Blood viscosity in the newborn.

Mackintosh, T. F.; Walker, Catherine

doi:10.1136/adc.48.7.547

Cited by 52 publications

(29 citation statements)

References 45 publications

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“…Those studies were done with a Wells-Brookfield viscometer, which has a different geometry than the viscometer used in this study. The fetal hematocrit was higher in all those studies, which might be due to the fact that blood was drawn from the placenta after delivery (3, 1 1) or from the newborn after delivery (21), where hematocrit is regularly about 60% (3,23). It is likely that the higher hematocrit accounts for the difference in whole blood viscosity between these earlier reports and the present data.…”

Section: Discussioncontrasting

confidence: 56%

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Rheology of Fetal and Maternal Blood

et al. 1985

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Section: Discussioncontrasting

confidence: 56%

“…This has now been confirmed also for the newborn lamb and adult sheep (32). Earlier reports described an increased whole blood viscosity in normal newborns (3,11,21). Those studies were done with a Wells-Brookfield viscometer, which has a different geometry than the viscometer used in this study.…”

Section: Discussionmentioning

confidence: 94%

Rheology of Fetal and Maternal Blood

et al. 1985

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“…Thus pups administered packed cells could have received more acid and less base than those receiving whole blood. In a previous experiment using a similar protocol where base excess and lactate were measured at 1 h posttransfusion, before necrotizing enterocolitis was evident although perhaps not before the pathologic process had begun, a rise in base deficit of 6 mEq/liter and a fall in pH, of 0.07 was seen in the polycythemic: group, but not in the control group [95% confidence interval (4,8) (1 1, -15) mg/dl, n = 4). Thus, the difference in transfused acid and base could conceivable account for as much as 50% of the acidosis seen in the polycythemic group in this study, if one uses the upper limit of the confidence interval for change in base deficit from my earlier experiment (22) attributes it all to difference in transfused acid and base and assumes no metabolic compensation occurs during the 4-h experiment.…”

Section: Discussionmentioning

confidence: 99%

Acute Polycythemia Increases the Disappearance Rate of Clottable Fibrinogen in the Newborn Dog

LeBlanc

Edwards

1986

Pediatr Res

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ABSTRACT. To explore the pathophysiology of the necrotizing enterocolitis caused by polycythemia in the newborn dog, the effect of acute polycythemia on fibrinogen disappearance rate was studied in 3 8 puppies (3-14 days). All pups received an exchange transfusion removing 6 5 ml/ kg of blood and transfusing 8 5 ml/kg of either whole blood (control, resulting hematocrit = 37), or packed red blood cells (polycythemia, resulting hematocrit = 68). Necrotizing enterocolitis was found in 1 5 of 19 polycythemic and four of 1 9 control pups ( p < 0.01). Iz5I fibrinogen and Evan's blue (an albumin marker) were injected 2 h after transfusion and the concentration of clottable labeled fibrinogen and albumin tracer were measured a t % and 2 h after injection. The fraction of the tracer that disappeared over the 1%-h period was calculated. In the polycythemic group 45 2 18 SD% of the clottable fibrinogen disappeared versus only 28 f 15% in the control group ( p < 0.01). In the polycythemic group 36 2 21% of the albumin tracer disappeared versus 31 f 12% in the control group (NS). Thus polycythemia in the newborn dog is associated with an increased disappearance rate of clottable fibrinogen not associated with a general increase in protein disappearance rate. Thus an intravascular coagulopathy is evident in the polycythemic animals. Whether this coagulopathy is the cause of the necrotizing enterocolitis or is secondary to the necrotizing enterocolitis seen in this animal model cannot be determined from this experiment. (Pediatr Res 20: 151-154,1986) Abbreviation pH,, arterial p H Polycythemia is a common condition in human newborns (1) that is thought to cause significant acute disease and possibly long-term neurologic sequelae (2-9). Hakanson and Oh (10) describe an association between polycythemic hyperviscosity and necrotizing enterocolitis in small for gestation age infants. We have demonstrated that polycythemia will cause necrotizing enterocolitis in the newborn dog (1 1). This article, as far as we are aware, was the only description of a disease seen in human infants with polycythemia, caused by polycythemia in an animal model. Since coagulation abnormalities have been associated with polycythemia in vitro (12-16) we sought to determine if coagulation abnormalities could be demonstrated in our model. Attempts to demonstrate coagulopathy in human infants with

