myeloma (MM) has been extensively studied. Our investigation regarded the behavior of whole-blood viscosity, plasma viscosity and erythrocyte deformability in MM. We enrolled 24 MM patients; 13 of them had been recently diagnosed and were at the initial stage of therapy, 6 were on consolidation/conservation therapy and 5 had achieved a complete remission. On fasting venous blood we evaluated whole-blood and plasma viscosity at high and low shear rates, haematocrit, the ratios between whole-blood viscosity (at high and low shear rate) and haematocrit×100, the ratio between plasma viscosity at low and high shear rate and the erythrocyte deformability examined by using laser diffractometry and expressed as elongation index. A significant increase in plasma viscosity at low shear rate and a marked decrease in haematocrit were observed in MM patients compared with normal controls. Also the ratio between the high shear rate whole-blood viscosity and haematocrit ×100 and the ratio between the low and high shear rate plasma viscosity were significantly increased in MM patients. A significant decrease in erythrocyte deformability, especially at low shear stresses, was found. We discuss some hypotheses that might explain the behavior of red blood cell deformability in MM, considering that its impairment, in addition to the increase of plasma viscosity, can alter the microcirculatory flow in these patients.

Hemorheological parameters in Monoclonal Gammopathy of Undetermined Significance (MGUS).

There is scarcity of information about the hemorheological pattern in subjects with Monoclonal Gammopathy of Undetermined Significance (MGUS). This preliminary research is focused on the behaviour of whole-blood and plasma viscosity, haematocrit and erythrocyte deformability in the above clinical condition. We enrolled 21 MGUS subjects (10 women and 11 men; mean age 66.4 ± 11.6 years). In fasting venous blood we examined whole-blood and plasma viscosity at high and low shear rates, haematocrit, the ratios between whole-blood viscosity (at high and low shear rate) and haematocrit × 100, the ratio between plasma viscosity at low and high shear rate, and the erythrocyte deformability expressed as elongation index. By comparing normal controls to MGUS subjects a significant increase in whole-blood viscosity at high shear rate and in plasma viscosity at low shear rate were observed. In MGUS subjects the ratios between the high and low shear rate blood viscosity and haematocrit × 100, as well as the ratio between the low and high shear rate plasma viscosity were significantly higher. In MGUS subjects a marked decrease in erythrocyte deformability was also observed. The alteration of the hemorheological profile found in these subjects might be involved in the pathogenesis of thromboembolic events, which occur with a high frequency in MGUS.

Decrease in Erythrocyte Deformability Promotes the Cell Accumulation near the Vessel Wall in Small Arterioles

This study demonstrated that the deformability‐impaired red blood cells (RBCs) preferentially accumulate near the vessel walls in arterioles in vivo. Chemically hardened RBCs (hRBCs) with fluorescent labeling from the donor rat were infused into the recipient rat circulatory system while maintaining the total blood volume. Fluorescent imaging analysis was performed to quantify the radial (R) distribution of the labeled hRBCs in small arterioles (~76 μm of diameter). In vivo experimental results showed that majority of the hRBCs (65%) were accumulated near the vessel wall (0.7R–0.9R). This near‐wall accumulation of hRBCs partly contributed to the decrease in the mean cell‐free layer width, and significantly increased the variation of cell‐free layer width (P < 0.05). Dynamic particle simulation by modeling individual RBCs was in agreement with the in vivo experiments by predicting that the hRBCs exhibit relatively weakened tank‐treading motion as compared with normal RBCs. Consequently, this leads to an attenuation in the inward migration of the cells toward the flow center. Our findings conclusively proposed that the preferential near‐wall accumulation of hRBCs in vivo could be attributed by the attenuated dispersion of hRBCs with reduced tank‐treading motion once they entered into the near‐wall zone. In addition, frequent sudden changes of lateral displacement of hRBCs while passing through multiple bifurcations partly contributed to their near‐wall accumulation despite the relatively shorter cell travel distance in vivo.Support or Funding InformationThis work was supported by National Medical Research Council (NMRC)/Cooperative Basic Research Grant (CBRG) No./0078/2014

The Rho kinase inhibitor Y-27632 increases erythrocyte deformability and low oxygen tension-induced ATP release

