Adrenergic vasoconstrictor activity in the cerebral circulation after inhibition of nitric oxide synthesis in conscious goats

The interaction between nitric oxide (NO) and adrenergic activity in the cerebral circulation was studied using conscious goats, where blood flow to one brain hemisphere (cerebral blood flow) was electromagnetically measured, and the effects of phentolamine and hexamethonium on cerebrovascular resistance were evaluated before (control) and after inhibition of NO synthesis with NW-nitro-L-arginine methyl ester (L-NAME). L-NAME (12 goats, 40 mg kg(-1) administered i.v.) reduced cerebral blood flow from 62 +/- 3 to 44 +/- 2 ml min(-1), increased mean systemic arterial pressure from 100 +/- 3 to 126 +/- 4 mm Hg, decreased heart rate from 79 +/- 5 to 50 +/- 4 beats min(-1) and increased cerebrovascular resistance from 1.63 +/- 0.08 to 2.91 +/- 0.016 mm Hg ml(-1)min(-1) (all P < 0.01). These hemodynamic variables normalized 48-72 h after L-NAME administration. Phentolamine (six goats, 1 mg), injected into the cerebral circulation. increased cerebral blood flow without changing systenic arterial pressure, but its cerebrovascular effects were augmented for about 24 h after L-NAME. The decrements in cerebrovascular resistance induced by phentolamine, in mm Hg ml(-1) min(-1), were: under control, 0.42 +/- 0.05; immediately after L-NAME, 1.38 +/- 0.09 (P < 0.01 compared with control); by about 24 h after L-NAME, 0.71 +/- 0.09 (P < 0.05 compared with control); and by about 48 h after L-NAME, 0.40 +/- 0.07 (P > 0.05 compared with control). Hexamethonium (six goats, 0.5-1 mg kg(-1) min(-1) i.v.) decreased mean systemic arterial pressure to about 75 mm Hg and caused tachycardia similarly before and after L-NAME, but the decrements in cerebrovascular resistance were augmented for about 24 h after L-NAME. The decrements in cerebrovascular resistance induced by hexamethonium, in mm Hg ml(-1).min(-1), were: under control. 0.61 +/- 0.09, immediately after L-NAME, 1.33 +/- 0.16 (P < 0.01 compared with control); by about 24 h after L-NAME, 1.18 +/- 0.10 (P < 0.01 compared with control): and by about 48 h after L-NAME, 0.99 +/- 0.10 (P > 0.05 compared with control). Therefore, these results suggest that adrenergic vasoconstrictor tone in cerebral vasculature may be augmented after inhibition of NO synthesis, and that this increment may contribute to the reduction of cerebral blood flow after inhibition of NO formation.     

Preservation of autoregulatory cerebral vasodilator responses to hypotension after inhibition of nitric oxide synthesis

Effects of inhibition of nitric oxide (NO) synthesis on the cerebrovascular autoregulatory vasodilator response to hypotension were studied in conscious rats. Cerebral blood flow (CBF) was determined with [¹⁴C]iodoantipyrine in a saline-treated control group and in three groups following inhibition of NO synthase activity by twice daily intraperitoneal injections of 50 mg/kg ofN^G-nitro-l-arginine methyl ester (l-NAME) for four days. In the saline-control group (n = 8) and in thel-NAME-treated Group (a) (n = 8) CBF was determined while systemic mean arterial blood pressure (MABP) remained at its resting level (means ± S.D., 128±6 and 151±11 mmHg, respectively). In the other groups CBF was determined after MABP was reduced by blood withdrawal to 118±9 and 88±8 mmHg in Groups (b) (n = 8) and (c) (n = 8), respectively. Despite the elevated MABP, global CBF was significantly lower inl-NAME-treated Group (a) than in the saline-controls (P < 0.005), indicating cerebral vasoconstriction striction resulting from inhibition of NO synthesis. Global CBF was not significantly reduced further in the two groups with hypotension. Local CBF in the hypotensive rats showed no significant reductions below values inl-NAME-treated control rats (Group (a)) in 31 of 32 brain structures; the only exception was in the auditory cortex of the severely hypotensive rats (Group (c)). The autoregulatory mechanism for cerebral vasodilatation to compensate for reduced arterial blood pressure is maintained following inhibition of NO synthesis.     

