Primate brain tolerance to temporary focal cerebral ischemia during isoflurane- or sodium nitroprusside-induced hypotension

Isoflurane has properties that suggest it may provide cerebral protection from ischemia. This study compared, in primates, neurologic outcome after a 45-min period of temporary focal ischemia during hypotension induced with either isoflurane or sodium nitroprusside (SNP). Fourteen macaque monkeys were studied. Seven animals received halothane and seven isoflurane anesthesia during surgical preparation. After transorbital exposure of the middle cerebral artery (MCA), in the halothane group, the inspired halothane was reduced to 0.75% and the mean blood pressure (BP) reduced to 50 mmHg by the infusion of SNP. In the isoflurane group, the isoflurane was titrated to reduce mean BP to 50 mmHg. Stable hypotension was maintained for 90 min, which included a 45-min period of MCA occlusion. Monitoring included intraarterial blood pressure, arterial blood gases, EEG, somatosensory evoked potentials (SEP), and temperature. After the procedure the animals were allowed to awaken and were assessed neurologically every 8 h. On the third postoperative day, they were reanesthetized and underwent magnetic resonance imaging (MRI) and SEP recording. Thereafter, they were killed with iv KCl and the brains fixed for neuropathology. All animals survived the surgical procedure, but two animals receiving halothane and none receiving isoflurane died prematurely (P less than 0.2). The SEP disappeared in all animals within 10 min of MCA occlusion and then returned partially or completely. There was no difference between groups in neurologic scores, in the size of the lesion as assessed by MRI (isoflurane 15.7 +/- 6%, halothane/SNP 10.5 +/- 4%), or in the extent or severity of the neuropathologic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral blood flow and cerebral oxygen consumption during nitroprusside-induced hypotension to less than 50 mmHg

The authors determined the effect of profound induced hypotension (i.e., mean arterial blood pressure less than 50 mmHg) during craniotomy for cerebral aneurysm on cerebral blood flow and cerebral metabolic rate for oxygen before, during, and after (20 min and 40 min after) the hypotensive period. The study was performed on nine adults (mean age, 29.2 yr) who were awake and conscious without peripheral neurologic deficits at the time of surgery. The study was conducted with the dura open with the use of a radial artery cannula, a 7-Fr thermodilution flow-directed pulmonary artery catheter, and an internal jugular vein catheter. The 133xenon intraarterial injection technique was used to determine regional cerebral blood flow (rCBF) in the nonoperated hemisphere. rCBF remained unchanged (from 22.8 +/- 4.1 ml.100 g-1.min-1 to 23.8 +/- 4.6 ml.100 g-1.min-1) during the hypotensive period (MAP from 87.8 +/- 10.4 mmHg to 40.0 +/- 4.4 mmHg; P less than 0.001) despite an increase in cardiac index since cerebral perfusion pressure and cerebrovascular resistance decreased to a similar degree. No gross cerebral metabolic disturbances were observed. A period of decreased cerebrovascular resistance and increased rCBF followed induced hypotension. rCBF increased from 23.8 +/- 4.6 ml.100 g-1.min-1 to 30.0 +/- 5.8 ml.100 g-1.min-1 (P less than 0.001) 20 min after sodium nitroprusside (SNP) was stopped without rebound hypertension. These modifications disappeared 20 min later. Reduction of mean arterial blood pressure to 40 mmHg by SNP was apparently safe for the brain, although the possibility of low perfused regions and local brain and cerebrospinal fluid lactoacidosis, particularly in the retracted hemisphere, cannot be excluded.     

The influence of hyperoxic ventilation during sodium nitroprusside-induced hypotension on skeletal muscle tissue oxygen tension

