Systemic hypotension in neurosurgery

1975 ◽  
Vol 43 (5) ◽  
pp. 579-589 ◽  
Author(s):  
David Yashon ◽  
Alfred P. Magness ◽  
W. Michael Vise
Keyword(s):  
Intracranial Pressure ◽  
Vascular Endothelial Cells ◽  
Systemic Blood Pressure ◽  
Vascular Endothelial ◽  
Content Type ◽  
Profound Hypotension ◽  
Clip Application ◽  
Low Glucose ◽  
The Brain ◽  
Elevated Lactate

✓ The authors review the intraoperative use of elective hypotension to reduce the probability of hemorrhage, to increase pliability of the aneurysmal sac for ease of clip application, and to control hemorrhage. The optimum agent and techniques for lowering systemic blood pressure remain controversial, but trimethaphan, sodium nitroprusside, and halothane have been found most useful. When cerebral blood flow falls below the brain's capacity to autoregulate, distinct time-related alterations occur biochemically and histologically. The profile of prolonged reduced adenosine triphosphate (ATP), low phosphocreatine, low glucose, and elevated lactate and lactate/pyruvate ratio is associated with swelling of perivascular astrocytes and “blebbing” of vascular endothelial cells with subsequent cerebral damage. To prevent permanent alteration it is desirable to observe time constraints and to employ other means of protection such as hypothermia, although the authors believe the latter unnecessary for short hypotensive periods. It has been proposed, but not substantiated, that anesthetics which depress rate of cerebral oxygen consumption but do not affect cerebral ATP level protect the brain from hypotension. Several investigations suggest that halothane, a vasodiltor, satisfies the safety requirement. The most prominent contraindication to halothane, however, is elevation of intracranial pressure. At present hypotensive surgery for aneurysmorrhaphy is usually performed when intracranial pressure has returned to normal. Experimentally the electroencephalogram has been observed to show alterations prior to biochemical parameters for following brain vulnerability, so that it conceivably could be an effective monitoring technique during prolonged profound hypotension.

Effect of Neuroinflammation on ABC Transporters: Possible Contribution to Refractory Epilepsy

2018 ◽  
Vol 17 (10) ◽  
pp. 728-735 ◽  
Author(s):  
Xiaolin Deng ◽  
Yangmei Xie ◽  
Yinghui Chen
Keyword(s):  
Antiepileptic Drugs ◽  
Abc Transporters ◽  
Refractory Epilepsy ◽  
Vascular Endothelial Cells ◽  
Efflux Transporters ◽  
Vascular Endothelial ◽  
Intracellular Signalling Pathways ◽  
The Brain ◽  
Transporter Expression

Background & Objective: Epilepsy is a common and serious chronic neurological disorder that is mainly treated with antiepileptic drugs. Although current antiepileptic drugs used in clinical practice have advanced to the third generation, approximately one-third of patients are refractory to these treatments. More efficacious treatments for refractory epilepsy are therefore needed. A better understanding of the mechanism underlying refractory epilepsy is likely to facilitate the development of a more effective therapy. The abnormal expression and/or dysfunction of efflux transporters, particularly ABC transporters, might contribute to certain cases of refractory epilepsy. Inflammation in the brain has recently been shown to regulate the expression and/or function of ABC transporters in the cerebral vascular endothelial cells and glia of the blood-brain barrier by activating intracellular signalling pathways. Conclusion: Therefore, in this review, we will briefly summarize recent research advances regarding the possible role of neuroinflammation in regulating ABC transporter expression in epilepsy.

Intracranial pressure in the normal monkey while awake and asleep

1979 ◽  
Vol 51 (2) ◽  
pp. 206-210 ◽  
Author(s):  
Gündüz Gücer ◽  
Lawrence J. Viernstein
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Systemic Blood Pressure ◽  
Macaque Monkey ◽  
Short Term ◽  
Content Type ◽  
Plateau Waves ◽  
Normal Monkey ◽  
The Mean ◽  
Cervical Ganglia

