Effect of treatment with fluosol and mannitol during temporary middle cerebral artery occlusion in cats

Four groups of seven cats each were subjected to 6 hours of temporary middle cerebral artery (MCA) occlusion followed by reperfusion. During the first 30 minutes of the occlusion, Group 1 received 20% Fluosol-DA (FDA) and Group 2 received 20% FDA and mannitol; Group 3 received 20% FDA and mannitol 30 minutes before the occlusion, and Group 4 (control) received an infusion of saline solution during the first 30 minutes of occlusion. All cats breathed 100% oxygen throughout the occlusion and during 2 hours of reperfusion. Blood pressure, PaO2, and pH remained stable for 8 hours. PaO2 increased from an average base line level of 102 +/- 15 (SD) torr to 520 +/- 45 torr in Group 1, 450 +/- 41 torr in Group 2, 480 +/- 28 torr in Group 3, and 396 +/- 151 torr in Group 4 during the administration of 100% oxygen. The average fluorocrit during occlusion was 6% in Groups 1, 2, and 3. The 24-hour mortality rate was 71% in Group 1, 43% in Group 2, 29% in Group 3, and 14% in Group 4; a midline shift and herniation were present after each fatal infarct. The survivors were sacrificed 10 days after the occlusion. There was a trend toward improvement of neurological function at sacrifice in Groups 2 and 3 compared with Groups 1 and 4. The infarct areas on coronal sections were 2.4 times larger in Group 1 (FDA only) than in Group 4 (control) (P less than 0.05). There was no significant difference in infarct size between Group 4 and Group 2 or 3.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of repeated temporary clipping of the middle cerebral artery on pial arterial diameter, regional cerebral blood flow, and brain structure in cats

Temporary clipping of the major arterial trunk is an important maneuver to control excessive unexpected bleeding in neurosurgical operations; however, repeated temporary clipping can give rise to severe neurological deficits after surgery. The present study was performed to confirm and explain these clinical findings. Initially, a single 20-minute or 1-hour occlusion of the middle cerebral artery was performed in each of 5 cats. Pial arterial diameter was determined by video imaging, regional cerebral blood flow was measured by autoradiography, and cerebral edema and infarction were observed. In the 20-minute occlusion group, no abnormal changes were found 5 hours after recirculation. In the 1-hour occlusion group, pial arteries were dilated by 45%, and regional cerebral blood flow increased to more than twice the resting cortical values. The extent of cerebral edema was 41.2 +/- 7.5% (SE) and infarction was 34.5 +/- 9.5% (SE) of the hemisphere. In the second experiment, three 20-minute occlusions of the middle cerebral artery in a 1-hour interval were performed in 20 cats. In 10 of them, thiopental (40 mg/kg) was used to protect the brain. In the group without barbiturate treatment, pial arteries were dilated by 40% at the end of experiment, regional cerebral blood flow decreased to about 70% compared with single 20-minute occlusion, cerebral edema was 19.5 +/- 8.1% (SE), and infarction was 8.1 +/- 3.7% (SE) of the hemisphere. In the treated group, these were only trivial changes. The effect of repeated clipping may cumulatively cause brain damage, and barbiturates should be used whenever repeated clipping is necessary.     

Changes in local cerebral blood flow,local EEG,and flow in the distal stump of the middle cerebral artery in cats with occlusion of the middle cerebral artery