Role of nitric oxide in the cerebral circulation during hypotension after hemorrhage, ganglionic blockade and diazoxide in awake goats

The role of nitric oxide in cerebrovascular response to hypotension was analyzed by evaluating the changes in cerebrovascular resistance after inhibition of nitric oxide synthesis with Nw-nitro-L-arginine methyl ester (L-NAME) during three types of hypotension in conscious goats. Blood flow to one brain hemisphere was electromagnetically measured, hypotension was induced by controlled bleeding, and by i.v. administration of hexametonium (ganglionic blocker) or of diazoxide (vasodilator drug), and L-NAME was injected by i.v. route (35 mg kg-1). Under control conditions (13 goats), L-NAME increased arterial pressure from 98 +/- 3 to 123 +/- 4 mmHg and decreased cerebral blood flow from 65 +/- 3 to 40 +/- 3 ml min-1 (all P < 0.001); cerebrovascular resistance increased from 1.52 +/- 0.04 to 3.09 +/- 0.013 mmHg ml-1 min-1 (P < 0.01) (delta = 1.59 +/- 0.12 mmHg ml-1 min-1). After bleeding (five goats), mean arterial pressure decreased to 60 +/- 4 mmHg and cerebral blood flow decreased to 37 +/- 4 ml min-1 (all P < 0.01); cerebrovascular resistance did not change (1.56 +/- 0.14 vs. 1.54 +/- 0.12 mmHg ml-1 min-1, P > 0.05). During this hypotension, L-NAME increased arterial pressure to reach the normotensive values an did not affect the hypotensive values for cerebral blood flow; cerebrovascular resistance increased from the hypotensive values to 2.91 +/- 0.19 mmHg ml-1 min-1 (P < 0.01) (delta = 1.37 +/- 0.16 mmHg ml-1 min-1), and this increment is comparable to that under control conditions (P > 0.05). Ganglionic blockade (six goats) decreased arterial pressure to 67 +/- 2 mmHg) and did not affect significantly cerebral blood flow; cerebrovascular resistance decreased from 1.71 +/- 0.11 to 1.05 +/- 0.09 mmHg ml-1 min-1 (P < 0.01). During this hypotension, L-NAME increased arterial pressure to 103 +/- 6 mmHg (P < 0.001), and did not affect cerebral blood flow; cerebrovascular resistance increased from the hypotensive values to 1.68 +/- 0.18 mmHg ml-1 min-1 (P < 0.01) (delta = 0.63 +/- 0.10 mmHg ml-1 min-1), and this increment was lower than under control conditions (P < 0.01). Diazoxide (six goats) decreased arterial pressure to 69 +/- 5 mmHg (P < 0.01) without changing cerebral blood flow; cerebrovascular resistance decreased from 1.89 +/- 0.11 to 1.16 +/- 0.14 mmHg ml-1 min-1 (P < 0.01). During this hypotension, L-NAME increased arterial pressure to 87 +/- 6 mmHg (P < 0.05) and did not affect the hypotensive values for cerebral blood flow (P > 0.05); cerebrovascular resistance increased from the hypotensive values to 1.53 +/- 0.13 mmHg ml-1 min-1 (P < 0.05) (delta = 0.36 +/- 0.06 mmHg-1 ml-1 min-1), and this increment was lower than under control conditions (P < 0.01). Therefore, the role of nitric oxide in cerebrovascular response to hypotension may differ in each type of hypotension, as this role during hemorrhagic hypotension may not change and during hypotension by ganglionic blockade or diazoxide may decrease. These differences may be related to changes in nitric oxide release as stimuli on the endothelium (shear stress and sympathetic activity) may vary in each type of hypotension.     

实验性脑血管痉挛时一氧化氮与超氧化物歧化酶对脑血流的作用研究

目的 探讨一氧化氮（ＮＯ）、超氧化物歧化酶（ＳＯＤ）分别及联合使用对大鼠实验性蛛网膜下腔出血（ＳＡＨ）后脑血管痉挛（ＣＶＳ）时脑血流（ＣＢＦ）的作用。方法 将３０只大鼠随机分成５组（每组６只）。Ａ组：假手术＋盐水,Ｂ组：ＳＡＨ＋盐水;Ｃ组：ＳＡＨ＋ＳＯＤ;Ｄ组：ＳＡＨ＋ＮＯＣ１２;Ｅ组：ＳＡＨ＋ＳＯＤ、ＮＯＣ１２。模拟制成４８ｈ后,通过Ｌａｓｅ－Ｄｏｐｐｌｅｒ血液仪观察各种药物持续静脉注射１ｈ内Ｃ     

Effects of hypoglycemia on the cerebral circulation in awake goats.