Low oxygen (O(2)) tension and mechanical deformation are stimuli for ATP release from erythrocytes. It has been shown previously that rabbit erythrocytes made less deformable with diamide, a thiol cross-linking agent, release less ATP in response to low O(2) tension, suggesting a link between these two stimuli. In nonerythroid cells, activation of the Rho/Rho kinase signaling pathway has been reported to decrease cell deformability by altering Rho kinase-dependent cytoskeleton-protein interactions. We investigated the hypothesis that the Rho kinase inhibitor Y-27632 would increase erythrocyte deformability and thereby increase low O(2) tension-induced ATP release from erythrocytes. Here we show that Y-27632 (1 μM) increases erythrocyte deformability (5%) and increases low O(2) tension-induced ATP release (203%) from healthy human erythrocytes. In addition, we found that, when erythrocytes were made less deformable by incubation with diamide (100 μM), Y-27632 restored both deformability and low O(2) tension-induced ATP release to levels similar to those measured in the absence of diamide. These findings suggest that the Rho kinase inhibitor Y-27632 is able to reverse the diamide-induced decrease in erythrocyte deformability and rescue low O(2) tension-induced ATP release. These results further support a link between erythrocyte deformability and ATP release in response to low O(2) tension.

Increased calcium deposits and decreased Ca 2+-ATPase in erythrocytes of ascitic broiler chickens

The decrease of erythrocyte deformability may be one of the predisposing factors for pulmonary hypertension and ascites in broiler chickens. In mammals, the cytoplasmic calcium is a major regulator of erythrocyte deformability. In this study, the erythrocyte deformability was measured, and the precise locations of Ca 2+ and Ca 2+-ATPase in the erythrocytes were investigated in chickens with ascites syndrome induced by low ambient temperature. The results showed that ascitic broilers had higher filtration index of erythrocyte compared with control groups, indicating a decrease in erythrocyte deformability in ascitic broilers. The more calcium deposits were observed in the erythrocytes of ascitic broilers compared with those of the age-matched control birds. The Ca 2+-ATPase reactive grains were significantly decreased on the erythrocyte membranes of ascitic broilers. Our data suggest that accumulation of intracellular calcium and inhibition of Ca 2+-ATPase might be important factors for the reduced deformability of the erythrocytes of ascitic broilers.

Reduced erythrocyte deformability in active and untreated Behçet’s disease patients

Although the etiology of Behcet's disease is not clarified yet, the vascular endothelial damage and thrombosis are prominent features of the disease. The underlying mechanisms of increased risk of thrombosis in Behcet's disease are not completely understood. It is stated that the changes in blood rheology such as erythrocyte deformability take part in the thrombosis. There are limited numbers of studies with conflicting results about the erythrocyte deformability in Behcet's disease. The previous studies were not limited to the untreated patients with active disease. Blood samples were filtered immediately by "Imugard- leukocyte removal filter". After plasma and erythrocytes were separated by centrifugation, 10% erythrocyte suspensions were prepared with isotonic Tris NaCl buffer solution. These erythrocyte suspensions were filtered under gravitational force by "Nucleopore" to determine the filtration time. The filtration times of the erythrocyte and buffer solutions were referred as t1 and t2 respectively. Finally, deformability indices were obtained by dividing the t1 by t2. A decrease in the deformability of the erythrocytes would result in an increase in the filtration time of the erythrocyte suspension and deformability indices. The median deformability indices were 3.090 and 2.170 for patients and control subjects respectively and the difference was statistically significant (P = 0.000). We suggest that the decrease in erythrocyte deformability in Behcet's disease may be related to oxidative damage of erythrocytes and subsequently takes part in the development of thrombosis in Behcet's disease.

Differential effect of high dietary fat intakes on haemorheological parameters in rats

High dietary intake of fats has been thought to be one of the major risk factors for the development of CVD. Less is known about the possible influence of fats from various sources on haemorheological abnormalities, which are considered an important factor in the pathogenesis of these diseases. The goal of the present study was to investigate effects of high-fat diets enriched in unsaturated fatty acids (USFA), SFA or trans-fatty acids (TFA), respectively, on haemorheological parameters in rats. Wistar female rats were divided into four groups and fed diets based on the AIN-93M formulation containing approximately 10 % energy from soyabean oil (control group) or 40 % energy from soyabean oil (USFA), palm oil (SFA) and vegetable shortening (TFA) for 8 weeks. The results showed that rats fed high-fat diets exhibited significant increases in serum TAG levels (P < 0.01), plasma viscosity (P < 0.01), whole blood viscosity (P < 0.01) and internal viscosity (P < 0.01) compared to the controls. The TFA group showed a significant decrease in erythrocyte deformability (P < 0.01) and increase in internal viscosity (P < 0.01) compared with the other groups. In addition, a significant increase in blood levels of free radicals (P < 0.01) was found in the TFA group, suggesting that the attack of oxygen-free radicals could be responsible for the impaired erythrocyte deformability. These impairments could be partly responsible for the development of various circulatory disorders. The present haemorheological study provides additional insights into the potential adverse effects of trans-fat and high-fat diets on haemorheological parameters.