Summary The local EEG, the local cerebral blood flow (1CBF), and the flow in the distal stump of the occluded middle cerebral artery were simultaneously recorded in 28 acute experiments in cats. Nembutal anaesthesia was used eleven times, and Halothane anaesthesia 17 times.The recordings were made via platinum electrodes: 12 in the ischaemic hemisphere, and 2–3 in the opposite non-ischaemic hemisphere. The flow in the occluded middle cerebral artery was recorded via a platinum electrode introduced into this artery via the transorbital approach. The changes in 1EEG, 1CBF, and middle cerebral artery flow were studied during normotension, hypertension, and hypotension. A beneficial effect of hypertension was noted in the acute phase of brain ischaemia. Hypertension counteracted also the diaschisis in the non-ischaemic part of the ischaemic hemisphere and in the opposite non-ischaemic hemisphere. A correlation between 1EEG changes and 1CBF changes was noted. In addition an interesting discrepancy was observed between the rapid H₂ clearance in the middle cerebral artery stump and the much slower H₂ clearance in the ischaemic brain area.Significant differences between experiments under Halothane and experiments under Nembutal anaesthesia were noted. In the acute phase those changes are probably the result of the different levels of blood pressure in those two groups.     

Failure of fluosol to influence the incidence of cerebral infarction or mortality in gerbils subjected to temporary carotid occlusion

Three hundred two gerbils were subjected to 2, 4, or 6 hours of temporary occlusion of the right common carotid artery. The animals were divided into four groups. The first two groups were given an infusion of Fluosol DA 20% (20 ml/kg) before arterial occlusion. One of these groups was kept in an environment of 100% oxygen during the time of occlusion and the other group was kept in room air. The two other groups of animals did not receive Fluosol. One of these groups was kept in 100% oxygen and the other group in room air during the time of arterial occlusion. The surviving animals were sacrificed 7 days later, and their brains were examined grossly and microscopically for evidence of cerebral infarction. There was a lesser incidence of early hemiparesis in the two groups treated with Fluosol, as well as in the untreated group that was kept in 100% oxygen. However, the incidence of infarction and the mortality were not significantly different in any of the groups.     

Results of hyperbaric oxygen therapy during temporary middle cerebral artery occlusion in unanesthetized cats

We evaluated the effect of hyperbaric oxygen (HBO) therapy on neurological function and infarct size in 33 unanesthetized cats subjected to temporary 6-hour or 24-hour occlusion of the middle cerebral artery (MCA) 7 to 10 days after transorbital implantation of a vessel occluder. HBO therapy (100% oxygen at 1.5 atmospheres absolute) was administered for 40 minutes during or after 6-hour occlusions and before, during, and after 24-hour occlusions. Neurological function was graded on a scale of 0 to 10 every 30 minutes before, during, and after occlusion and HBO treatments until it stabilized and then daily until the cats were killed 10 days after occlusion. The results were compared with observations in 13 untreated controls and 6 cats that received 100% O2 at atmospheric pressure during a 6-hour MCA occlusion. HBO therapy during the 1st or 3rd hour of a 6-hour MCA occlusion resulted in a four-grade improvement of the initial neurological function; this effect persisted during the remainder of the occlusion. The average grade of neurological deficit at death was 94% less than in the untreated cats (P less than 0.03). Infarct size in the HBO-treated group was 58% less than in controls (P less than 0.03). There was no significant difference in infarct size between the untreated cats and those treated with 100% O2 at atmospheric pressure. HBO therapy during the 4th hour of a 6-hour MCA occlusion had no statistically significant effect on infarct size, even though the mean neurological deficit was 73% less than in controls (P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of mannitol on cerebral blood flow and microcirculation during experimental middle cerebral artery occlusion

Regional cerebral blood flow (rCBF) was measured during and after a 2-3 hour occlusion period of the middle cerebral artery (MCA) in cats with the hydrogen clearance technique. The effects of mannitol upon rCBF were studied. Transient hypotension during occlusion dropped the blood flow to near zero on the occluded side, leading to postischemic hypoperfusion. Mannitol failed to modify blood flow during the occlusion period, but was effective in preventing any further decrease of blood flow during hypotension. Animals receiving mannitol had an improved postischemic recovery of blood flow. The correlation of ischemic severity and postischemic brain damage and the effects of mannitol on these parameters are discussed.     