✓ Intracranial pressure (ICP) was recorded continuously by telemetry in seven normal monkeys trained to eat, sleep, and live in a primate chair. Electroencephalography, electromyography, and blood pressure were also measured by conventional means. During wakefulness and all stages of sleep except desynchronized sleep, the ICP record showed small short-term variations in pressure. However, during desynchronized sleep, the mean ICP rose on the average to 170 ± 6 mm H2O above the ICP levels in the other states of sleep, and the pulsation pressure variation increased by a factor of three. The episodes occurred 10 ± 2 times during the night and lasted for 6.8 ± 1.4 minutes, during which the average systemic blood pressure decreased by 19 ± 1.6 mm Hg. These ICP waves occurring during desynchronized sleep resemble the plateau waves described by Lundberg, but are of smaller magnitude and they appear to be a normal characteristic of sleep in the macaque monkey. Bilateral sympathectomy of the superior cervical ganglia in four of the monkeys did not alter significantly the duration, amplitude, or frequency of occurrence of the ICP waves during desynchronized sleep.

scholarly journals Distribution of the Cystine/Glutamate Antiporter System x−c in the Brain, Kidney, and Duodenum

2006 ◽  
Vol 54 (5) ◽  
pp. 549-557 ◽  
Author(s):  
Joseph Burdo ◽  
Richard Dargusch ◽  
David Schubert
Keyword(s):  
Oxidative Stress ◽  
Vascular Endothelial Cells ◽  
Ependymal Cells ◽  
Vascular Endothelial ◽  
Specific Antibodies ◽  
Glutathione Status ◽  
Border Areas ◽  
Low Levels ◽  
Rate Limiting ◽  
The Brain

System x−c, one of the main transporters responsible for central nervous system cystine transport, is comprised of two subunits, xCT and 4F2hc. The transport of cystine into cells is rate limiting for glutathione synthesis, the major antioxidant and redox cofactor in the brain. Alterations in glutathione status are prevalent in numerous neurodegenerative diseases, emphasizing the importance of proper cystine homeostasis. However, the distribution of xCT and 4F2hc within the brain and other areas has not been described. Using specific antibodies, both xCT and 4F2hc were localized predominantly to neurons in the mouse and human brain, but some glial cells were labeled as well. Border areas between the brain proper and periphery including the vascular endothelial cells, ependymal cells, choroid plexus, and leptomeninges were also highly positive for the system x−c components. xCT and 4F2hc are also present at the brush border membranes in the kidney and duodenum. These results indicate that system x−c is likely to play a role in cellular health throughout many areas of the brain as well as other organs by maintaining intracellular cystine levels, thereby resulting in low levels of oxidative stress. (J Histochem Cytochem 54: 549–557, 2006)

Interleukin-6 overexpression as a marker of malignancy in human gliomas

2001 ◽  
Vol 94 (1) ◽  
pp. 97-101 ◽  
Author(s):  
Christine Rolhion ◽  
Frédérique Penault-Llorca ◽  
Jean-Louis Kémény ◽  
Jean-Jacques Lemaire ◽  
Christiane Jullien ◽  
...  
Keyword(s):  
Gene Expression ◽  
Interleukin 6 ◽  
Vascular Endothelial Cells ◽  
Immunohistochemical Analysis ◽  
Vascular Endothelial ◽  
Content Type ◽  
Major Interest ◽  
Polymerase Chain ◽  
The Relationship ◽  
Fine Print

Object. Glioblastomas multiforme (GBMs) grow rapidly and are highly resistant to treatment compared with other glioma types and grades. Consequently, it is of major interest to identify markers of aggressiveness in these tumors that could represent new therapeutic targets. Interleukin (IL)—6 is frequently produced in gliomas and, given its manifold properties, could be considered as a candidate marker. Expression of IL-6 may be involved in cell growth, resistance to chemotherapy and radiotherapy (via an antiapoptotic pathway), and angiogenesis. This study was conducted to test this hypotheses and to evaluate the suitability of IL-6 as a target in the treatment of GBMs. Methods. The authors studied the relationship between the level of IL-6 gene expression as assessed using semiquantitative reverse transcription—polymerase chain reaction and by determining various histological types and grades in a series of 59 gliomas. It was found that GBMs displayed a significantly higher level of IL-6 expression than other types of glioma (p < 0.001). Immunohistochemical analysis revealed that IL-6 was produced mainly by malignant cells and a few vascular endothelial cells. Conclusions. It can be inferred from these findings that IL-6 gene expression is related to glioma aggressiveness and that IL-6 may play a central role in GBM behavior. Interleukin-6, therefore, could be considered as a new potential target in the treatment of GBMs.