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“…The relationship between packed cell volume and viscosity was compared to published data from similar studies utilizing red blood cells from human newborns and adults (18,23,26,29,30).…”

Section: Methodsmentioning

confidence: 99%

“…The hypoglycemia found commonly (12,13,15,18) in the hyperviscous newborn is unexplained. Many hyperviscous infants are small for gestational age or infants of diabetic mothers, suggesting that th& hypogly&ia might reflect limitations of gluconeogenesis, hyperinsulinism, or both.…”

Section: Speculationmentioning

confidence: 99%

Glucose Perturbation in Experimental Hyperviscosity

et al. 1980

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SummaryHyperviscosity was produced in one member of each of 7 sets of twin newborn lambs by an exchange transfusion with 500 ml maternal packed red blood cells. The remaining seven control twin lambs underwent an identical exchange with maternal whole blood.Postexchange hematocrits were 63 f 6 and 29.0 * 3% (mean f S.E.), respectively ( P < 0.01). Whole blood viscosity measured at 3 rpm increased from 3.2 f 0.4 centipoise (cps) to 14.4 f 6.1 cps in the lambs made hyperviscous ( P < 0.01) and remained unchanged in the control lambs (2.2 f 0.2 versus 2.8 f 0.3 cps).A 2-hr steady state glucose infusion was performed on each lamb before and after the packed cell or whole blood exchange transfusion. Mean steady state plasma glucose concentrations were significantly decreased from pre-exchange steady state glucose infusion levels in the same lambs made hyperviscous ( P < 0.05), whereas steady state glucose levels increased from preexchange levels in the twin lambs exchanged with maternal whole blood. Mean plasma insulin and glucagon values for the hyperviscous and control lambs remained unchanged during the glucose infusion. SpeculationThe fmding of an abnormality in glucose homeostasis in the absence of a hormonal or substrate disturbance in hyperviscous lambs suggests that there may be rapid glucose utilization from increased cerebral extraction of glucose and/or a reduction in endogenous glucose production caused by sluggish hepatic circulation.There are many studies relating neonatal hypoglycemia to decreased glycogen stores (22, 25), hyperinsulinism (1, 8), increased metabolic demand (5, 7), and abnormalities in gluconeogenesis (14, 21). The hypoglycemia found commonly (12,13,15,18) in the hyperviscous newborn is unexplained. Many hyperviscous infants are small for gestational age or infants of diabetic mothers, suggesting that th& hypogly&ia might reflect limitations of gluconeogenesis, hyperinsulinism, or both.In a previousstudy (l&j utilizing intravenous (IV) glucose tolerance tests, we demonstrated increased glucose disappearance rates when hyperviscous infants (infants of diabetic mothers, small for gestational age infants, and infants whose hyperviscosity was of unknown etiology) were compared to control infants matched for conceptual age (16). In the hyperviscous infants, glucose disappearance rates decreased towards control values after partial exchange transfusion. Basal and stimulated plasma insulin, alanine, and growth hormone levels were similar to control values throughout the study period. Thus, there was suggestive evidence that the rapid rate constant for glucose outflow in the neonatal hyperviscosity syndrome was on the basis of mechanisms other than absolute hyperinsulinism or deficiency of a key gluconeogenic substrate (14) and was perhaps related to pathophysiologic considerations more fundamental to the underlying clinical diagnosis.In the present study, we utilized the hyperviscous lamb model described by Fouron and Hebert (1 1) to investigate further the effects of hyperviscosity on glucose...

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Blood viscosity in the newborn.

Cited by 52 publications

References 45 publications

Rheology of Fetal and Maternal Blood

Rheology of Fetal and Maternal Blood

Acute Polycythemia Increases the Disappearance Rate of Clottable Fibrinogen in the Newborn Dog

Glucose Perturbation in Experimental Hyperviscosity

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