Continuous monitoring of regional cerebral blood flow during temporary arterial occlusion in aneurysm surgery

OBJECT: Temporary arterial occlusion (TAO) during aneurysm surgery carries the risk of ischemic sequelae. Because monitoring of regional cerebral blood flow (rCBF) may limit neurological damage, the authors evaluated a novel thermal diffusion (TD) microprobe for use in the continuous and quantitative assessment of rCBF during TAO. METHODS: Following subcortical implantation of the device at a depth of 20 mm in the middle cerebral artery or anterior cerebral artery territory, rCBF was continuously monitored by TD microprobe (TD-rCBF) throughout surgery in 20 patients harboring anterior circulation aneurysms; 46 occlusive episodes were recorded. Postoperative radiographic evidence of new infarction was used as the threshold for failure of occlusion tolerance. The mean subcortical TD-rCBF decreased from 27.8+/-8.4 ml/100 g/min at baseline to 13.7+/-11.1 ml/100 g/min (p < 0.0001) during TAO. The TD microprobe showed an immediate exponential decline of TD-rCBF on clip placement. On average, 50% of the total decrease was reached after 12 seconds, thus rapidly indicating the severity of hypoperfusion. Following clip removal, TD-rCBF returned to baseline levels after an average interval of 32 seconds, and subsequently demonstrated a transient hyperperfusion to 41.4+/-18.3 ml/l 00 g/min (p < 0.001). The occurrence of postoperative infarction (15%) and the extent of postischemic hyperperfusion correlated with the depth of occlusion-induced ischemia. CONCLUSIONS: The new TD microprobe provides a sensitive, continuous, and real-time assessment of intraoperative rCBF during TAO. Occlusion-induced ischemia is reliably detected within the 1st minute after clip application. In the future, this may enable the surgeon to alter the surgical strategy early after TAO to prevent ischemic brain injury.     

The effect of hypervolemic hemodilution with and without hypertension on cerebral blood flow following middle cerebral artery occlusion in rats anesthetized with isoflurane

The effect of hypervolemic hemodilution or hypervolemic hemodilution with dopamine-induced hypertension on cerebral blood flow (CBF) was investigated during 1.2 MAC isoflurane anesthesia in rats (n = 24) subjected to middle cerebral artery occlusion (MCAO). Prior to MCAO each animal was randomized to one of the following groups: 1) control, mean arterial pressure (89 +/- 10 mmHg [mean +/- SD]), blood volume, and hematocrit (46 +/- 1) were not manipulated; 2) hypervolemic hemodilution (HH), 30 min before MCAO, 5% albumin was administered to reduce the hematocrit to 29-32%; or 3) hypervolemic hemodilution/dopamine hypertension (HH/Dop), hemodilution was accomplished and dopamine (10 micrograms.kg-1.min-1) was infused during the ischemic period to achieve a mean arterial pressure of 111 +/- 10 mmHg (mean +/- SD). Ten minutes after occlusion of the left middle cerebral artery, CBF was determined using 14C-iodoantipyrine. Five coronal brain sections were analyzed to determine the area within each brain section with CBF ranges of 0-15 ml.100 g-1.min-1 and 15-23 ml.100 g-1.min-1. The area of 0-15 ml.100 g-1.min-1 CBF was less in both the HH and HH/Dop groups compared with control (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Induced hypertension during restoration of flow after temporary middle cerebral artery occlusion in the rat: effect on neuronal injury and edema

The effect of hypertension instituted during restoration of flow after focal ischemia was studied. After the middle cerebral artery (MCA) of 12 rats was occluded for 2 hours, the ligatures were released and flow was restored for a period of 2 hours. In the control group, mean arterial pressure (MAP) was not manipulated. In the hypertensive group, the MAP was elevated by 25-30 mm Hg immediately after reestablishment of MCA patency. The area of neuronal injury, determined by 2,3,5-triphenyltetrazolium staining, was significantly smaller in the hypertensive group. Specific gravity, determined by microgravimetry, did not differ between groups. The data demonstrate that modest hypertension, when induced during reperfusion after 2 hours of MCA occlusion, reduces neuronal injury and does not exacerbate edema formation.     