scholarly journals Pathogenic Mechanism of Mouse Brain Damage Caused by Oral Infection with Shiga Toxin-Producing Escherichia coliO157:H7

2000 ◽  
Vol 68 (3) ◽  
pp. 1207-1214 ◽  
Author(s):  
Eiji Kita ◽  
Yoshihisa Yunou ◽  
Takaaki Kurioka ◽  
Hiroko Harada ◽  
Shinji Yoshikawa ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Brain Damage ◽  
Shiga Toxin ◽  
Vascular Endothelial Cells ◽  
Oral Infection ◽  
Target Cells ◽  
Vascular Endothelial ◽  
Short Term Exposure ◽  
Tnf Α ◽  
The Brain

ABSTRACT In a previous study, we showed that infection with Shiga toxin (Stx)-producing Escherichia coli O157:H7 (strain SmrN-9) caused neurologic symptoms in malnourished mice with positive immunoreactions of Stx2 in brain tissues. The present study explores the mechanism of how Stx injures the vascular endothelium to enter the central nervous system in mice. Oral infection with strain SmrN-9 elicited a tumor necrosis factor alpha (TNF-α) response in the blood as early as 2 days after infection, while Stx was first detected at 3 days postinfection. In the brain, TNF-α was detected at day 3, and its quantity was increased over the next 3 days. Frozen sections of the brains from moribound mice contained high numbers of apoptotic cells. Glycolipids recognized by an anti-Gb3 monoclonal antibody were extracted from the brain, and purified Stx2 was able to bind to the glycolipids. In human umbilical vascular endothelial cells (HUVEC) cultured with fluorescein-labeled Stx2 (100 ng/ml), TNF-α (20 U/ml) significantly facilitated the intracellular compartmentalization of fluorescence during 24 h of incubation, suggesting the enhanced intracellular processing of Stx2. Consequently, higher levels of apoptosis in HUVEC were found at 48 h. Short-term exposure of HUVEC to Stx2 abrogated their apoptotic response to subsequent incubation with TNF-α alone or TNF-α and Stx2. In contrast, primary exposure of HUVEC to TNF-α followed by exposure to Stx2 alone or TNF-α and Stx2 induced apoptosis at the same level as obtained after 48-h incubation with these two agents. These results suggest that the rapid production of circulating TNF-α after infection induces a state of competence in vascular endothelial cells to undergo apoptosis, which would be finally achieved by subsequent elevation of Stx in the blood. In this synergistic action, target cells must be first exposed to TNF-α. Such cell injury may be a prerequisite to brain damage after infection with Stx-producing E. coliO157:H7.

scholarly journals Enhanced brain angiogenesis in chronic cerebral hypoperfusion after administration of plasmid human vascular endothelial growth factor in combination with indirect vasoreconstructive surgery

2005 ◽  
Vol 103 (5) ◽  
pp. 882-890 ◽  
Author(s):  
Noboru Kusaka ◽  
Kenji Sugiu ◽  
Koji Tokunaga ◽  
Atsushi Katsumata ◽  
Ayumi Nishida ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Control Group ◽  
Vascular Endothelial ◽  
Content Type ◽  
Endothelial Growth Factor ◽  
The Brain ◽  
Brain Angiogenesis ◽  
Fine Print

Object. Vascular endothelial growth factor (VEGF) is a secreted mitogen associated with angiogenesis. The conceptual basis for therapeutic angiogenesis after plasmid human VEGF gene (phVEGF) transfer has been established in patients presenting with limb ischemia and myocardial infarction. The authors hypothesized that overexpression of VEGF using a gene transfer method combined with indirect vasoreconstruction might induce effective brain angiogenesis in chronic cerebral hypoperfusion, leading to prevention of ischemic attacks. Methods. A chronic cerebral hypoperfusion model induced by permanent ligation of both common carotid arteries in rats was used in this investigation. Seven days after induction of cerebral hypoperfusion, encephalomyosynangiosis (EMS) and phVEGF administration in the temporal muscle were performed. Fourteen days after treatment, the VEGF gene therapy group displayed numbers and areas of capillary vessels in temporal muscles that were 2.2 and 2.5 times greater, respectively, in comparison with the control group. In the brain, the number and area of capillary vessels in the group treated with the VEGF gene were 1.5 and 1.8 times greater, respectively, relative to the control group. Conclusions. In rat models of chronic cerebral hypoperfusion, administration of phVEGF combined with indirect vasoreconstructive surgery significantly increased capillary density in the brain. The authors' results indicate that administration of phVEGF may be an effective therapy in patients with chronic cerebral hypoperfusion, such as those with moyamoya disease.

