Influence of hematocrit on whole blood glucose levels: new evidence from marine mammals

1989 ◽  
Vol 256 (6) ◽  
pp. R1220-R1224 ◽  
Author(s):  
M. A. Castellini ◽  
J. M. Castellini

The water content and glucose concentration in the whole blood of marine mammals were found to be correlated to red blood cell concentration. Because hematocrit (Hct) undergoes significant periodic shifts in these mammals during periods of apnea and/or diving, the measured values of whole blood glucose change due to alterations in Hct, independent of shifts in metabolite regulatory pathways. In contrast to humans, where red blood cell and plasma glucose concentrations are equivalent, in most other mammalian species red blood cell glucose concentration is much lower than that in plasma. Therefore, as Hct increases, the whole blood concentration of glucose must decrease in a linear manner, depending on the magnitude of the Hct change and the concentration of glucose in the blood cells. This study demonstrates that water and metabolite distribution must be considered when interpreting whole blood metabolite data. The results suggest that plasma or serum analysis of metabolites would avoid distribution problems. This is especially critical in species where Hct varies during the course of the experiment, as in exercising or diving mammals.

Author(s):  
Adam Attila Matrai ◽  
Gabor Varga ◽  
Bence Tanczos ◽  
Barbara Barath ◽  
Adam Varga ◽  
...  

BACKGROUND: The effects of temperature on micro-rheological variables have not been completely revealed yet. OBJECTIVE: To investigate micro-rheological effects of heat treatment in human, rat, dog, and porcine blood samples. METHODS: Red blood cell (RBC) - buffer suspensions were prepared and immersed in a 37, 40, and 43°C heat-controlled water bath for 10 minutes. Deformability, as well as mechanical stability of RBCs were measured in ektacytometer. These tests were also examined in whole blood samples at various temperatures, gradually between 37 and 45°C in the ektacytometer. RESULTS: RBC deformability significantly worsened in the samples treated at 40 and 43°C degrees, more expressed in human, porcine, rat, and in smaller degree in canine samples. The way of heating (incubation vs. ektacytometer temperation) and the composition of the sample (RBC-PBS suspension or whole blood) resulted in the different magnitude of RBC deformability deterioration. Heating affected RBC membrane (mechanical) stability, showing controversial alterations. CONCLUSION: Significant changes occur in RBC deformability by increasing temperature, showing inter-species differences. The magnitude of alterations is depending on the way of heating and the composition of the sample. The results may contribute to better understanding the micro-rheological deterioration in hyperthermia or fever.


2010 ◽  
Vol 298 (5) ◽  
pp. E1088-E1096 ◽  
Author(s):  
Diego Pérez-Tilve ◽  
Lucas González-Matías ◽  
Benedikt A. Aulinger ◽  
Mayte Alvarez-Crespo ◽  
Manuel Gil-Lozano ◽  
...  

Exendin-4 (Ex-4), an agonist of the glucagon-like peptide-1 receptor (GLP-1R), shares many of the actions of GLP-1 on pancreatic islets, the central nervous system (CNS), and the gastrointestinal tract that mediates glucose homeostasis and food intake. Because Ex-4 has a much longer plasma half-life than GLP-1, it is an effective drug for reducing blood glucose levels in patients with type 2 diabetes mellitus (T2DM). Here, we report that acute administration of Ex-4, in relatively high doses, into either the peripheral circulation or the CNS, paradoxically increased blood glucose levels in rats. This effect was independent of the insulinotropic and hypothalamic-pituitary-adrenal activating actions of Ex-4 and could be blocked by a GLP-1R antagonist. Comparable doses of GLP-1 did not induce hyperglycemia, even when protected from rapid metabolism by a dipeptidyl peptidase IV inhibitor. Acute hyperglycemia induced by Ex-4 was blocked by hexamethonium, guanethidine, and adrenal medullectomy, indicating that this effect was mediated by sympathetic nervous system (SNS) activation. The potency of Ex-4 to elevate blood glucose waned with chronic administration such that after 6 days the familiar actions of Ex-4 to improve glucose tolerance were evident. These findings indicate that, in rats, high doses of Ex-4 activate a SNS response that can overcome the expected benefits of this peptide on glucose metabolism and actually raise blood glucose. These results have important implications for the design and interpretation of studies using Ex-4 in rats. Moreover, since there are many similarities in the response of the GLP-1R system across mammalian species, it is important to consider whether there is acute activation of the SNS by Ex-4 in humans.


1959 ◽  
Vol 196 (3) ◽  
pp. 619-624 ◽  
Author(s):  
G. S. Kanter

When unanesthetized dogs are exposed to heat (120°F) for 4 hr. with no water available for drinking, hypoglycemia results. One would expect that the dehydration, which also occurs, should physically cause an increase in blood glucose concentration as is usually found in man. The tendency is present in dogs but the utilization of glucose is sufficiently rapid to offset the hemoconcentration and cause a fall in glucose levels even when exogenous glucose is given at the rate of 1% body wt/hr. of 11% glucose by stomach tube. This increased utilization has been demonstrated to be mainly due to involvement of the respiratory muscles which are used in the panting mechanism for no fall in blood glucose occurs under similar conditions when the animal is curarized. The evidence indicates that the hypoglycemic mechanism present in dogs is not a species phenomenon but is probably also present in man under appropriate conditions. In both man and the dog whether hypoglycemia occurs will depend upon the degree of involvement of the respiratory apparatus.