Melatonin prevents lipid peroxidation in human erythrocytes but augments deterioration of deformability after in vitro oxidative stress

Oxidative stress decreases the deformability of erythrocytes. Anti-oxidant measures may alleviate, pro-oxidative damage may augment this decrease. Melatonin is reported to exert both anti-oxidant and pro-oxidant properties on erythrocytes. The aim of the present study was to evaluate the effects of melatonin on erythrocyte deformability under oxidative stress conditions induced by the combination of hydrogen peroxide (20 mM) and sodium azide (100 microM). Erythrocyte suspensions were incubated for 10 min with melatonin (1-1000 microM) prior to oxidative stress. Erythrocyte deformability was measured by Laser-assisted Optical Rotational Cell Analyzer (LORCA). Lipid peroxidation was determined via malondialdehyde (MDA) measurements by HPLC. Melatonin alone did not change erythrocyte deformability. Oxidative stress alone decreased the deformability of erythrocytes by 25.8 +/- 3.1% (P<0.05). Melatonin pre-treatment augmented the decrease in erythrocyte deformability but prevented lipid peroxidation. Melatonin (1 microM) did not cause any additional effect on erythrocyte deformability. Higher concentrations (10-1000 microM) further decreased deformability (P<0.05). Erythrocytes exposed to oxidative stress had MDA levels of 116.3 +/- 14.3 micromol/g Hb. Melatonin (1 microM) slightly increased MDA levels, but 1000 microM melatonin reduced it by 35% (P<0.05). These findings indicate that melatonin exerts antioxidant effect on lipids. Deterioration of erythrocyte deformability may be due to a separate pro-oxidative action on proteins.

Hemorheological Mechanisms in Alzheimer's Disease

The aim of the present study was to elucidate the underlying mechanisms responsible for hemorheological abnormalities in elderly patients with Alzheimer's disease (AD). Twenty-one patients with AD and twenty-three age-matched healthy controls (CON) were studied. We used a controlled-shear rate rheometer generating various flow fields in vitro for simulating blood flow in vivo. The applied experimental techniques provided valid and quantitative data for the analysis of hemorheological abnormalities associated with AD. Principal blood biochemical parameters and hemorheological parameters, including blood viscosity, erythrocyte deformability, erythrocyte aggregation and oxygen transport efficiency of blood were assessed. The results show no statistically significant difference in most of the blood biochemical parameters between the AD patients and the CON, except that fibrinogen concentration and mean corpuscular cell volume level of erythrocytes (MCV) were significantly higher in the AD patients. Hemorheological parameters including blood viscosity, plasma viscosity, and blood viscoelasticity in the AD patients were considerably higher than the respective factors in the CON. Owing to the MDA levels of the AD patients being significantly higher than that of the CON, the AD patients also showed a decrease in erythrocyte deformability and an increase in blood flow resistance despite the lack of any significant difference in erythrocyte rigidity. In addition, the erythrocyte aggregation of AD patients was higher than that of the CON and reduced oxygen transport efficiency of blood was observed in the AD patients. The hemorheological abnormalities found in AD patients may be explained by the parallel findings of oxidative damage on erythrocyte membranes that could result in a decrease of erythrocyte deformability. Furthermore, the oxidative stress-induced elevation of fibrinogen concentration could lead to accelerated erythrocyte aggregation as a consequence of a rise in blood viscosity and blood viscoelasticity. Taken together, these factors may impair the oxygen transport efficiency of blood in AD patients.

Red blood cell dysfunction in septic glucose-6-phosphate dehydrogenase-deficient mice.