The effect of nimodipine on intracranial pressure

1987 ◽  
Vol 67 (3) ◽  
pp. 387-393 ◽  
Author(s):  
Mark N. Hadley ◽  
Robert F. Spetzler ◽  
Mary S. Fifield ◽  
William D. Bichard ◽  
John A. Hodak
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Systemic Blood Pressure ◽  
Artery Occlusion ◽  
Content Type ◽  
Arterial Blood ◽  
Increased Risk ◽  
Before And After ◽  
The Right ◽  
Cerebral Artery Occlusion

✓ Nimodipine was administered by intravenous infusion to six male baboons before, during, and after 6 hours of middle cerebral artery occlusion. Intracranial pressure (ICP) and systemic blood pressure were monitored continuously. An epidural balloon was inflated at regular intervals at three levels of arterial CO2 tension (25, 35, and 50 mm Hg) before and after the administration of nimodipine, and volume-pressure curves were generated. In every case, curves generated after intravenous nimodipine infusion were lower and shifted more to the right than the same set of curves generated before nimodipine administration, regardless of the baseline ICP. The reduction in ICP following nimodipine infusion was not due to a reduction in mean arterial blood pressure and was statistically significant at all three levels of pCO2 (p < 0.01). These results suggest that, in the presence of elevated ICP due to cerebral infarction, there is no increased risk of exacerbating intracranial hypertension with the addition of nimodipine.

Autoregulation of cerebral blood flow after experimental fluid percussion injury of the brain

1980 ◽  
Vol 53 (4) ◽  
pp. 500-511 ◽  
Author(s):  
W. Lewelt ◽  
L. W. Jenkins ◽  
J. Douglas Miller
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Injury ◽  
Content Type ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Fluid Percussion Injury ◽  
The Brain

✓ To test the hypothesis that concussive brain injury impairs autoregulation of cerebral blood flow (CBF), 24 cats were subjected to hemorrhagic hypotension in 10-mm Hg increments while measurements were made of arterial and intracranial pressure, CBF, and arterial blood gases. Eight cats served as controls, while eight were subjected to mild fluid percussion injury of the brain (1.5 to 2.2 atmospheres) and eight to severe injury (2.8 to 4.8 atmospheres). Injury produced only transient changes in arterial and intracranial pressure, and no change in resting CBF. Impairment of autoregulation was found in injured animals, more pronounced in the severe-injury group. This could not be explained on the basis of intracranial hypertension, hypoxemia, hypercarbia, or brain damage localized to the area of the blood flow electrodes. It is, therefore, concluded that concussive brain injury produces a generalized loss of autoregulation for at least several hours following injury.

Cultured Vascular Endothelial Cells of the Brain.

1996 ◽  
Vol 45 (3) ◽  
pp. 183-199 ◽  
Author(s):  
Mária A Deli ◽  
Ferenc Joó
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
The Brain

Hydrostatically raised intracranial pressure

1972 ◽  
Vol 37 (6) ◽  
pp. 695-699 ◽  
Author(s):  
Timo Kuurne ◽  
Henry Troupp
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Respiratory Arrest ◽  
Carbon Dioxide Tension ◽  
Experimental Models ◽  
Raised Intracranial Pressure ◽  
Acid Base Balance ◽  
Content Type ◽  
Base Balance ◽  
The Brain

✓ Hydrostatic pressure with artificial cerebrospinal fluid (CSF) was applied through a needle inserted into the cisterna magna of rabbits breathing spontaneously. Blood pressure, confluens sinuum pressure and oxygen tension, respiratory rate and volume, and acid-base balance were recorded until respiratory arrest. Blood pressure and confluens sinuum pressure and respiratory volume rose; confluens sinuum oxygen and arterial carbon dioxide tension dropped. The significant similarities and differences in changes in the same parameters following local cold injury to the brain are discussed. Comparisons between different experimental models for raised intracranial pressure must take into consideration the differing reactions of the brain.

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