We electromagnetically measured blood flow to one cerebral hemisphere and determined cerebrovascular reactivity to vasoconstrictor and vasodilator stimuli during normoglycemia and insulin-induced hypoglycemia in unanesthetized goats. Control blood glucose concentration was 84 +/- 4 mg, and insulin, injected intravenously, decreased glycemia with a concomitant increment in cerebral blood flow and reduction in cerebrovascular resistance in all the animals. When glycemia decreased to 60 to 65 mg/dl, the animals began to show signs of increased adrenergic activity, and when it decreased to less than 30 mg/dl, they showed signs of CNS depression. Cerebral blood flow began to rise significantly at a glycemia of 50 to 55 mg/dl, and progressively increased to reach an increment of 36% +/- 4% when glycemia was less than 30 mg/dl. Norepinephrine (0.3 to 9 micrograms), tyramine (50 to 500 micrograms), and 5-hydroxytryptamine (0.1 to 9 micrograms) reduced cerebral blood flow, and this effect was lower during severe hypoglycemia. Acetylcholine (0.01 to 1 microgram), isoproterenol (0.03 to 3 micrograms), diazoxide (0.3 to 9 mg), and inhalation of 10% CO2 in air increased cerebral blood flow, and this effect was also lower during severe hypoglycemia. The results show that insulin-induced hypoglycemia causes cerebral vasodilation and reduction of the capacity of cerebral blood vessels to constrict and dilate. They also show that the glycemic thresholds for increasing cerebral blood flow are near to, or slightly lower than, the thresholds for hypoglycemic symptoms. This experimental model of hypoglycemia closely resembles the conditions in hypoglycemic patients and permits serial evaluation of the cerebrovascular effects of hypoglycemia without using anesthesia.     

Effects of shear stress on nitric oxide levels of human cerebral endothelial cells cultured in an artificial capillary system

Nitric oxide (NO) is an important vasodilator with various activities in the cerebral vasculature. Although the response of NO levels to shear stress has been investigated in various models using systemic endothelium, no study has evaluated human cerebral endothelial cells (HCE). We determined the NO levels of HCE cultured in an artificial capillary system in response to changes in shear stress. With direct measurement by a porphyrinic microsensor, we found that NO levels increased immediately with a peak at 7 h after changes in shear stress, and by 24 h dropped to a constant elevated baseline. Shear stress-mediated increases in NO levels were confirmed by the measurement of citrulline, an indirect measure of NO. Furthermore, NO levels by HCE were shown to decrease with decreasing shear stress levels. This study presents a novel system to study NO production by microvascular HCE, and indicates a linear relationship between shear stress and NO levels. As cerebral vessels age and lose transmural compliance, shear stress-mediated production of NO may play a greater role in cerebrovascular function and dysfunction.     

7-nitroindazole reduces cerebral blood flow following chronic nitric oxide synthase inhibition

Blood flow and glucose utilization were measured in rat brain after chronic L-NAME treatment followed by acute 7-nitroindazole. Following chronic L-NAME, blood flow was not significantly different from control. Treatment with acute 7-nitroindazole reduced blood flow to the same extent in both chronic saline and L-NAME groups. Glucose utilization was unaffected. These results suggest that residual NOS activity in brain is sufficient to provide tonic, NO-dependent cerebrovascular dilator tone.     

Role of nitric oxide in cerebrovascular reactivity to NMDA and hypercapnia during prenatal development in sheep

