Effect of Hyperglycemia on Brain Penetrating Arterioles and Cerebral Blood Flow Before and After Ischemia/Reperfusion

Cipolla, Marilyn J.; Godfrey, Julie A.

doi:10.1007/s12975-010-0014-8

Cited by 27 publications

(24 citation statements)

References 42 publications

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“…The mechanism of the effects of hyperglycaemia on lacunar stroke is not yet known. Experiments have also found that the effect of ischaemia was not different between normoglycaemic and hyperglycaemic animals with end-artery infarcts, 27,28 suggesting that it was related to ischaemia and reperfusion rather than to hyperglycaemia. However, in subcortical strokes, the magnetic resonance spectroscopy also provided evidence of metabolically compromised area.…”

Section: Discussionmentioning

confidence: 98%

Hyperglycaemia in acute lacunar stroke: A Chinese hospital-based study

Yuan

Zhang

et al. 2012

Diabetes and Vascular Disease Research

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Admission hyperglycaemia is very common in acute ischaemic stroke (IS) patients and is associated with worse outcome in non-lacunar infarction, but its association with lacunar infarction remains controversial. We investigated the association between hyperglycaemia and clinical outcome in patients with acute lacunar stroke in a hospitalised Chinese population. Consecutive patients with acute IS were enrolled and classified into lacunar and non-lacunar stroke groups based on clinical criteria according to the Oxfordshire Community Stroke Project (OCSP) and findings on brain computed tomography (CT) or magnetic resonance imaging (MRI) scan. Hyperglycaemia was defined as blood glucose > 6.1 mmol/L. Univariate and multivariate analyses were used to examine the association between hyperglycaemia and outcomes in diabetic and non-diabetic groups. The main outcome measure was a poor outcome [defined as modified Rankin Scale (mRS) score ≥ 3] at 12 months after stroke. Of the 2020 acute ISs, 689 (34.1%) were acute lacunar strokes, of which 159 (23%) were diabetic and the other 530 (77%) were non-diabetic. In non-lacunar stroke, admission hyperglycaemia was independently associated with increased risk of poor outcome at 1 year (odds ratio (OR) = 1.782; 95% confidence interval (CI) = 1.340-2.370, p = 0.0005). In lacunar stroke, hyperglycaemia was not associated with functional outcome (OR = 1.337; 95% CI = 0.939-1.093, p = 0.086) irrespective of the diabetic status.

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Section: Discussionmentioning

confidence: 98%

Hyperglycaemia in acute lacunar stroke: A Chinese hospital-based study

Yuan

Zhang

et al. 2012

Diabetes and Vascular Disease Research

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“…Basal tone was reduced in both normoglycemic and hyperglycemic animals to the same degree suggesting that it was due to ischemia/reperfusion injury and independent of glucose. They also demonstrated that acute hyperglycemia had no effect on endothelium dependent vasodilator production in penetrating arterioles which may explain why lacunar strokes are not worsened by hyperglycemia [71]. However, studies done on cortical stroke revealed a deleterious effect of acute hyperglycemia on vascular reactivity.…”

Section: Preclinical Evidencementioning

confidence: 99%

Hyperglycemia, Acute Ischemic Stroke, and Thrombolytic Therapy

Hafez

Coucha

Bruno

et al. 2014

Transl. Stroke Res.

104

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Ischemic stroke is a leading cause of disability and is considered now the 4th leading cause of death. Many clinical trials have shown that stroke patients with acute elevation in blood glucose at onset of stroke suffer worse functional outcomes, longer in-hospital stay and higher mortality rates. The only therapeutic hope for these patients is the rapid restoration of blood flow to the ischemic tissue through intravenous administration of the only currently proven effective therapy, tissue plasminogen activator (tPA). However, even this option is associated with the increased risk of intracerebral hemorrhage. Nonetheless, the underlying mechanisms through which hyperglycemia (HG) and tPA worsen the neurovascular injury after stroke are not fully understood. Accordingly, this review summarizes the latest updates and recommendations about the management of HG and co-administration of tPA in a clinical setting while focusing more on the various experimental models studying: 1. the effect of HG on stroke outcomes; 2. the potential mechanisms involved in worsening the neurovasular injury; 3. the different therapeutic strategies employed to ameliorate the injury, and finally; 4. the interaction between HG and tPA. Developing therapeutic strategies to reduce the hemorrhage risk with tPA in hyperglycemic setting is of great clinical importance. This can best be achieved by conducting robust preclinical studies evaluating the interaction between tPA and other therapeutics in order to develop potential therapeutic strategies with high translational impact.

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“…Blood gases and pH were maintained within normal ranges (Table 1). CBF was continuously measured using laser Doppler flowmetry (Perimed Periflux 5010 Laser Doppler System, North Royalton, OH, USA), as previously described (Cipolla et al, 2001;Cipolla and Godfrey, 2010). Briefly, the flow probe was affixed over a thinned area of skull posterior to the coronal suture and lateral to the sagittal suture over the MCA perfusion domain.…”

Section: Peroxynitrite Decomposition Catalyst Treatmentmentioning

confidence: 99%

Peroxynitrite Decomposition with FeTMPyP Improves Plasma-Induced Vascular Dysfunction and Infarction during Mild but not Severe Hyperglycemic Stroke

Palomares

Gardner‐Morse

Sweet

et al. 2012

J Cereb Blood Flow Metab

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We investigated mechanisms by which circulating factors during hyperglycemic (HG) stroke affect cerebrovascular function and the role of peroxynitrite in stroke outcome. Middle cerebral arteries (MCAs) were isolated from male Wistar rats and perfused with plasma from rats that were hyperglycemic for 5 to 6 days by streptozotocin and underwent either MCA occlusion (HG MCAO) or Sham surgery (HG Sham) compared with MCA perfused with physiologic saline (No plasma). Myogenic responses and endothelial function were compared in untreated MCA (n = 8/group) or with inhibitors of NADPH oxidase (apocynin; n = 8), peroxynitrite (FeTMPyP; n = 8) or endothelin-1 (ET-1) A (BQ-123; n = 8). Finally, animals were treated in vivo before reperfusion after mild ( < 68% cerebral blood flow (CBF) decrease) or severe ( > 68% CBF decrease) MCAO with FeTMPyP (n = 12) or vehicle (n = 12) and CBF and infarction measured. The HG MCAO plasma increased tone in MCA versus No plasma (P < 0.05) that was reversed by FeTMPyP, but not by apocynin or BQ-123. The HG Sham plasma also increased tone in MCA (P < 0.05) that was reversed by BQ-123 only. In vivo, FeTMPyP was neuroprotective during mild, but not severe ischemia. These results show that circulating factors in plasma can affect cerebrovascular function through peroxynitrite generation and ET-1. In addition, peroxynitrite decomposition improves stroke outcome acutely during mild, but not severe HG ischemia.

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Effect of Hyperglycemia on Brain Penetrating Arterioles and Cerebral Blood Flow Before and After Ischemia/Reperfusion

Cited by 27 publications

References 42 publications

Hyperglycaemia in acute lacunar stroke: A Chinese hospital-based study

Hyperglycaemia in acute lacunar stroke: A Chinese hospital-based study

Hyperglycemia, Acute Ischemic Stroke, and Thrombolytic Therapy

Peroxynitrite Decomposition with FeTMPyP Improves Plasma-Induced Vascular Dysfunction and Infarction during Mild but not Severe Hyperglycemic Stroke

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