Intracranial pressure, blood pressure, and pulse rate after occlusion of a middle cerebral artery in cats.

The left middle cerebral artery was occluded in 12 tranquilized but unanesthetized cats with use of a device implanted transorbitally 5 to 7 days earlier. Bilateral epidural pressures, mean aortic blood pressure, and pulse rate were measured at intervals for up to 48 hours after occlusion. The relationships of these measurements to each other and to the extent and severity of cerebral infarcts is described.     

半肝全血流阻断联合肝固有动脉暂时阻断在半肝切除中应用的临床效果

目的半肝全血流阻断联合肝固有动脉暂时阻断半肝切除的临床效果。方法回顾性分析我院2001年6月-2007年12月行半肝全血流阻断联合肝固有动脉暂时阻断半肝切除35例与同期半肝全血流阻断半肝切除36例的术中平均出血量和术后肝功能等级恶化发生率。结果半肝全血流阻断联合肝固有动脉暂时阻断半肝切除组和半肝全血流阻断半肝切除组术中平均出血量分别为（320±50）ml和（390±80）ml,两组间有显著性差异（P〈0．05）;两组术后肝功能等级恶化发生率分别为17．1％和16．6％（P〉0．05）。结论半肝全血流阻断联合肝固有动脉暂时阻断半肝切除能显著减少术中的出血量,不增加术后肝功能恶化加级的发生率。     

Effect of calcium antagonist nimodipine and induced hypertension on cerebral vessel reactivities, cerebral blood flow, cerebral edema and infarction in cats with one hour middle-cerebral-artery occlusion

Treatment with the calcium entry blocker nimodipine is recommended as effective therapy for cerebral ischemia due to cerebral vasospasm or cerebral thrombosis. On the other hand, treatment with induced hypertension is a widely accepted measure to reverse ischemic deficits caused by vasospasm. Thus, a combination of the two regimens--nimodipine and induced hypertension--may have real benefits for cerebral ischemia. But it is possible that the benefit of one is abolished by adverse effects of the other, or that a combination of both may not be as effective as the use of only one therapy. In order to investigate these problems, the effects of nimodipine and induced hypertension on cerebral vessel, cerebral blood flow, cerebral edema and cerebral infarction using a one hour middle-cerebral-artery occlusion model in cats. Twenty-one anesthetized cats were divided into a control group, the nimodipine-treated group, and the nimodipine-and-induced-hypertension group. There were seven cats in each group. Occlusion of the middle cerebral artery (MCA) was continued for one hour in each animal. Induced hypertension was a little higher than resting values, and it was continued for only one hour during MCA occlusion, brought on by instillation of dopamine. Cerebral pial arteries dilated much more prominently during and after the occlusion of MCA in the nimodipine-and-induced-hypertension group than other groups. Although cerebral blood flow in the nimodipine group, and the nimodipine-and-induced-hypertension group increased more in the non-ischemic hemisphere, the most remarkable increase was seen around the infarcted cortex in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)     

SEM evaluation of endothelial damage following temporary middle cerebral artery occlusion in dogs

Microsurgical clips and tourniquets were used to occlude middle cerebral arteries of dogs for 45-minute periods. Scanning electron microscopy and light microscopy studies revealed significant endothelial damage in many of these arteries. Less traumatic microsurgical clips are needed for temporary small vessel occlusion.     

Local cerebral blood flow after middle cerebral artery occlusion in rabbits following transposition of omentum to the brain

Transposition of pedicled omental grafts to the brain has been shown to minimize the effects of cerebral infarction in dogs and monkeys. An experimental study in which pedicled omental grafts and free non-revascularized omental grafts were placed on the brains of rabbits is reported. With the use of a modified inhaled hydrogen clearance technique to measure blood flow in the brain tissue, it was determined that the pedicled omental graft minimized the effects of middle cerebral artery occlusion by maintaining a collateral blood supply and limiting the decline of local cerebral flow. Superposition of free omental grafts on the brain had no effect on the threshold for infarction.     