BACKGROUND: Increasing inspired oxygen concentrations might provide a simple and effective intervention to increase oxygen tension in tissues during controlled hypotension. To test this hypothesis, the influence of hyperoxic ventilation (100% O2) on skeletal muscle oxygen partial pressure (Ptio2) in patients receiving sodium nitroprusside-induced controlled hypotension was studied. METHODS: Forty-two patients undergoing radical prostatectomy were prospectively studied and randomly divided into three groups as follows: (1) Controlled hypotension induced by sodium nitroprusside (mean arterial blood pressure, 50 mmHg) and hyperoxic ventilation (CH-100%; n = 14); (2) controlled hypotension and ventilation with 50% O2 in nitrous oxide (CH-50%; n = 14); and (3) standard normotensive anesthesia with 50% O2 in nitrous oxide (control; n = 14). Ptio2 values were measured continuously in all patients using implantable polarographic microprobes. Arterial blood gases and lactate concentrations were analyzed in 30-min intervals. RESULTS: Surgical blood loss and transfusion requirements were significantly reduced in both groups receiving hypotensive anesthesia. During surgery, arterial partial pressure of oxy-gen and arterial oxygen content were significantly higher in patients of the CH-100% group. Baseline values of Ptio2 were comparable between the groups (CH-50%: 25.0 +/- 0.7 mmHg; CH-100%: 25.2 +/- 0.2 mmHg; control: 24.5 +/- 0.2 mmHg). After a transient increase in Ptio2 in the CH-100% group during normotension, Ptio2 values returned to baseline and remained unchanged in the control group. Ptio2 decreased significantly during the hypotensive period in the CH-50% group. The lowest mean Ptio2 values were 15.0 +/- 4.1 mmHg in the CH-50% group, 24.2 +/- 4.9 mmHg in the CH-100% group, and 23.5 +/- 3.8 mmHg in the control group. There were no significant changes in lactate plasma concentrations in any group throughout the study period. CONCLUSIONS: Hyperoxic ventilation improved skeletal muscle tissue oxygenation during sodium nitroprusside-induced hypotension. This improved local tissue oxygenation seems to be most likely due to an increase in convective oxygen transport and the attenuation of hyperoxemia-induced arteriolar vasoconstriction by sodium nitroprusside.     

Monitoring of somatosensory evoked potentials during temporary arterial occlusion in cerebral aneurysm surgery

Somatosensory evoked potentials (SSEP) have been used during cerebral aneurysm surgery to monitor the integrity of neural pathways. The purpose of this study was to evaluate the effectiveness of SSEP monitoring as a predictor of neurological outcome during temporary arterial occlusion. In a series of 157 patients monitored, 97 patients had temporary occlusion of the feeding artery. Twenty-three patients developed a SSEP change during temporary occlusion, 15 reversible (recovery of the change after the release of occlusion), and 8 persistent (no recovery) changes. A persistent change predicted a postoperative neurological deficit in each case, whereas, of the 15 patients with reversible changes, only 5 had postoperative deficits. Seventy-four patients had no change on SSEP monitoring but 10 patients did have new neurological deficits postoperatively. The false positive rate was 43% and the false negative rate was 14%. SSEP was a better predictor of neurological deficits in patients with aneurysms of the carotid circulation than of the vertebral-basilar arteries. Despite these limitations, we find SSEP monitoring useful during temporary occlusion in cerebral aneurysm surgery.     

七氟醚和硝普钠控制性降压对患者一氧化氮、内皮素及氧自由基的影响

目的 探讨七氟醚和硝普钠(SNP)控制性降压对患者一氧化氮(NO)、内皮素(ET)和氧自由基的影响.方法 择期手术病人48例,年龄28～64岁,ASA Ⅰ或Ⅱ级,随机分为3组(n=16):七氟醚常压组(Ⅰ组)、七氟醚降压组(Ⅱ组)和SNP降压组(Ⅲ组).3组麻醉诱导后均吸入七氟醚1 MAC.手术开始后10 min,Ⅱ组吸入七氟醚浓度增加至3 MAC,Ⅲ组开始持续静脉输注0.01% SNP 2～5 μg·kg-1·min-1,使平均动脉压(MAP)快速降至基础值的60%-70%(55-73 mm Hg),再调整七氟醚呼气末浓度(1.87～2.54 MAC)和SNP输注速率(1.5～4 μg·ks-1·min-1)维持降压,降压40 min后,Ⅱ组七氟醚呼气末浓度降至0.8 MAC;Ⅲ组停止输注SNP,使血压很快升至降压前水平.分别于手术开始后10 min(降压前即刻,T0)、降压20 min(T1)、40 min(T2)和停止降压后20 min(T3)采集静脉血,测定血浆NO、ET、丙二醛(MDA)浓度及超氧化物歧化酶(SOD)活性.结果 与T0比较,Ⅰ组和Ⅱ组血浆NO浓度在T1～3时降低,Ⅲ组血浆NO浓度在T1,2时升高,Ⅲ组在T1,2时血浆ET浓度升高,3组在T1～3,时血浆MDA和SOD浓度均升高(P＜0.05或0.01);与Ⅰ组比较,Ⅱ组在T1,2时血浆NO浓度降低,Ⅲ组在T1～3时血浆NO浓度升高,Ⅲ组血浆ET浓度在T1～3时升高(P＜0.05),Ⅱ组各时点血浆NO浓度差异无统计学意义(P＞0.05);Ⅱ组在T1～3时血浆MDA和SOD水平升高(P＜0.05).结论 七氟醚控制性降压可降低患者血浆NO浓度,SNP控制性降压可升高血浆NO及ET浓度;七氟醚控制性降压及硝普钠控制性降压均可导致患者氧自由基生成增加,七氟醚控制性降压使氧自由基增加的程度更高.     

