Comparison of crystalloids and colloids for hemodilution in a model of focal cerebral ischemia

1990 ◽  
Vol 73 (4) ◽  
pp. 576-584 ◽  
Author(s):  
Kazuyoshi Korosue ◽  
Roberto C. Heros ◽  
Christopher S. Ogilvy ◽  
Akio Hyodo ◽  
Yong-Kwang Tu ◽  
...  
Keyword(s):  
Arterial Occlusion ◽  
Acute Stage ◽  
Control Group ◽  
Total Protein Content ◽  
Oncotic Pressure ◽  
Content Type ◽  
Ringer’S Solution ◽  
Arterial Blood ◽  
Lactated Ringer's Solution ◽  
Fine Print

✓ Forty dogs were subjected to 6 hours of occlusion of the left internal carotid and middle cerebral arteries. They were divided into two “hemodilution groups” of 13 dogs each and a control “nonhemodiluted group” of 14 dogs. Thirty minutes after arterial occlusion, isovolemic hemodilution was performed by phlebotomy and infusions of low-molecular weight (MW) dextran in one group and of lactated Ringer's solution in the other group. The animals were sacrificed 1 week after temporary arterial occlusion. Hemodilution reduced the hematocrit to a level of 33% to 34%, which lasted throughout the week in both groups. After hemodilution there was a very significant reduction in blood viscosity, plasma total protein content, and fibrinogen levels in both groups in the acute stage; these levels gradually returned to baseline by the end of the week. In the group with lactated Ringer's solution hemodilution, both osmotic and oncotic pressures were decreased by hemodilution in the acute stage. In the control and low-MW dextran groups, osmotic and oncotic pressure remained unaltered throughout the week. Hemodilution resulted in a slight decrease in mean arterial blood pressure in all groups in the acute stage, but there were no significant changes in central venous, pulmonary arterial, or pulmonary wedge pressures. During the week of study, there were no differences in the cardiac index and total blood volume between the groups, and no significant changes in hematological parameters with the exception of a slight increase in bleeding time immediately after hemodilution with low-MW dextran. Daily neurological assessment showed consistently poorer condition during the first 5 days in the group with lactated Ringer's solution compared to either the control group or the group receiving low-MW dextran. Based on Mann-Whitney U-testing, the infarct volume of the lactated Ringer's solution recipients, expressed as a percentage of the total volume of that hemisphere (median 15.7%, range 6.6% to 25.2%) was significantly larger than that of the group receiving low-MW dextran (median 2.2%, range 0% to 15.8%) and that of the control group (median 11.9%, range 0% to 39.9%). The results indicate that, in this model, hemodilution with colloids was beneficial, whereas hemodilution with crystalloids was deleterious. It is likely that the decrease in oncotic pressure observed after hemodilution with lactated Ringer's solution is one of the most important reasons for its detrimental effect.

Experimental brain injury: successful therapy with the weak base, tromethamine

1984 ◽  
Vol 60 (5) ◽  
pp. 961-971 ◽  
Author(s):  
Michael J. Rosner ◽  
Donald P. Becker
Keyword(s):  
Brain Injury ◽  
Control Group ◽  
Weak Base ◽  
Post Injury ◽  
Content Type ◽  
Ringer’S Solution ◽  
Fluid Percussion Injury ◽  
Lactated Ringer's Solution ◽  
Injury Control ◽  
Fine Print