Cerebral vasodilatory responses evoked by activation of NMDA receptors and by hypercapnia are important factors in the integrated vascular response to perinatal cerebral ischemia. Cerebral vasodilation to NMDA is mediated by nitric oxide in adult and newborn animals, whereas vasodilation to hypercapnia is thought to become modulated by nitric oxide, at least in swine, after the newborn period. The developmental role of nitric oxide in the cerebral blood flow response to NMDA and hypercapnia was investigated at mid- and late gestation in fetal sheep. Superfusion of 300microM NMDA over the cerebral cortex through a closed cranial window on the exteriorized head of an anesthetized fetus increased laser-Doppler flow by 41+/-7% (+/-S.E.) at 0.65 gestation. The increase was reduced by superfusion of a nitric oxide synthase inhibitor (18+/-8%). At 0.9 gestation, the response to NMDA was augmented (85+/-24%) compared to that at 0.65 gestation and was reduced by a nitric oxide synthase inhibitor (32+/-6%). In unanesthetized fetal sheep, hypercapnic reactivity of microsphere-determined cerebral blood flow was not significantly attenuated by nitric oxide synthase inhibition at 0.65 gestation (4.6+/-0.7 to 3.7+/-1.0% change/mmHg pCO2) or at 0.9 gestation (4.0+/-0.7 to 3.5+/-0.9% change/mmHg pCO2). Therefore, nitric oxide-dependent cerebrovascular dilation to NMDA-receptor activation is present as early as 0.65 gestation in fetal sheep and increases further during the last trimester, whereas vasodilation to hypercapnia remains unchanged and independent of nitric oxide during the last trimester. Hence, cerebrovascular reactivities to different stimuli do not mature concurrently.     

Inhibition of nitric oxide synthesis extends cerebrovascular autoregulation during hypertension

In anesthetized intact rats, cerebral blood flow is autoregulated until mean arterial blood pressure (MAP) exceeds 150 mmHg. At higher pressures cerebral blood flow breaks through autoregulation and rapidly increases. However, interruption of the arterial baroreceptor reflex eliminates breakthrough of autoregulation. Thus, breakthrough may reflect active rather than passive vasodilatation. We, therefore, sought to determine if breakthrough depends upon synthesis of the vasodilator nitric oxide. Thirty-eight anesthetized adult male Sprague-Dawley rats were studied. In all, MAP was raised by slow i.v. infusion of phenylephrine. In rats pretreated with the nitric oxide synthase inhibitor L-nitroarginine (L---NA; 22 mg/kg i.v.) or with a combination of L---NA plus D-arginine (D---Arg; 240 mg/kg i.v.), breakthrough did not occur even when MAP exceeded 185 mmHg (L---NA) and 165 mmHg (D---Arg). In contrast, breakthrough occurred in rats treated with L---NA plus L-arginine (L---Arg; 240 mg/kg i.v.) and in rats whose basal vascular tone had been increased by pretreatment with arginine vasopressin prior to infusion of phenylephrine. Removal of sympathetic innervation to cerebral vessls attenuated, but did not eliminate, effects of L---NA on breakthrough. Thus, vasodilatation seen with breakthrough of autoregulation depends upon release of nitric oxide or a nitric oxide donor.     

脑梗死患者脑血管反应性研究

目的应用经颅多普勒超声结合屏气试验评价脑梗死患者的脑血管反应性（CVR）。方法采用经颅多普勒超声结合屏气试验检测30例急性期颈内动脉系统脑梗死患者,30例急性期腔隙性脑梗死患者的屏气指数（BHI）,并与60例健康者进行对比。结果急性期颈内动脉系统脑梗死患者和腔隙性脑梗死患者屏气指数均显著低于对照组,颈内动脉系统脑梗死侧显著低于对侧和腔隙性脑梗死患者。结论脑血管反应性与脑梗死有密切关系,检测脑血管反应性对于预测脑卒中风险至关重要。     

慢性脑供血不足患者的脑血流及颈动脉粥样硬化研究

目的研究慢性脑供血不足患者的脑血流及颈动脉粥样硬化特点.方法分别对100例慢性脑供血不足患者和100例正常对照者及100例脑梗死患者行颈动脉彩色多普勒及经颅多普勒检查,并测量相关指标.结果观察组颈动脉粥样斑块发生率为60%,内膜粗糙率为31%,颈动脉内膜中层厚度＞1.00 mm者占24%,颈动脉狭窄率为23%,颅内血流异常率为60%,颅内血管狭窄率为16%,而正常对照组分别为18%,4%,4%,6%,8.1%,4.8%;脑梗死对照组分别为90%,62%,51%,45%,88.9%,50%,观察组与正常对照组比较有显著差异(P＜0.01),脑梗死对照组与观察组比较也有显著差异(P＜0.01).结论慢性脑供血不足是动脉粥样硬化过程的一个阶段,是缺血性脑卒中的预兆.     

