Increased Cerebral Blood Flow and Plasma Epinephrine in Hypoglycemic, Preterm Neonates

PEDIATRICS ◽  
1990 ◽  
Vol 85 (2) ◽  
pp. 172-176 ◽  
Author(s):  
O. Pryds ◽  
N. J. Christensen ◽  
B. Friis-Hansen

Cerebral blood flow, plasma epinephrine, and plasma norepinephrine were measured in 25 spontaneously breathing, preterm neonates (mean gestational age 30.4 weeks) 2 hours after birth, during a routine screening for low blood glucose levels. Increased cerebral blood flow and plasma epinephrine values were observed when blood glucose levels were low, whereas plasma norepinephrine was constant throughout the blood glucose range. Hypoglycemia (defined as blood glucose concentration <30 mg/dL) was found in 13 neonates who were treated with intravenous glucose and milk enterally. Blood glucose levels were normal in the remaining 12 control neonates who received milk by a gastric line. Approximately 30 minutes after treatment with intravenous glucose and/or milk, cerebral blood flow had decreased by a mean of 11.3% in the 13 hypoglycemic neonates but was still 37.5% higher than cerebral blood flow in the control neonates despite normalization of plasma epinephrine concentration. Mean arterial blood pressure and blood gas values were identical between groups throughout the investigation. It is suggested that a normal coupling between cerebral metabolic demands and flow is present in very preterm neonates and that epinephrine may play a role in the cerebral hyperperfusion. Although none of the neonates had clinical signs of hypoglycemia, the data suggest that counterregulatory mechanisms are invoked when blood glucose values are <30 to 45 mg/dL.

1993 ◽  
Vol 265 (4) ◽  
pp. R883-R887 ◽  
Author(s):  
W. J. Powers ◽  
P. J. Boyle ◽  
I. B. Hirsch ◽  
P. E. Cryer

To determine if increases in plasma epinephrine and norepinephrine caused by hypoglycemia are associated with increments in cerebral blood flow (CBF), we measured CBF with positron emission tomography in normal humans at ambient fasting arterial plasma glucose levels and at clamped plasma glucose levels of 5.3, 3.5, and 2.8 mmol/l using the hyperinsulinemic, stepped hypoglycemic clamp technique. Despite significant increases in plasma epinephrine to 7,340 +/- 350 (SE) pmol/l and in plasma norepinephrine to 3.32 +/- 0.35 nmol/l, mean hemispheric CBF (41 +/- 1, 49 +/- 1, 48 +/- 2, and 51 +/- 3 ml x 100 g-1 x min-1) remained constant at the ambient (5.2), 5.3, 3.5, and 2.8 mmol/l glycemic levels, respectively. Furthermore, there was no correlation between CBF and either plasma epinephrine levels ranging from 160 to 10,580 pmol/l or plasma norepinephrine levels ranging from 0.56 to 5.10 nmol/l. Failure to demonstrate any dose-response relationship between plasma catecholamine levels and CBF argues against their primary role in cerebrovascular control during hypoglycemia.


2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Sarah Docherty ◽  
Crystal Haskell-Ramsay

AbstractBaobab fruit contains high levels of phenolic compounds and vitamin C. Previous work has associated these phenolic compounds and vitamin C with a range of health benefits including improvements in cerebral blood flow and cognition. In vivo, it has been demonstrated that consumption of baobab fruit can reduce the glycaemic response, which may provide a mechanism for cognitive benefits as other research has shown that variations in blood glucose levels can modulate cognitive performance. Preliminary work found that consumption of 15 g baobab fruit extract significantly improved reaction time but increased number of errors on an executive function task. Taken together it would suggest baobab fruit has the potential to improve cognitive performance that could be attributed to changes in cerebral blood flow and blood glucose levels.The current study aimed to determine the effect of baobab fruit on cognitive performance, cerebral blood flow and blood glucose levels in a healthy young sample.This randomised, placebo-controlled, double-blind, counterbalanced-crossover study assessed the effect of 10 g baobab fruit powder or sugar matched control in 24 healthy participants (17 female, 7 male, mean age = 22.91 SD = 3.37). All participants completed the cognitive assessments, a subset of 14 completed the cerebral blood flow and blood glucose assessments (mean age = 23.21, SD = 2.46). Participants completed baseline tasks before consuming a drink containing either 10 g baobab fruit powder or placebo, there was then a 45-minute absorption period before participants completed cognitive tasks again. Seven days after participants returned and completed the same procedure but consumed the opposite drink. In the 14 participant subset, cerebral blood flow was measured throughout using Near Infrared Spectroscopy (NIRS) and blood glucose was measured before testing, after absorption period and upon completion of post doseUsing the MIXED procedure in SPSS, results showed that after consumption of baobab there was improved accuracy on a sustained attention task and fewer errors on the last repetition of a serial subtraction task. Baobab consumption led to increased blood glucose levels but there was no significant effect on cerebral blood flow.Results show that, in this sample, 10 g baobab fruit can improve certain aspects of cognitive performance and increase circulating blood glucose levels, which may explain these improvements. However, there was no significant effect on any cerebral blood flow measures. Future work may wish to explore further glucoregulation activity (in particular insulin response) after baobab consumption as a potential underlying mechanism.