✓ The presence of lactic acidosis in the cerebrospinal fluid of patients suffering brain injury as the result of trauma, subarachnoid hemorrhage, neoplasia, or ischemia has been well documented. The authors theorized that this acidosis becomes harmful in itself, and that treatment with an alkalinizing agent (tris(hydroxymethyl)aminomethane: tromethamine) capable of penetrating the blood-brain barrier would be efficacious. Fifteen pairs of mongrel cats were subjected to a 2.85-atmosphere fluid-percussion injury (LD80), and were supported by respirators for up to 72 hours prior to being placed in cages for an additional 4 days of observation. Experimental cats underwent continuous infusion of tromethamine (begun 10 minutes after injury); control animals were infused with an equal volume of lactated Ringer's solution. Twenty percent of the control group survived until sacrificed on Day 7 post-injury. Survival in the tromethamine group was 60% (p < 0.05), and morbidity also appeared to be reduced in the treated cats. Intracranial pressure (ICP) in treated cats was 60% (p < 0.05) of that in the control cats after respirator support for 3 days. Tromethamine infusion was associated with improved survival, decreased morbidity, and decreased ICP when compared with results in control animals. The literature with regard to central nervous system acidosis has been reviewed in an attempt to clarify and define this problem.

The influence of hemodynamic stress factors on intracranial aneurysm formation

2001 ◽  
Vol 95 (5) ◽  
pp. 764-770 ◽  
Author(s):  
Carole L. Turner ◽  
Susan Tebbs ◽  
Piotr Smielewski ◽  
Peter J. Kirkpatrick
Keyword(s):  
Intracranial Aneurysms ◽  
Augmentation Index ◽  
Applanation Tonometry ◽  
Stress Factors ◽  
Control Group ◽  
Content Type ◽  
Arterial Blood ◽  
Analysis System ◽  
The Right ◽  
Fine Print

Object. Applanation tonometry is a noninvasive method of assessing both peripheral and central arterial blood pressure (BP) profiles. In this study the authors examine whether there are differences in these profiles in patients with intracranial aneurysms when compared with age-matched controls. Methods. Carotid artery (CA) and derived aortic BP waveforms were obtained using a pulse wave analysis system. The ratio of the pressure wave amplitude above the systolic shoulder to the total systolic BP (augmentation index [AI]) was recorded. One hundred seventy-three patients with intracranial aneurysms (23 unruptured lesions) and 173 healthy control volunteers were examined. For the patients with aneurysms the right and left CA AIs (mean ± standard deviation) were 125.6 ± 23.1% and 128.3 ± 22.1%, respectively. Corresponding values for the control group were 118.4 ± 22.6% and 119.4 ± 21.8%. The calculated AI for the ascending aorta was 29.8 ± 10.5% and 25.6 ± 12.2% for patients with aneurysms and control volunteers, respectively. Significant asymmetry in CA AI was seen in patients with aneurysms, the left being greater (p = 0.002). No significant differences were seen in mean BP (108 ± 14 mm Hg in patients with aneurysms compared with 106 ± 16 mm Hg in controls; p = 0.2). Multivariate analysis excluded the influence of BP and other potential confounding vascular risk factors for increased AI. Conclusions. Significant differences in AI, both in magnitude and symmetry, were identified in patients with intracranial aneurysms when compared with matched controls.

scholarly journals Recruitment of neutrophils across the blood-brain barrier: the role of posttraumatic hepatic ischemia

2003 ◽  
Vol 18 (5) ◽  
pp. 392-397
Author(s):  
Mario Mantovani ◽  
Mauro José Fontelles ◽  
Elcio Shiyoiti Hirano ◽  
Rosana Celestina Morandin ◽  
André Almeida Schenka
Keyword(s):  
Hemorrhagic Shock ◽  
Tissue Perfusion ◽  
Serum Lactate ◽  
Control Group ◽  
Shock State ◽  
Hepatic Ischemia ◽  
Ringer’S Solution ◽  
Arterial Blood ◽  
Lactated Ringer's Solution ◽  
The Brain