Glucose-6-phosphate dehydrogenase (G-6-PDH) deficiency is the most common known human genetic polymorphism. This study tested the hypothesis that G-6-PDH deficiency worsens sepsis-induced erythrocyte dysfunction. Sepsis (24 h) was induced by cecal ligation and puncture in wild-type (WT) and G-6-PDH-deficient (G-6-PDH activity 15% of WT) mice. Erythrocyte responses were tested in whole blood as well as in subpopulations of circulating erythrocytes. Whereas erythrocyte deformability was similar in unchallenged deficient and WT animals, sepsis decreased erythrocyte deformability that was more pronounced in deficient than WT animals. Sepsis also resulted in anemia and hemolysis in deficient compared with WT animals. Mean corpuscular hemoglobin content and erythrocyte deformability decreased in younger erythrocyte subpopulations from septic deficient compared with WT animals. Sepsis decreased the reduced-to-oxidized glutathione ratio in erythrocytes from both deficient and WT animals; however, plasma glutathione increased more in deficient than in WT animals. Erythrocyte content of band 3 associated with the cytoskeleton was elevated in deficient compared with WT erythrocytes. The antioxidant N-acetyl-l-cysteine in vivo alleviated the sepsis-induced decrease in erythrocyte deformability in deficient animals compared with sham-operated control animals. This study demonstrates that a mild degree of G-6-PDH deficiency (comparable to the human class III G-6-PDH deficiencies) worsens erythrocyte dysfunction during sepsis. Increased erythrocyte rigidity and tendency for hemolysis together with alterations in band 3-spectrin interactions may contribute to the immunomodulatory effects of G-6-PDH deficiency observed after major trauma and infections in humans.

Protective effect of quercetin against cigarette tar extract-induced impairment of erythrocyte deformability

Quercetin (3,3′,4′,5,7-pentahydroxyflavone) is one of the most abundant flavonol-type flavonoids rich in diet and suggested to possess a beneficial role in blood circulation. This study was conducted to know the effect of quercetin aglycone and one of its possible metabolite, quercetin-3- O-β- D-glucuronide on cigarette tar extract-induced impairment of erythrocyte deformability. Erythrocyte suspension containing quercetin aglycone, quercetin-3- O-β- D-glucuronide or quercetin-3- O-β- D-glucoside was forced to flow through microchannels with equivalent diameter of 7 μm and its transit time was measured as an index of erythrocyte deformability using microchannel array method. Both quercetin aglycone and quercetin-3- O-β- D-glucuronide, but not quercetin-3- O-β- D-glucoside, substantially increased erythrocyte deformability indicating that the former two compounds affect the physicochemical state of erythrocyte by interacting with its membranes. Aqueous cigarette tar extract caused marked decrease in erythrocyte deformability with concomitant increase of membranous lipid peroxidation. In that case, quercetin aglycone suppressed the impairment of erythrocyte deformability as well as membranous lipid peroxidation. The same effect was found in quercetin-3- O-β- D-glucuronide, eventhough its effect was lower than that of quercetin aglycone. Thus, not only quercetin aglycone but also its conjugate metabolite protects erythrocyte membrane from the damage of smoking by scavenging reactive oxygen species generated from cigarette tar. Intake of quercetin-rich food may be helpful to protect membranous damage in erythrocytes from smoking.

Protective effect of alpha-tocotrienol against free radical-induced impairment of erythrocyte deformability.

Alpha-tocotrienol (alpha-T3) has been suggested to protect cellular membranes against free radical damage. This study was done to estimate the effect of alpha-T3 on free radical-induced impairment of erythrocyte deformability by comparing it to alpha-tocopherol (alpha-T). An erythrocyte suspension containing 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH) was forced to flow through microchannels with an equivalent diameter of 7 microm for measuring erythrocyte deformability. A higher concentration of AAPH caused a marked decrease in erythrocyte deformability with concomitant increase of membranous lipid peroxidation. Treatment of erythrocytes with alpha-T or alpha-T3 suppressed the impairment of erythrocyte deformability as well as membranous lipid peroxidation and they also increased erythrocyte deformability even in the absence of AAPH. In these cases, the protecting effect of alpha-T3 was significantly higher than that of alpha-T. We emphasize that higher incorporating activity of alpha-T3 into erythrocyte membranes seems to be the most important reason for higher protection against erythrocyte oxidation and impairment its deformability.

Haemorheological variables in a rat model of hypertriglyceridaemic obesity and diabetes.