1991 ◽  
Vol 156 (1) ◽  
pp. 233-248 ◽  
Author(s):  
S. THOMAS ◽  
R. KINKEAD ◽  
P. J. WALSH ◽  
C. M. WOOD ◽  
S. F. PERRY

The sensitivity of red blood cell Na+/H+ exchange to exogenous adrenaline was assessed in vitro using blood withdrawn from catheterized rainbow trout (Oncorhynchus mykiss) maintained under normoxic conditions [water PO2, (PwO2)=20.66 kPa] or after exposure to moderate hypoxia (PwO2=6.67-9.33 kPa) for 48 h, which chronically elevated plasma adrenaline, but not noradrenaline, levels. Peak changes in whole-blood extracellular pH over a 30 min period after adding 50–1000 nmoll−1 adrenaline were employed as an index of sensitivity; the blood was pre-equilibrated to simulate arterial blood gas tensions in severely hypoxic fish (PaO2=2.0 kPa, PaCO2=0.31 kPa). Blood pooled from normoxic fish displayed a dose-dependent reduction in whole-blood pH after addition of adrenaline. Blood pooled from three separate groups of hypoxic fish, however, displayed diminished sensitivity to adrenaline, ranging from complete desensitization to a 60%reduction of the response. Subsequent experiments performed on blood from individual (i.e. not pooled) normoxic or hypoxic fish demonstrated an inverse correlation between the intensity of H+ extrusion (induced by exogenous adrenaline addition) and endogenous plasma adrenaline levels at the time of blood withdrawal. However, acute increases in plasma adrenaline levels in vitro did not affect the responsiveness of the red blood cell to subsequent adrenergic stimulation. The intensity of H+ extrusion was inversely related to the PaO2in vivo between 2.67 and 10.66 kPa, and directly related to the logarithm of the endogenous plasma adrenaline level. The results suggest that desensitization of Na+/H+ exchange in chronically hypoxic fish is related to persistent elevation of levels of this catecholamine. This desensitization can be reversed in vitro as a function of time, but only when blood is maintained under sufficiently aerobic conditions.


Blood ◽  
1984 ◽  
Vol 64 (6) ◽  
pp. 1270-1276 ◽  
Author(s):  
TN Estep ◽  
RA Pedersen ◽  
TJ Miller ◽  
KR Stupar

Abstract Di-(2-ethylhexyl) phthalate (DEHP) accumulates in blood brought into contact with materials utilizing this compound as a plasticizer. To determine whether this phthalate diester affects red blood cell integrity, we have compared cell morphology, plasma hemoglobin accumulation, micro-vesicle production, and the concentration of intracellular metabolites and electrolytes of erythrocytes from blood stored at 4 degrees C with and without DEHP. When sufficient emulsified DEHP was mixed with blood to give a final concentration of 300 micrograms/mL, plasma hemoglobin accumulation was reduced by an average of 70%, the percentage of cells exhibiting normal morphology was enhanced by at least 20-fold, and the volume of microvesicles released from red blood cells was reduced by 50% after 35 days of refrigerated storage compared to the values obtained from corresponding samples stored without added phthalate. Similar effects were observed regardless of whether blood was stored in nonplasticized polypropylene or tri-(2-ethylhexyl) trimellitate plasticized polyvinylchloride containers and with DEHP solubilized by a variety of emulsifiers. When 300 micrograms/mL DEHP was added to stored blood containing erythrocytes predominantly in the echinocyte conformation, many of the cells reverted to the normal discoid morphology. The addition of this quantity of DEHP to blood had no significant effect on the course of storage-induced changes in erythrocyte adenosine triphosphate (ATP), 2,3-diphosphoglycerate (2,3-DPG), sodium or potassium concentrations. The data are consistent with the hypothesis that DEHP inhibits the deterioration of the red blood cell membrane that results from the refrigerated storage of whole blood.


The Analyst ◽  
2019 ◽  
Vol 144 (9) ◽  
pp. 3144-3157 ◽  
Author(s):  
Byung Jun Kim ◽  
Ye Sung Lee ◽  
Alexander Zhbanov ◽  
Sung Yang

In this study, a microfluidic-based physiometer capable of measuring the whole blood viscosity, hematocrit, and red blood cell (RBC) deformability on a chip is introduced.


2018 ◽  
Vol 104 (3) ◽  
pp. 707-710 ◽  
Author(s):  
Robert M Cohen ◽  
Robert S Franco ◽  
Eric P Smith ◽  
John M Higgins

Commentary placing genetic ancestry markers and racial difference in HbA1c in the context of more common variations in the HbA1c-average glucose relationship and their clinical implications.


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