PURPOSE: To study the effects of total hepatic ischemia, and reperfusion on the accumulation of neutrophils in the brain of rats submitted to normovolemic conditions as well as to controlled hemorrhagic shock state. METHODS: Thirty two adult male Wistar rats, were divided into four groups: the Control group, was submitted to the standard procedures for a period of 60 min of observation; Shock group, was submitted to controlled hemorrhagic shock (mean arterial blood pressure=40mmHg, 20min) followed by volemic resuscitation (lactated Ringer's solution + blood, 3:1) and reperfusion for 60min; Pringle group, was submitted to total hepatic ischemia for 15min and reperfusion for 60min. The total group was submitted to controlled hemorrhagic shock for 20min followed by volemic resuscitation (lactated Ringer's solution + blood, 3:1), total hepatic ischemia for 15min and reperfusion for 60min. Measurements of serum lactate and base excess were used to characterize the hemorrhagic shock state with low tissue perfusion. The counting of neutrophils on the brain was performed after the euthanasia of animals. RESULTS: The values for the counting of neutrophils on the brain indicate that did not occur difference among studied groups (p=0.196) (Control 0.12± 0.11, Shock 0.12± 0.13, Pringle 0.02± 0.04, Total 0.14± 0.16). CONCLUSION: Hemorrhagic shock associated to total hepatic ischemia for 15 minutes, followed by 60 minutes of reperfusion, did not causes significant neutrophils accumulation in the brain of rats.

Effects of head elevation on intracranial hemodynamics in patients with ventriculoperitoneal shunts

1994 ◽  
Vol 81 (6) ◽  
pp. 829-836 ◽  
Author(s):  
Sotaro Higashi ◽  
Kazuya Futami ◽  
Hiroshi Matsuda ◽  
Junkoh Yamashita ◽  
Masaaki Hashimoto ◽  
...  
Keyword(s):  
Photon Emission ◽  
Fluid Pressure ◽  
Upright Position ◽  
Differential Pressure ◽  
Control Group ◽  
Content Type ◽  
Arterial Blood ◽  
Head Elevation ◽  
The Mean ◽  
Fine Print

✓ The present study was performed to investigate the effects of head elevation on intracranial hemodynamics in patients with ventriculoperitoneal (VP) shunts. The series included 35 hydrocephalic patients and five individuals without hydrocephalus who were used as controls. The hydrocephalic patients were divided into three groups: 15 patients who received VP shunts with a differential-pressure valve (DP group); 11 who received VP shunts with a variable-resistance valve (VR group), and 13 hydrocephalic patients (Hyd group) who had not received shunts (four underwent VP shunts later). The cerebral blood flow (CBF) of patients in the supine and upright positions was measured by technetium-99m hexamethylpropylenamine oxide (HMPAO) single-photon emission computerized tomography in each patient, using the subtraction technique. Cerebral perfusion pressure (CPP) was taken as the difference between the mean arterial blood pressure and ventricular fluid pressure, both referenced to the level of the foramen of Monro. The patients' heads were elevated stepwise from supine to upright. Percent changes of the mean CBF in the upright position (%ΔmCBFupr) were 24.9% ± 4.3% (mean ± standard error of the mean) in the DP group, 6.2% ± 2.7% in the VR group, 3.5% ± 2.6% in the Hyd group, and 4.5% ± 2.2% in the control group. Patients in the DP group showed a pathological increase in CPP with head elevation, whereas those in the Hyd and VR groups showed a physiological decrease in CPP. Three patients with differential-pressure valves, whose %ΔmCBFupr was markedly high, developed low-intracranial pressure syndrome. In conclusion, shunted patients with a DP valve showed pathological intracranial hemodynamics in the upright position. This pathological hemodynamic stress in patients with long-standing differential-pressure valve implantation may induce pathological changes in the brain such as subependymal gliosis.