1999 ◽  
Vol 19 (3) ◽  
pp. 288-297 ◽  
Author(s):  
Lars Gisselsson ◽  
Maj-Lis Smith ◽  
Bo K. Siesjö

The influence of hyperglycemic ischemia on tissue damage and cerebral blood flow was studied in rats subjected to short-lasting transient middle cerebral artery (MCA) occlusion. Rats were made hyperglycemic by intravenous infusion of glucose to a blood glucose level of about 20 mmol/L, and MCA occlusion was performed with the intraluminar filament technique for 15, 30, or 60 minutes, followed by 7 days of recovery. Normoglycemic animals received saline infusion. Perfusion-fixed brains were examined microscopically, and the volumes of selective neuronal necrosis and infarctions were calculated. Cerebral blood flow was measured autoradiographically at the end of 30 minutes of MCA occlusion and after 1 hour of recirculation in normoglycemic and hyperglycemic animals. In two additional groups with 30 minutes of MCA occlusion, CO2 was added to the inhaled gases to create a similar tissue acidosis as in hyperglycemic animals. In one group CBF was measured, and the second group was examined for tissue damage after 7 days. Fifteen and 30 minutes of MCA occlusion in combination with hyperglycemia produced larger infarcts and smaller amounts of selective neuronal necrosis than in rats with normal blood glucose levels, a significant difference in the total volume of ischemic damage being found after 30 minutes of MCA occlusion. After 60 minutes of occlusion, when the volume of infarction was larger, only minor differences between normoglycemic and hyperglycemic animals were found. Hypercapnic animals showed volumes of both selective neuronal necrosis and infarction that were almost identical with those observed in normoglycemic, normocapnic animals. When local CBF was measured in the ischemic core after 30 minutes of occlusion, neither the hyperglycemic nor the hypercapnic animals were found to be significantly different from the normoglycemic group. Brief focal cerebral ischemia combined with hyperglycemia leads to larger and more severe tissue damage. Our results do not support the hypothesis that the aggravated injury is caused by any disturbances in CBF.


1997 ◽  
Vol 17 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Naoaki Horinaka ◽  
Nicole Artz ◽  
Jane Jehle ◽  
Shinichi Takahashi ◽  
Charles Kennedy ◽  
...  

Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [14C]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 m M, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3– concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p. injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 m M) or pharmacological doses of deoxyglucose.


1997 ◽  
Vol 176 (1) ◽  
pp. S164 ◽  
Author(s):  
I. Ingemarsson ◽  
I. Amer-Wåhlin ◽  
R. Liedman ◽  
C. Lindoff ◽  
M. Westgren

2017 ◽  
Vol 107 (2) ◽  
pp. 138-144 ◽  
Author(s):  
K. M. Järvelä ◽  
N. K. Khan ◽  
E. L. Loisa ◽  
J. A. Sutinen ◽  
J. O. Laurikka ◽  
...  

Background and Aims: To describe the incidence of and risk factors for postoperative infections and the correlation between postoperative hyperglycemia despite tight blood glucose control with infectious and other complications after contemporary cardiac surgery. Material and Methods: The study comprised 1356 consecutive adult patients who underwent cardiac surgery between January 2013 and December 2014 and were followed up for 6 months. Patients surviving the first 2 days were included in the analysis. Preoperative demographic information, medical history, procedural details, and the postoperative course were recorded. The target range for blood glucose levels was 4–7 mmol/L and repeated arterial blood samples were obtained during the intensive care unit stay. The associations of blood glucose levels during the first postoperative day and the occurrence of postoperative infections and other significant complications were analyzed. Results: Of the study cohort, 9.8% developed infectious complications which were classified as major surgical site infections in 2.2%, minor surgical site infections in 1.1%, lung infections in 2.0%, unclear fever or bacteremia in 0.3%, cannula or catheter related in 2.6%, multiple in 1.5%, and other in 0.2%. The incidence of deep sternal wound infection was 2.0%. Repeated hyperglycemia occurred in 39.7% of patients and was associated with increased rates of postoperative infections, 12.1% versus 8.2%, p = 0.019; stroke, 4.9% versus 1.5%, p < 0.001; and mortality, 6.1% versus 2.1%, p < 0.001, when compared to patients with single or no hyperglycemia. Conclusion: Every 10th patient develops infectious complications after cardiac surgery. Repeated hyperglycemia is associated with increased rates of infectious complications, stroke, and mortality.