Evaluation of cerebral circulation and oxygen metabolism in infants using near-infrared light

Bedside monitoring of cerebral circulation or oxygen metabolism in infants to appropriately manage circulation and establish the oxygen dose, aiming at improving the neurological prognosis, is needed in general clinical practice. Near-infrared spectroscopy is used for measurements of neonatal cerebral Hb oxygen saturation, cerebral blood volume, cerebral blood flow and cerebral metabolic rate of oxygen. Near-infrared time-resolved spectroscopy is particularly useful for bedside evaluation of cerebral circulation and oxygen metabolism because of its simple measurement procedure. Combined evaluation of cerebral blood volume and cerebral Hb oxygen saturation is expected to contribute to treatment centering on the brain in neonatal medical care.     

An experimental study on the effects of DMSO and indomethacin on cerebral circulation and intracranial pressure

Albino rabbits with a cryogenic lesion to the left parieto-occipital cortex had cerebral blood flow studies (CBF) with the hydrogen clearance technique 24 hours after the insult. Similar subgroups were treated with DMSO (1 g/kg) bolus, DMSO (2 g/kg) infusion, indomethacin (20 mg/kg) bolus, and indomethacin followed by DMSO. Following DMSO bolus administration there was an immediate rise in CBF over both hemispheres, with a significant paradoxical decrease at 30 minutes, followed by a second smaller rise at 60 minutes. With DMSO infusion, the rise in CBF was sustained throughout the infusion period with no paradoxical decrease. With indomethacin there was an initial decrease immediately following the drug, and at 60 minutes there was a rise in the insulted left hemisphere, more than the right one. Indomethacin administration 15 minutes prior to DMSO failed to halt the immediate increase in CBF noted following DMSO bolus injection. These results, together with the changes that occurred in intracranial pressure and brain water content, are analyzed.     

The role of nitric oxide in the regulation of cerebral blood flow

The role of nitric oxide in the cerebral circulation under basal conditions and when exposed to hypoxic, hypercapnic and hypotensive stimuli, was studied in mechanically ventilated rats using a venous outflow technique, by examining the effects of inhibition of nitric oxide synthase with N-nitro-l-arginine methyl ester (l-NAME).l-NAME (10 or 30 mg/kg injected intravenously) raised mean arterial blood pressure by 14% and 24%, and increased cerebrovascular resistance (CVR) by 20% and 24%, respectively. Cerebral blood flow (CBF) was unaltered, as were blood gases and pH. The increases in MABP and CVR were attenuated byl-arginine (300 mg/kg). Following the administration ofl-NAME, the increases in CBF elicited by ventilation with 8% oxygen for 25 s were unaltered, in comparison to control responses.l-NAME attenuated the increases in CBF and reduced the time for recovery to basal flow rates evoked by ventilation with 10% carbon dioxide. These effects were reversed byl-, but not byd-, arginine. Autoregulation by CBF during hypotensive episodes, as measured by comparisons of CVR values, was unaffected byl-NAME. The results suggest that endogenous nitric oxide is involved in the responses of the cerebral vasculature to elevated levels of CO₂ in the arterial blood. Nitric oxide does not appear to play a major role in autoregulation to increases or decreases in MABP, or in hypoxia-evoked vasodilation.     

Effects of transient loss of shear stress on blood-brain barrier endothelium: role of nitric oxide and IL-6

Loss of blood-brain barrier (BBB) function may contribute to post-ischemic cerebral injury by yet unknown mechanisms. Ischemia is associated with anoxia, aglycemia and loss of flow (i.e. shearing forces). We tested the hypothesis that loss of shear stress alone does not acutely affect BBB function due to a protective cascade of mechanisms involving cytokines and nitric oxide (NO). To determine the relative contribution of shear stress on BBB integrity we used a dynamic in vitro BBB model based on co-culture of rat brain microvascular endothelial cells (RBMEC) and astrocytes. Trans-endothelial electrical resistance (TEER), IL-6 release and NO levels were measured from the lumenal and ablumenal compartments throughout the experiment. Flow-exposed RBMEC were challenged with 1 h of normoxic-normoglycemic flow cessation (NNFC) followed by reperfusion for 2 to 24 h. NNFC caused a progressive drop in nitric oxide production during flow cessation followed by a time-dependent increase in ablumenal IL-6 associated with a prolonged NO increase during reperfusion. The nitric oxide synthetase (NOS) inhibitor L-NAME (10 microM) abrogated all effects of NNFC, including changes in NO and cytokine production. BBB permeability did not increase during or after NNFC/reperfusion, but was increased by treatment with L-NAME or when the effects of IL-6 were blocked. Flow adapted RBMEC and astrocytes respond to NNFC/reperfusion by overproduction of IL-6, possibly secondary to increased production of NO during the reperfusion. Maintenance of BBB function during and following NNFC appears to depend on intact NO signaling and IL-6 release.     