Cerebral arterial responses to induced hypertension following subarachnoid hemorrhage in the monkey

1978 ◽  
Vol 49 (1) ◽  
pp. 75-83 ◽  
Author(s):  
Donald P. Boisvert ◽  
Thomas R. Overton ◽  
Bryce Weir ◽  
Michael G. Grace
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Control Group ◽  
Content Type ◽  
Csf Pressure ◽  
Arterial Blood ◽  
Subarachnoid Injection ◽  
Arterial Responses ◽  
Fine Print

✓ Regional cerebral blood flow (rCBF), angiographic cerebral arterial caliber, and cerebrospinal fluid (CSF) pressure were measured in rhesus monkeys to determine the effect of experimentally induced subarachnoid hemorrhage (SAH) on cerebral arterial responses to graded increases in blood pressure. These measurements were also performed in a control group of monkeys subjected to a mock SAH by injection of artificial CSF into the cerebral space. Before subarachnoid injection of blood or artificial CSF, graded increases in mean arterial blood pressure (MABP) to a level 40% to 50% above baseline values had no effect on rCBF. The major cerebral arteries constricted and CSF pressure remained unchanged. Similar responses were observed after injection of artificial CSF. When MABP was increased in animals that had been subjected to subarachnoid injection of blood, rCBF increased and was associated with dilatation of the major cerebral arteries and moderate increases in CSF pressure. These results demonstrate that cerebral arterial responses to increases in blood pressure may be abnormal in the presence of subarachnoid blood. The manner in which abnormal cerebral arterial reactivity, changes in blood pressure, and vasospasm combine to determine the level of cerebral perfusion following SAH is postulated.

Temporal changes in perivascular concentrations of oxyhemoglobin, deoxyhemoglobin, and methemoglobin after subarachnoid hemorrhage

1998 ◽  
Vol 88 (3) ◽  
pp. 557-561 ◽  
Author(s):  
Ryszard M. Pluta ◽  
John K. B. Afshar ◽  
Robert J. Boock ◽  
Edward H. Oldfield
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Blood Clot ◽  
Saline Control ◽  
Control Group ◽  
Content Type ◽  
Delayed Cerebral Vasospasm ◽  
Arterial Blood ◽  
Fine Print

Hemoglobin released from hemolysed erythrocytes has been postulated to be responsible for delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). However, the evidence is indirect and the mechanisms of action are unclear. Cerebrovascular tone is regulated by a dynamic balance of relaxing and contracting factors. Loss of the endothelium-derived relaxing factor—nitric oxide in the presence of oxyhemoglobin and overproduction of endothelin-1 stimulated by oxyhemoglobin have been postulated as causes of delayed cerebral vasospasm after SAH. Object. The authors aimed to investigate this hypothesis using in vivo microdialysis to examine time-dependent changes in the perivascular concentrations of oxyhemoglobin, deoxyhemoglobin, and methemoglobin in a primate model of SAH. Methods. Nine cynomolgus monkeys underwent right-sided frontotemporal craniectomy and placement of a semipermeable microdialysis catheter adjacent to the right middle cerebral artery (MCA). Saline (control group, three animals) or an arterial blood clot (SAH group, six animals) was then placed around the MCA and the catheter. Arteriographically confirmed vasospasm had developed in all animals with SAH but in none of the control animals on Day 7. The dialysate was collected daily for 12 days. Levels of oxyhemoglobin, deoxyhemoglobin, and methemoglobin were measured by means of spectrophotometry. Perivascular concentrations of oxyhemoglobin, deoxyhemoglobin, and methemoglobin peaked on Day 2 in the control monkeys and could not be detected on Days 5 to 12. Perivascular concentrations of oxyhemoglobin and deoxyhemoglobin peaked on Day 7 in the SAH group, at which time the concentrations in the dialysate were 100-fold higher than in any sample obtained from the control animals. Methemoglobin levels increased only slightly, peaking between Days 7 and 12, at which time the concentration in the dialysate was 10-fold higher than in samples from the control animals. Conclusions. This study provides in vivo evidence that the concentrations of oxyhemoglobin and deoxyhemoglobin increase in the cerebral subarachnoid perivascular space during the development of delayed cerebral vasospasm. The results support the hypothesis that oxyhemoglobin is involved in the pathogenesis of delayed cerebral vasospasm after SAH and implicate deoxyhemoglobin as a possible vasospastic agent.