Chronic AT1-receptor blockade does not alter cerebral oxygen supply/demand ratio during cardiopulmonary bypass in hypertensive patients

Background: The angiotensin II receptor type 1 antagonist candesartan has been hypothesized to alter vasopressor requirements and brain–blood flow by changing cerebrovascular autoregulation. Therefore, we assessed the effects of a pre-anaesthetic treatment course with candesartan on cerebral arterial-jugular bulb oxygen content difference, middle cerebral artery blood velocity, and vasopressor requirements in hypertensive patients undergoing elective on-pump coronary artery bypass graft surgery.
Methods: In a randomized, double-blind, placebo-controlled study, we evaluated the effects of candesartan (8 mg po/d, given for 6–8 days before surgery) in 35 hypertensive patients. The mean arterial pressure was maintained above 60 mmHg by bolus administration of phenylephrine, if required, and dosages were recorded.
Results: Candesartan did not significantly alter oxygen content difference across the cerebral circulation, mean middle cerebral artery blood velocity during cardiopulmonary bypass, or phenylephrine requirements either before (0.0067 μg/kg/min±0.0042 vs. 0.0056 μg/kg/min±0.0049, P =0.48) or during cardiopulmonary bypass (0.0240 μg/kg/min±0.0240 vs. 0.0250 μg/kg/min±0.0190, P =0.97) compared with placebo.
Conclusion: Thus, a 6–8-day treatment course with candesartan does not alter global cerebral perfusion and oxygen supply/demand ratio during cardiopulmonary bypass, or vasopressor requirements in hypertensive patients undergoing on-pump coronary artery bypass graft surgery, and no deleterious consequences of AT1-receptor blockade were detected.     

Phenylephrine does not limit myocardial blood flow or oxygen delivery during isoflurane-induced hypotension in dogs.

Experiments were performed on seven fentanyl-pentobarbital-anesthetized, open-chest dogs to determine whether stimulation of coronary alpha 1-adrenergic receptors by phenylephrine causes coronary vasoconstriction and impaired myocardial oxygen delivery when phenylephrine is infused to correct isoflurane-induced hypotension. Myocardial blood flow was measured with radioactive microspheres, and myocardial oxygen and lactate extraction were determined. The Fick equation was used to calculate myocardial oxygen consumption. Measurements were obtained (a) under control conditions, (b) after a 30-min inhalation of isoflurane sufficient to decrease mean aortic pressure by 30%, and (c) while maintaining administration of isoflurane, 5-10 min after restoration of mean aortic pressure by intravenous infusion of phenylephrine. Isoflurane-induced hypotension was accompanied by a baroreceptor-mediated increase in heart rate and by a decrease in myocardial oxygen consumption; however, myocardial blood flow was maintained, resulting in decreased oxygen extraction and increased coronary sinus PO2, thus implying a direct coronary vasodilating effect for isoflurane. Lactate extraction was unaffected. Phenylephrine infusion during inhalation of isoflurane returned mean aortic pressure and heart rate to their respective control values, and it did not change myocardial oxygen consumption, myocardial blood flow, myocardial oxygen extraction, coronary sinus PO2, or lactate extraction from values obtained during isoflurane alone. These latter findings are consistent with undiminished coronary vasodilation by isoflurane in the presence of phenylephrine. In conclusion, infused phenylephrine to restore aortic pressure during isoflurane administration had no vasoconstrictor effect in the coronary circulation and did not impair myocardial oxygen delivery. Apparently, the direct coronary vasodilating action of isoflurane completely nullified phenylephrine-induced vasoconstriction via local alpha 1-adrenergic receptors.     