1990 ◽  
Vol 258 (1) ◽  
pp. E212-E219 ◽  
Author(s):  
X. F. Zhou ◽  
K. H. Jhamandas ◽  
B. G. Livett

We have studied the glucose response and catecholamine (CA) response to insulin in the conscious rat to evaluate the role of sensory fibers in these responses in animals pretreated with capsaicin as neonates. In contrast to previous results obtained in anesthetized rats (Z. Khalil, B.G. Livett, and P.D. Marley. J. Physiol. Lond. 370: 201-215, 1986; Z. Khalil, B.G. Livett, and P.D. Marley. J. Physiol. Lond. 391: 511-526, 1987.), in conscious rats, insulin (1 IU/kg iv) produced only a mild hypoglycemia, which quickly returned to resting levels and caused no significant changes in plasma epinephrine levels. Somatostatin and SMS-(201-995), a somatostatin analogue, both potentiated and prolonged the insulin-induced hypoglycemia, resulting in an increase in circulating CA levels that was suppressed by hexamethonium and atropine. In capsaicin-pretreated rats the blood glucose levels at 90 min after insulin were significantly lower than those in vehicle-pretreated rats both in the presence (1 IU/kg insulin, 48 +/- 6 vs. 92 +/- 6 mg/100 ml, P less than 0.01) and absence (10 IU/kg insulin, 38 +/- 4 vs. 51 +/- 2 mg/100 ml, P less than 0.01) of SMS-(201-995). The CA levels in capsaicin-pretreated rats at 90 min after insulin were higher than in vehicle-pretreated rats (epinephrine levels: 27 +/- 4 vs. 10 +/- 1 pmol/ml in 1 IU/kg insulin, P less than 0.01; 64 +/- 14 vs. 25 +/- 5 pmol/ml in 10 IU/kg insulin, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)


2011 ◽  
Vol 301 (2) ◽  
pp. F288-F294 ◽  
Author(s):  
Kyungjoon Lim ◽  
Paul Lombardo ◽  
Michal Schneider-Kolsky ◽  
Lucinda Hilliard ◽  
Kate M. Denton ◽  
...  

Intrauterine growth restriction (IUGR) leads to a reduction in nephron endowment at birth and is linked to renal dysfunction in adulthood. The aim of the present study was to determine whether kidneys of IUGR rat offspring are more vulnerable to a secondary insult of hyperglycemia. IUGR was induced in Wistar-Kyoto rats by maternal protein restriction. At 24 wk of age, diabetes was induced in male IUGR and non-IUGR offspring by streptozotocin injection; insulin was injected daily to maintain blood glucose levels at either a mild (7–10 mmol/l; n=8/group) or a moderate (10–15 mmol/l; n=8/group) level. At 32 wk of age, renal function was assessed using ultrasound and [3H]inulin and [14C]para-aminohippurate clearance techniques. Conscious mean arterial blood pressure and heart rate were unchanged in IUGR offspring. Relative kidney length was increased significantly in IUGR offspring, and renal function was altered significantly; of importance, there was a significant increase in filtration fraction, indicative of glomerular hyperfiltration. Induction of hyperglycemia led to marked impairment of renal function. However, the response to hyperglycemia was not different between IUGR and non-IUGR offspring. Maintaining blood glucose levels at a mild hyperglycemic level led to marked improvement in all measures of renal function in IUGR and non-IUGR offspring. In conclusion, while the IUGR offspring showed evidence of hyperfiltration, the response to hyperglycemia was similar in IUGR and non-IUGR kidneys in adulthood. Importantly, maintaining blood glucose levels at a mild hyperglycemic level markedly attenuated the renal dysfunction associated with diabetes, even in IUGR offspring.


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