Effect of mannitol on local cerebral blood flow after temporary complete cerebral ischemia in rats

1992 ◽  
Vol 76 (3) ◽  
pp. 486-492 ◽  
Author(s):  
Reizo Shirane ◽  
Philip R. Weinstein
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
External Carotid ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Content Type ◽  
Arterial Blood ◽  
Permanent Occlusion ◽  
Fine Print

✓ The effects of pretreatment with mannitol on local cerebral blood flow (CBF) after permanent or temporary global cerebral ischemia were evaluated with 14C-iodoantipyrine autoradiography in rats under halothane-N2O endotracheal anesthesia. Blood pressure, pulse rate, arterial blood gas levels, and electroencephalographic (EEG) tracings were monitored throughout the experiments. After permanent occlusion of the basilar artery and both external carotid and pterygopalatine arteries, severe global ischemia was induced by permanent occlusion of the common carotid arteries (CCA's) or by a 30-minute temporary CCA occlusion followed by 5 minutes of reperfusion. Intravenous mannitol (25%, 1 gm/kg) or saline solution was administered 5 minutes before occlusion of the CCA's. Cerebral blood flow was measured in 24 anatomical regions. The EEG tracings flattened within 2 to 3 minutes after the onset of ischemia, and no recovery was observed during reperfusion. In the mannitol-treated rats and the saline-treated controls, autoradiographic studies after permanent occlusion showed no CBF in the forebrain or cerebellum, although brain-stem and spinal cord CBF values were normal. After 5 minutes of reperfusion, CBF in the cortex, basal ganglia, and white matter was 100% to 200% higher in mannitol-treated rats and 50% to 100% higher in saline-injected rats than in the nonischemic anesthetized control group. Heterogeneously distributed areas of no-reflow were seen in all saline-injected rats but were observed in none of the mannitol-treated rats. Pretreatment with mannitol prevented postischemic obstruction of the microcirculation during 5 minutes of recirculation after 30 minutes of severe temporary ischemia, but the EEG signals did not recover. Further studies of the functional and morphological responses to longer periods of postischemic recirculation are needed to verify the extent to which these mannitol-induced effects are protective.

Optimum degree of hemodilution for brain protection in a canine model of focal cerebral ischemia

1994 ◽  
Vol 80 (3) ◽  
pp. 469-475 ◽  
Author(s):  
Sun Ho Lee ◽  
Roberto C. Heros ◽  
John C. Mullan ◽  
Kazuyoshi Korosue
Keyword(s):  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Arterial Occlusion ◽  
Canine Model ◽  
Control Group ◽  
Left Middle Cerebral Artery ◽  
Content Type ◽  
Infarction Size ◽  
Infarction Volume ◽  
Fine Print

✓ The ability of hemodilution to lower blood viscosity and increase cerebral blood flow has been proven experimentally; however, the optimum hematocrit for maximum oxygen delivery to ischemic brain tissue is not known, and a study was designed to determine this. Fifty dogs were selected for inclusion in the study using criteria based on changes in somatosensory evoked potentials at the time of arterial occlusion, which were found in a previous study to predict the development of a moderate infarction of relatively constant size. Infarctions were induced by permanent occlusion of the left middle cerebral artery and the azygous anterior cerebral artery. The animals selected for inclusion were divided into five groups of 10 dogs each: 1) a control group; 2) a group with 25% hematocrit; 3) a group with 30% hematocrit; 4) a group with 35% hematocrit; and 5) a group with 40% hematocrit. Isovolemic hemodilution was accomplished 1 hour after occlusion of vessels using dextran infusion and blood withdrawal. The animals were sacrificed after 6 days and infarction volume was determined from fluorescein-stained sections. Statistical analysis was performed using Student's t-test and one-way analysis of variance. Mean infarction volume for each group, expressed as a percentage of total hemispheric volume ± 1 standard error of the mean, was 28.3% ± 2.8% for the control group, 33.6% ± 3.4% for the 25% hematocrit group, 17.1% ± 2.2% for the 30% hematocrit group, 29.2% ± 4.3% for the 35% hematocrit group, and 29.9% ± 2.1% for the 40% hematocrit group. The 30% hematocrit group showed the smallest average infarction size and this size differed significantly (p = 0.02) from the average infarction size in the control animals. These results show that, in this model of focal ischemia, a hematocrit of approximately 30% is optimum for protecting the brain.