Changes in canine conjunctival and cerebral oxygen tension during hemorrhagic hypotension

On-line conjunctival oxygen tension (PcjO2) and cerebral cortical oxygen tension (PcxO2) were measured simultaneously using polarographic oxygen sensors during hemorrhagic hypotension in dogs. Mean arterial pressure (MAP) decreased from a control value of 119 +/- 7 to 52 +/- 1 (SEM) mmHg during initial bleeding of 30 minutes, and then this level of MAP was maintained for another 150min by adjusting the height of the reservoir. During the early phase of arterial hypotension, PcjO2 fell sharply, and this was accompanied by a parallel decrease of carotid artery blood flow and cardiac output, whereas PcxO2 remained unaffected with this level of hypovolemic hypotension which was possibly due to the cerebral tissue autoregulatory mechanism. Thus, it was demonstrated that despite the anatomical similarity and proximity of their blood supply, the conjunctival tissue responded differently to the intracranial cerebral tissues when compared during hemorrhagic hypotension. The study also suggests that monitoring the PcjO2 during surgery may be a useful monitoring tool in detecting early signs of tissue ischemia and hypoxia during hypovolemic shock.     

Posterior tibial nerve and median nerve somatosensory evoked potential monitoring during carotid endarterectomy

PURPOSE: Somatosensory evoked potential (SSEP) monitoring using the median nerve (MN) modality during carotid endarterectomy is well established. This study assessed the usefulness of monitoring the posterior tibial nerve (PTN) SSEP as an adjunct to MNSSEP for detection of cerebral ischemia and as an indicator for the insertion of a shunt in patients undergoing a carotid endarterectomy. METHODS: All patients undergoing carotid endarterectomy during three years who had routine bilateral MNSSEP were also monitored with bilateral PTNSSEP. Patients received a shunt if there was a significant change (> 50% decrease in amplitude of cortical peak (N20) in the MNSSEP after cross clamping. The incidence, timing, and duration of all PTNSSEP changes were compared to MNSSEP changes. RESULTS: One hundred fifty-three patients were studied. Significant changes in MNSSEP after cross clamp lead to insertion of a shunt in six patients. Changes in PTNSSEP occurred at almost the same time in three patients, four minutes before MNSSEP in one, three minutes later in one and no change in one patient. Good quality baseline tracings were obtained in 99% MNSSEP as compared to 88% PTNSSEP (P < 0.05). New postoperative neurological deficits occurred in four patients (2.6%), only one had significant evoked potential changes. CONCLUSION: Monitoring of PTNSSEP is feasible and may be considered for an adjunct to MNSSEP or as an alternative modality if there are difficulties with MNSSEP. However, there may be a greater incidence of poor quality baseline tracings for PTNSSEP.     

Reduced regional and global cerebral blood flow during fenoldopam-induced hypotension in volunteers.

Dopamine has a wide spectrum of receptor and pharmacologic actions that may affect cerebral blood flow (CBF). A new, selective dopamine-1 agonist, fenoldopam, is a potent systemic vasodilator with moderate alpha(2)-receptor affinity. However, the effects of fenoldopam on the cerebral circulation are undefined. We therefore hypothesized that infusion of fenoldopam would decrease mean arterial blood pressure (MAP) and might concurrently decrease CBF via vascular alpha(2)-adrenoreceptor activation in awake volunteers. We studied nine healthy normotensive subjects, using positron emission tomography to measure CBF in multiple cortical and subcortical regions of interest. In addition, bioimpedance cardiac output and middle cerebral artery blood flow velocity were determined during fenoldopam-induced hypotension. Three men and four women, aged 25-43 yr, completed the study. Fenoldopam infused at 1.3 +/- 0.4 microg. kg(-1). min(-1) (mean +/- SD) reduced MAP 16% from baseline: from 94 (89-100) mm Hg (mean [95% confidence interval]) to 79 [74-85] mm Hg (P < 0.0001). During the fenoldopam infusion, both cardiac output (+39%), and heart rate (+45%) increased significantly, whereas global CBF decreased from baseline, 45.6 [35.6-58.5] mL. 100 g(-1). min(-1), to 37.7 [33.9-42.0] mL. 100 g(-1). min(-1) (P < 0.0001). Despite restoration of baseline MAP with a concurrent infusion of phenylephrine, global CBF remained decreased relative to baseline values at 37.9 [34.0-42.3] mL. 100 gm(-1). min(-1) (P < 0.0001). Changes in middle cerebral artery velocity did not correlate with positron emission tomography-measured changes of CBF induced by fenoldopam, with or without concurrent phenylephrine. Implications: In awake volunteers with (presumably) intact cerebral autoregulation,fenoldopam-induced hypotension significantly decreased global cerebral bloodflow (CBF). Clinicians should be aware of these pharmacodynamic effects when choosing a vasodilator to control blood pressure, especially in situations where control of CBF, cerebral blood volume, and intracranial pressure are therapeutic priorities.     

