Postischemic generation of superoxide anion by newborn pig brain

Armstead, William M.; Mirro, R.; Busija, David W.; Leffler, Charles W.

doi:10.1152/ajpheart.1988.255.2.h401

Cited by 100 publications

(110 citation statements)

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“…After ischemia and reperfusion, in piglets, the major deficit appears to be the lack of increased production of vasodilator prostanoids to hypercapnia rather than impaired vascular response to prostanoids that are applied locally (4). Our finding of preserved CBF response to hypercapnia after ischemia in piglets receiving PEG-SOD is consistent with the hypothesis that oxygen radicals produced during ischemia and reperfusion (8,16) can lead to inhibition of cyclooxynenase activity with decreased vostischemic production of vasodilator prostanoids. This finding implies that oxygen radical injury in brain occurs during reperfusion and that PEG-SOD is able to at least partially access one site of oxygen radical production that affects vascular smooth muscle during ischemia and reperfusion.…”

Section: Ischrmiasupporting

confidence: 90%

Polyethylene Glycol-Conjugated Superoxide Dismutase Improves Recovery of Postischemic Hypercapnic Cerebral Blood Flow in Piglets

et al. 1993

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Section: Ischrmiasupporting

confidence: 90%

Polyethylene Glycol-Conjugated Superoxide Dismutase Improves Recovery of Postischemic Hypercapnic Cerebral Blood Flow in Piglets

et al. 1993

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“…The differences in results could be due to the magnitude or location of the damage. Clearly, ischemia followed by reperfusion immediately exposes all cerebral neurons, glial cells, and blood vessels to major changes in their environment, 17 while topical application of blood exposes a more limited population of cells on the cortical surface to potentially damaging conditions. Thus, our results indicate that the presence of blood by itself is not detrimental to cerebrovascular function, at least in the short term.…”

Section: Discussionmentioning

confidence: 99%

Selective attenuation by perivascular blood of prostanoid-dependent cerebrovascular dilation in piglets.

Busija

Leffler

1991

Stroke

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Cerebral hemorrhagic insults are common in neonates. However, the consequences of intracranial blood on cerebral hemodynamics are poorly understood. We examined the effects of perivascular blood on cerebrovascular dilator responses in 29 piglets. Fresh, autologous blood (n=15) or cerebrospinal fluid (n = 14) was placed under the dura mater over the parietal cortex, and the piglets were allowed to recover from anesthesia. One to four days later, a closed cranial window was placed over the parietal cortex and pial arteriolar responses to arterial hypercapnia (Paco 2 >55 mm Hg), hemorrhagic hypotension (mean arterial blood pressure <35 mm Hg), or topical application of 10~6 and 10* M isoproterenol were determined. Pial arterioles in the cerebrospinal fluid group dilated 27±4% (mean±SEM) (n=ll) in response to hypercapnia, 26±5% (n=9) in response to hypotension, and 26±3% in response to 10~6 M and 40±4% in response to 10~4 M isoproterenol (n=ll). In the group in which blood was placed on the parietal cortex, pial arterioles did not dilate significantly in response to hypercapnia (8 ±3%, n = l l ) or hypotension (2±5%, t=13) but dilated normally in response to isoproterenol (25±5% in response to 10" 6 M and 36±7% in response to 10~4 M, n = 13). We conclude that prolonged contact of pial arterioles with extravascular blood selectively attenuates cerebrovascular dilation in piglets. (Stroke 1991 £2:484-488) I ntracranial hemorrhage (ICH) is a serious problem in preterm and full-term infants. The most common types are subdural, primary subarachnoid, intraparenchymal, and intraventricular hemorrhages.1 -4 Depending on the location and extent of bleeding, the neurologic sequelae can be quite serious. Several mechanisms contribute to immediate and later derangements of cerebral blood flow (CBF). First, rupture of arteries and capillaries leads to ischemia in areas served by those vessels. Second, increased intracranial pressure due to blood and edema causes extraluminal compression of vessels, which can reduce CBF. Third, the presence of blood and/or macrophages leads to production of substances that could damage vessels and, consequently, alter cerebral vascular responsiveness. For example, we have shown that fresh, Supported by grants HL-30260 and HL-34059 from the National Institutes of Health Heart, Lung, and Blood Institute.Address for reprints: David W. Busija, PhD, Department of Physiology and Pharmacology, Bowman Gray School of Medicine, 300 South Hawthorne Road, Winston-Salem, NC 27103.Received September 11, 1990; accepted December 18, 1990. autologous blood placed on the brain surface generates superoxide anion in piglets, 5 and free radicals have been implicated in the altered responsiveness of cerebral resistance vessels. -7In adult animal models of ICH, the perivascular presence of blood alters cerebrovascular responsiveness. 8 -12 In particular, responses involving endothelium-derived relaxing factor (EDRF) and arterial hypercapnia 13 can be reduced. On the other hand, little is known concerning the effect...

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“…Indomethacin, which decreases ROS production in newborn piglet brain after ischemia (2) and asphyxia (26), has been shown to preserve the NMDA response after asphyxia (12), ischemia (18), and hypoxia (4). Similar protective effects have been obtained following administration of superoxide dismutase (4) or the selective blockade of COX-2.…”

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confidence: 77%

“…However, vascular responses to NO remain intact, indicating that the attenuation of NMDA vascular responsiveness that follows hypoxia or ischemia is due to effects from the insult that occurs at the level of the neurons (13,16). These local neuronal effects appear to involve events related to the production of superoxide anion and other reactive oxygen species (ROS) via the activated cyclooxygenase (COX) pathway and from damaged mitochondria (2,4,5,16,17,26,29).…”

mentioning

confidence: 99%

Effects of hypothermia on neuronal-vascular function after cerebral ischemia in piglets

Perciaccante

Domoki

Puskar

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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We determined whether cerebral arteriolar dilation to N-methyl-d-aspartate (NMDA), a response dependent on stimulation of cortical neurons and inhibited by anoxic stress, would be preserved by hypothermia during and following ischemia. Pial arteriolar diameters in anesthetized piglets were determined via intravital microscopy. Arteriolar responses to NMDA (10, 50, and 100 μmol/l) were measured before and 1 h after 10 min of global ischemia. Piglets were exposed to either total body or selective brain cooling (33–34°C). Arteriolar dilation to lower doses or to 100 μmol/l NMDA was not affected by hypothermia alone (51 ± 3 vs. 46 ± 7%, normothermia vs. hypothermia; n = 7) in nonischemic animals. However, arteriolar responses to 100 μmol/l NMDA were clearly attenuated after ischemia despite body cooling during ischemia (53 ± 3 vs. 32 ± 6%; n = 8), hypothermia during ischemia and early reperfusion (49 ± 10 vs. 20 ± 3%; n = 8), or selective brain cooling (48 ± 5 vs. 20 ± 5%; n = 10). In contrast, pretreatment with indomethacin resulted in complete preservation of NMDA-induced vasodilation after ischemia. Thus, hypothermia fails to protect against neuronal dysfunction during ischemia.

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Postischemic generation of superoxide anion by newborn pig brain

Cited by 100 publications

References 0 publications

Polyethylene Glycol-Conjugated Superoxide Dismutase Improves Recovery of Postischemic Hypercapnic Cerebral Blood Flow in Piglets

Polyethylene Glycol-Conjugated Superoxide Dismutase Improves Recovery of Postischemic Hypercapnic Cerebral Blood Flow in Piglets

Selective attenuation by perivascular blood of prostanoid-dependent cerebrovascular dilation in piglets.

Effects of hypothermia on neuronal-vascular function after cerebral ischemia in piglets

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