Transient cerebral vasodilatory effect of neuropeptide y mediated by nitric oxide

The effects of intracarotidly injected neuropeptide Y (NPY; 0.1 μg/kg) on the local cerebral blood volume (CBV) and blood flow (CBF) in the parieto-temporal cortex were examined by the photoelectric method in 17 anesthetized cats. CBV reflects the cumulative crosssectional area of the cerebral microvascular beds. NPY immediately caused transient but significant increases in CBV and CBF, which lasted for less than 5 min. Thereafter, CBV returned to and remained at the control level, although CBF was decreased by 30–40% for 60 min during the monitoring period. The CBV increases after NPY were prevented by a 15-min preinjection of 0.35 mg/kg/min of N^g-monomethyl-L-arginine (L-NMMA), which is a competitive blocker of nitric oxide synthesis. The CBV increases after NPY reappeared following a 15-min administration of 0.25 mg/kg/min of L-arginine, which is a precursor of nitric oxide. We conclude that NPY administered in vivo exerts a previously unreported effect of transient vasodilatation on the cerebral microvessels. This action appears to be mediated by nitric oxide, which is a major candidate as an endothelium-derived relaxing factor (EDRF).     

Role of nitric oxide in regulation of cerebral microvascular tone and autoregulation of cerebral blood flow in cats

The role of nitric oxide in the regulation of cerebrocortical microvascular tone and autoregulation of cerebral blood flow (CBF) was examined in 24 anesthetized cats. The local cerebral blood volume (CBV), mean transit time of blood (MTT), and CBF in the cortex were measured by our photoelectric method. CBV represents the cumulative dimensions of the cerebral microvessels. Intravenous injection of 0.35–0.7 mg/kg/minN^G-monomethyl-l-arginine (l-NMMA), an inhibitor of nitric oxide synthesis, significantly increased mean arterial blood pressure (MABP; 8.4–14.1%,P < 0.01), decreased CBV (15.2–28.7%,P < 0.01), and decreased CBF (20.0–29.8%,P < 0.01) in a dose-related manner. The changes in MABP, CBV, and CBF elicited byl-NMMA were inhibited (P < 0.05) by simultaneous infusion of 35 mg/kg/minl-arginine. Autoregulation of CBF was examined during controlled hypotension of −30 to −40 mmHg (artificial bleeding) and recovery of blood pressure (reinfusion of blood). Although CBF remained constant with blood pressure changes in the control state (ΔCBF/ΔMABP of 0.037±0.155 with hypotension), CBF became dependent on blood pressure changes (ΔCBF/ΔMABP of 0.478±0.135, P < 0.05) during infusion of 0.35 mg/kg/minl-NMMA. It is concluded that nitric oxide participates in both the regulation of basal tone of cerebral microvessels and the autoregulation of CBF.     

大鼠脑缺血再灌流脑区一氧化氮变化的研究

目的研究大鼠脑缺血及再灌流后脑部一氧化氮的变化。方法采用荧光法和放射免疫法测定４个脑区一氧化氮（ＮＯ）代谢产物ＮＯ２和环磷酸鸟苷（ｃＧＭＰ）。结果脑缺血１０ｍｉｎ,各脑区ＮＯ２和ｃＧＭＰ含量明显增高;脑缺血３０ｍｉｎ,各脑区ＮＯ２和ｃＧＭＰ含量开始下降。缺血１０ｍｉｎ再灌流１５ｍｉｎ以及缺血３０ｍｉｎ再灌流１５ｍｉｎ,各脑区ＮＯ２和ｃＧＭＰ含量再次增加,与单纯脑缺血组相比,有显著差异性（Ｐ＜０．０５或Ｐ＜０．０１）。结论ＮＯ参与了脑缺血再灌流的损伤过程