Spinal and cortical somatosensory evoked potential monitoring during corrective spinal surgery with 108 patients

To reduce the incidence of neurologic complications following spinal surgery, somatosensory evoked potentials (SEPs) were monitored in 108 patients. An electrode with four in-line contacts was used to record spinal SEPs in the epidural space in 33 patients at locations both rostral and caudal to the surgical site. Cortical SEPs were successfully monitored in 107/108 patients and spinal SEPs in all 33 attempted epidurally. Spinal conduction velocities were found to range from 43.9 to 110.5 m/s depending on vertebral level and the time location of the measured peak in the response waveform. Frequency power spectra of the SEP waveforms were found to be a reliable adjunct to peak latency amplitude analysis in the time domain. Use of caudal and rostral epidural, subcortical, and cortical electrode sites were found to be the most reliable technique for the maximum patient safety.     

Comparison of transcranial electric motor and somatosensory evoked potential monitoring during cervical spine surgery

BACKGROUND: There has been little enthusiasm for somatosensory evoked potential monitoring in cervical spine surgery as a result, in part, of the increased risk of motor tract injury at this level, to which somatosensory monitoring may be insensitive. Transcranial electric motor evoked potential monitoring allows assessment of the motor tracts; therefore, we compared transcranial electric motor evoked potential and somatosensory evoked potential monitoring during cervical spine surgery to determine the temporal relationship between the changes in the potentials demonstrated by each type of monitoring and neurological sequelae and to identify patient-related and surgical factors associated with intraoperative neurophysiological changes. METHODS: Somatosensory evoked potential and transcranial electric motor evoked potential data recorded for 427 patients undergoing anterior or posterior cervical spine surgery between January 1999 and March 2001 were analyzed. All patients who showed substantial (at least 60%) or complete unilateral or bilateral amplitude loss, for at least ten minutes, during the transcranial electric motor evoked potential and/or somatosensory evoked potential monitoring were identified. RESULTS: Twelve of the 427 patients demonstrated substantial or complete loss of amplitude of the transcranial electric motor evoked potentials. Ten of those patients had complete reversal of the loss following prompt intraoperative intervention, whereas two awoke with a new motor deficit. Somatosensory evoked potential monitoring failed to identify any change in one of the two patients, and the change in the somatosensory evoked potentials lagged behind the change in the transcranial electric motor evoked potentials by thirty-three minutes in the other. No patient showed loss of amplitude of the somatosensory evoked potentials in the absence of changes in the transcranial electric motor evoked potentials. Transcranial electric motor evoked potential monitoring was 100% sensitive and 100% specific, whereas somatosensory evoked potential monitoring was only 25% sensitive; it was, however, 100% specific. CONCLUSIONS: Transcranial electric motor evoked potential monitoring appears to be superior to conventional somatosensory evoked potential monitoring for identifying evolving motor tract injury during cervical spine surgery. Surgeons should strongly consider using this modality when operating on patients with cervical spondylotic myelopathy in general and on those with ossification of the posterior longitudinal ligament in particular.     

Changes of latency and amplitude of short latency somatosensory evoked potentials during slow induction of anesthesia with sevoflurane

In the present study, changes of latency and amplitude of short latency somatosensory evoked potentials (SSEPs) were evaluated continuously during slow induction of anesthesia from sevoflurane awake to deep levels of anesthesia in eight scheduled surgical patients. Not consistent with other previous investigations, the latency of N20 was significantly shortened with sevoflurane after 25 minutes from the beginning of inhalation compared with the awake control levels. No increase of latency was observed. The amplitudes of N20 were decreased with sevoflurane anesthesia in relation to duration of anesthesia. These results suggest that sevoflurane alone might have no marked pharmacological properties to change the latency of SSEPs even in the deep level of anesthesia.     

异氟醚控制性降压对颅内动脉瘤夹闭术病人血液动力学及组织氧合的影响

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