Obesity is a heterogeneous condition of variable aetiology, generally associated with pathologies such as arterial hypertension, hyperlipidaemia, diabetes and cardiac disease. These conditions, either themselves or because of the various treatments used, may further modify blood rheology in an arbitrary manner. Therefore, analyses of changes in the blood rheology induced by obesity in humans have had differing and controversial results. In our laboratory, a model of hypertriglyceridaemic obesity is provided by an inbred rat strain; the beta genotype from the IIMb/Fm strain, presenting a syndrome of moderate obesity with apparent peripubertal onset, associated with hypertriglyceridaemia and glucose intolerance that turns into diabetes. The alpha genotype, originated from the same IIM/Fm stock, represents the control. The present study describes a comparative analysis of the variables determining the rheological behaviour of the blood in obese and control strains. Our results, agreeing with some other studies performed in humans, confirmed the haemorheological changes associated with obesity, and the fact that these changes became more evident in the presence of pathologies such as diabetes. It appears that triglyceridaemia. cholesterolaemia and hyperglycaemia may influence the rheological behaviour of the cell membrane and this damage may provoke a decrease in erythrocyte deformability and, consequently, hyperviscosity of the blood.

Exercise-induced oxidative stress affects erythrocytes in sedentary rats but not exercise-trained rats.

Oxidant stress is one of the factors proposed to be responsible for damaged erythrocytes observed during and after exercise. The impact of exertional oxidant stress after acute exhaustive treadmill running on erythrocyte damage was investigated in sedentary (Sed) and exercise-trained (ET) rats treated with or without antioxidant vitamins C and E. Exhaustive exercise led to statistically significant increments in the levels of thiobarbituric acid-reactive substance (TBARS) and H2O2-induced TBARS in Sed rats and resulted in functional and structural alterations in erythrocytes (plasma hemoglobin concentrations, methemoglobin levels, and rise in osmotic fragility of erythrocytes with decrease in erythrocyte deformability). Administration of antioxidant vitamin for 1 mo before exhaustive exercises prevented lipid peroxidation (TBARS, H2O2-induced TBARS) in Sed rats without any functional or structural alterations in erythrocytes. Parameters indicating erythrocyte lipid peroxidation and deterioration after exhaustive exercise in rats trained regularly with treadmill running for 1 mo were not different from those in Sed controls. Erythrocyte lipid peroxidation (TBARS) increased in exhausted-ET rats compared with ET controls; however, the plasma hemoglobin, methemoglobin levels, and erythrocyte osmotic fragility and deformability did not differ. Exhaustive exercise-induced lipid peroxidation in ET rats on antioxidant vitamin treatment was prevented, whereas functional and structural parameters of erythrocytes were not different from those of the ET controls. We conclude that exertional oxidant stress contributed to erythrocyte deterioration due to exercise in Sed but not in ET rats.

Erythrocyte deformability is a nitric oxide-mediated factor in decreased capillary density during sepsis.

Erythrocyte deformability has been recognized as a determinant of microvascular perfusion. Because nitric oxide (NO) is implicated in the modulation of red blood cell (RBC) deformability and NO levels increase during sepsis, we tested the hypothesis that a NO-mediated decrease in RBC deformability contributes to decreased functional capillary density (CD) in remote organs. With the use of a peritonitis model of sepsis in the rat [cecal ligation and perforation (CLP)] and aminoguanidine (AG) to prevent increases in NO, we measured CD in skeletal muscle (intravital microscopy), mean erythrocyte membrane deformability (; micropipette aspiration), systemic NO production [plasma nitrite/nitrate (NO(x)) chemiluminescence], and NO accumulation in RBC [NO bound to hemoglobin (HbNO) detected by electron paramagnetic resonance spectroscopy]. In untreated CLP animals relative to sham, NO(x) increased 254% (P < 0.05), stopped flow capillaries increased 149% (P < 0.05), and decreased 12.7% (P < 0.05), with a subpopulation (5%) of RBC with deformabilities below the normal range. AG prevented increases in NO(x), accumulation of HbNO, and decreases in both and functional CD. We found no evidence of leukocyte plugging postcapillary venules. Our findings suggest that decreased functional CD during sepsis resulted from a NO-mediated decrease in erythrocyte deformability.