Prevention of cerebrovasospasm following subarachnoid hemorrhage in rabbits by the platelet-activating factor antagonist, E5880

1996 ◽  
Vol 84 (5) ◽  
pp. 826-830 ◽  
Author(s):  
Yutaka Hirashima ◽  
Shunro Endo ◽  
Ryoko Kato ◽  
Akira Takaku
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intravenous Administration ◽  
Basilar Artery ◽  
Platelet Activating Factor ◽  
Control Group ◽  
Distilled Water ◽  
Dependent Manner ◽  
Content Type ◽  
Arterial Blood ◽  
Fine Print

✓ Recently, an important role of platelet-activating factor (PAF), an inflammation mediator, has been demonstrated in the genesis of cerebral vasospasm following subarachnoid hemorrhage (SAH). In the current study, the authors examined whether intravenous administration of the novel PAF antagonist, E5880, can prevent vasospasm following SAH in rabbits. A vasospasm model was produced in three groups of rabbits using two subarachnoid injections of autologous arterial blood, followed by intravenous administration of distilled water (control), a low dose of E5880 (0.1 mg/kg in distilled water), or a high dose of E5880 (0.5 mg/kg in distilled water). Neurological deterioration was largely prevented in the rabbits that received E5880. Basilar artery constriction was also reduced by both doses of E5880. Histological examination at autopsy predominantly showed ischemic changes in the brain. Animals in each E5880-treated group exhibited ischemic changes less frequently than those in the control group. Plasma thromboxane B2 concentrations were reduced in rabbits treated with E5880. Platelet-activating factor was immunolocalized in the intima and media of the basilar artery in the control group. The PAF immunoreactivity demonstrated in the basilar artery was decreased in the E5880 groups in a dose-dependent manner. Thus, this study provides evidence that PAF may play a role in the pathogenesis of vasospasm after SAH and that intravenous administration of E5880 is a promising approach in preventing vasospasm.

Evaluation of endorphin content in the CSF of patients with trigeminal neuralgia before and after Gasserian ganglion thermocoagulation

1981 ◽  
Vol 55 (6) ◽  
pp. 935-937 ◽  
Author(s):  
Giuseppe Salar ◽  
Salvatore Mingrino ◽  
Marco Trabucchi ◽  
Angelo Bosio ◽  
Carlo Semenza
Keyword(s):  
Cerebrospinal Fluid ◽  
Trigeminal Neuralgia ◽  
Control Group ◽  
Gasserian Ganglion ◽  
Content Type ◽  
Group Of Seven ◽  
Idiopathic Trigeminal Neuralgia ◽  
Significant Difference ◽  
Before And After ◽  
Fine Print

✓ The β-endorphin content in cerebrospinal fluid (CSF) was evaluated in 10 patients with idiopathic trigeminal neuralgia during medical treatment (with or without carbamazepine) and after selective thermocoagulation of the Gasserian ganglion. These values were compared with those obtained in a control group of seven patients without pain problems. No statistically significant difference was found between patients suffering from trigeminal neuralgia and those without pain. Furthermore, neither pharmacological treatment nor surgery changed CSF endorphin values. It is concluded that there is no pathogenetic relationship between trigeminal neuralgia and endorphins.

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