Distribution of cerebral blood flow during deep isoflurane vs. pentobarbital anesthesia in rats with middle cerebral artery occlusion

While previous studies have identified a protective effect for barbiturate anesthesia during focal cerebral ischemia, no such effect has been demonstrated for isoflurane. To better understand the effects of these anesthetics on cerebral blood flow and metabolism that might have relevance to their respective potential for cerebral protection, fasted physiologically stable rats underwent autoradiographic determination of CBF and CMRglu during deep isoflurane or pentobarbital anesthesia (burst suppression of EEG). As expected, cerebral blood flow was significantly greater during isoflurane anesthesia (isoflurane = 157 +/- 18 and pentobarbital = 54 +/- 12 ml/100 g/min) while CMRglu values were nearly identical (isoflurane = 35 +/- 5 and pentobarbital = 33 +/- 4 mumol/100 g/min). Additional identically anesthetized rats underwent middle cerebral artery occlusion with CBF autoradiographically determined 1 h later. While the insult resulted in a significant reduction in the ipsilateral hemispheric and cortical blood flow in both anesthetic groups, flow remained at least twofold greater in isoflurane as opposed to pentobarbital-anesthetized rats. When regional flow was assessed, no difference between groups was observed with respect to the area of tissue with flow values falling between 0-10 ml/100 g/min. In contrast, isoflurane-anesthetized rats had significantly less hemispheric and cortical area with flow values in the ranges of 10-20 and 20-30 ml/100 g/min, respectively. These data, therefore, do not support the contention that isoflurane causes maldistribution of CBF during focal ischemia.     

Characterization of the cerebral blood flow response to balloon deflation after temporary internal carotid artery test occlusion

The authors tested the hypothesis that cerebral blood flow (CBF) would increase after acute and relatively brief internal carotid artery (ICA) test occlusion, and examined the relationship of the postdeflation CBF to the development of neurologic symptoms. In 16 patients undergoing ICA test occlusion with deliberate hypotension, the authors measured intracarotid 133Xe CBF at baseline, occlusion, and deflation. Four patients developed neurologic symptoms during occlusion. As positive controls, 11 other patients received intracarotid verapamil or papaverine before deflation as part of another protocol. Balloon occlusion was 23.1 +/- 10.5 minutes (mean +/- standard deviation) in duration. At 1.3 +/- 1.6 minutes after balloon deflation, there was a trend (12 +/- 31%) for CBF to increase (48 +/- 9 mL/100 g/min versus 53 +/- 17 mL/100 g/min, P =.15), and a 16 +/- 27% decrease in cerebrovascular resistance (CVR; 2.1 +/- 0.6 mm Hg/100 g/min/mL versus 1.7 +/- 0.6 mm Hg/100 g/min/mL, P =.03) compared with baseline values. By comparison, patients who received a intracarotid dilator demonstrated a 53 +/- 55% increase in CBF (48 +/- 10 mL/100/min versus 70 +/- 23 mL/100 g/min, P = .007) and a 33 +/- 31% decrease in CVR (2.2 +/- 0.6 mm Hg/100 g/min/mL versus 1.4 +/- 0.6 mm Hg/100 g/min/mL, P = .0007) compared with baseline. Analysis of variance and regression analysis showed no other relationships between postocclusion CBF and balloon occlusion duration, distal internal carotid occlusion ("stump") pressure, or the development of neurologic symptoms. Acute, temporary interruption of ICA blood flow resulted in minimal postocclusive changes in cerebrovascular hemodynamics, even in those patients who developed neurologic symptoms during the period of test occlusion.