Direct Measurement of Erythrocyte Deformability in Diabetes Mellitus with a Transparent Microchannel Capillary Model and High-Speed Video Camera System

To measure erythrocyte deformability in vitro, we made transparent microchannels on a crystal substrate as a capillary model. We observed axisymmetrically deformed erythrocytes and defined a deformation index directly from individual flowing erythrocytes. By appropriate choice of channel width and erythrocyte velocity, we could observe erythrocytes deforming to a parachute-like shape similar to that occurring in capillaries. The flowing erythrocytes magnified 200-fold through microscopy were recorded with an image-intensified high-speed video camera system. The sensitivity of deformability measurement was confirmed by comparing the deformation index in healthy controls with erythrocytes whose membranes were hardened by glutaraldehyde. We confirmed that the crystal microchannel system is a valuable tool for erythrocyte deformability measurement. Microangiopathy is a characteristic complication of diabetes mellitus. A decrease in erythrocyte deformability may be part of the cause of this complication. In order to identify the difference in erythrocyte deformability between control and diabetic erythrocytes, we measured erythrocyte deformability using transparent crystal microchannels and a high-speed video camera system. The deformability of diabetic erythrocytes was indeed measurably lower than that of erythrocytes in healthy controls. This result suggests that impaired deformability in diabetic erythrocytes can cause altered viscosity and increase the shear stress on the microvessel wall.

Blood viscosity and blood pressure: role of temperature and hyperglycemia

We planned a study to research the relations among blood pressure (BP), viscosity, and temperature in healthy subjects and among BP, viscosity, and glucose in diabetics. With simple random sampling method, 53 healthy and 29 diabetes mellitus (DM) type II subjects were selected. Parameters were determined with capillary viscometer and glucometer at 22°C, 36.5°C, and 39.5°C in healthy subjects, and at 22°C on diabetic patients during OGTT with 75 g of glucose. Statistical evaluations of the data were made with regression analysis, Student t test, Spearman’s correlation, and analysis of variance. When temperature decreased from 36.5°C to 22°C, blood viscosity increased 26.13%. This increase resulted in a 20.72% decrease in blood flow rate. According to the Hagen-Poiseuille equation, the required BP increase for compensation of the resulting tissue ischemia was 20.72%. Also, a 34.73% decrease in erythrocyte deformability and 18.71% increase in plasma viscosity were seen. When temperature increased from 36.5° to 39.5°C, blood viscosity decreased 10.38%. This caused 11.15% decrease in blood flow rate, and 11.15% decrease in BP, according to the equation. Erythrocyte deformability increase of 9.92% and plasma viscosity decrease of 4.99% arose from the temperature rise. There is a correlation between total data for temperatures and viscosities (r = −0.84, P < .001). When the mean value of blood glucose increased from 100 to 400 mg/dL, viscosity increased 25% (r = 0.59, P = .002). In this state, blood flow rate decrease was 20% and BP increase for physiological compensation was 25%. Consequently, temperature, glucose and viscosity levels of blood are important factors for BP.

A review of myocardial normothermia: its theoretical basis and the potential clinical benefits in cardiac surgery

Myocardial protection during cardiac surgery aims to preserve myocardial function while providing a bloodless and motionless operating field to make surgery easier. Myocardial protection is achieved by decreasing the oxygen needs using hypothermia and producing electromechanical cardiac arrest using potassium infusion which allows surgery to be performed on a non-beating heart. The deleterious effects of hypothermia include dysfunction of enzymatic systems, development of acidosis, a decrease in tissue oxygen delivery, an increase in blood viscosity and a decrease in erythrocyte deformability. Ninety percent of the decrease in oxygen consumption is obtained by inducing electromechanical arrest and inducing hypothermia has little additional benefit. Maintenance of systemic and myocardial normothermia reduces problems and provides a more physiological approach for cardiopulmonary bypass (CPB). The current results obtained using normothermic protection are very encouraging, and it is an easier inexpensive option. This review summarizes the current knowledge on the benefits of normothermia, based upon experimental and clinical studies.

Chlorpromazine-induced Erythrocyte Shape Change in Ratswith Obstructive Cholestasis

Cholestasis is associated with an accumulation of endogenous opioids in plasma which are known to reduce erythrocyte deformability in-vitro. We compared chlorpromazine-induced erythrocyte shape change in bile duct ligated (cholestatic), sham-operated and control rats to evaluate the effect of cholestasis on erythrocyte deformability. Cell shape change was measured using a polarized light scattering method. Cholestasis reduced erythrocyte shape change induced by chlorpromazine and the decrease in erythrocyte deformability correlated with the duration of cholestasis. Doses of chlorpromazine which produced 50% effect on erythrocyte shape change in cholestatic groups were significantly (P < 0.001) higher than controls. Erythrocyte osmotic fragility was also measured. Cholestasis produced increased resistance to osmotic shock in erythrocytes. Erythrocyte shape change is reduced in cholestasis probably due to the accumulation of endogenous opioids in plasma.