scholarly journals Regional Cerebral Metabolic Activity in the Rat following Experimental Subarachnoid Hemorrhage

1987 ◽  
Vol 7 (2) ◽  
pp. 193-198 ◽  
Author(s):  
Robert A. Solomon ◽  
Robert L. Lovitz ◽  
Margaret T. Hegemann ◽  
George B. Schuessler ◽  
William L. Young ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Metabolic Activity ◽  
Subarachnoid Space ◽  
Brain Function ◽  
Brain Regions ◽  
Intravenous Injections ◽  
Arterial Blood ◽  
Subarachnoid Injection ◽  
Experimental Subarachnoid Hemorrhage ◽  
Brain Metabolic Activity

A new experimental model was employed to investigate alterations of cerebral metabolic activity in rats subjected to extensive subarachnoid hemorrhage (SAH). The hemorrhages were produced in anesthetized animals by inserting 0.37 ml fresh autologous arterial blood into the subarachnoid space. Rats that underwent sham operations received subarachnoid injections of mock CSF to study the effects of sudden raised intracranial pressure (ICP). Forty-eight hours after subarachnoid injection, the unanesthetized rats were given intravenous injections of [14C]2-deoxyglucose. Experiments were terminated 45 min later by decapitation, and the brains were removed and frozen. Regional brain metabolic activity was studied employing quantitative autoradiography. In comparison with control animals, cerebral metabolic activity was diffusely decreased following SAH. Statistically significant decreases in metabolic activity of <34% were observed in 17 of 30 brain regions studied. The largest percentage reductions were in regions displaying the highest basal metabolic rates. Subarachnoid injections of mock CSF also produced depression of cerebral metabolic activity, but quantitatively these changes were not as pronounced as in the hemorrhage group. These studies demonstrate regional changes in brain function following SAH. The data relate these changes to both the presence of blood in the subarachnoid space and sudden raised ICP.

scholarly journals Brain temperature regulation in poor-grade subarachnoid hemorrhage patients – A multimodal neuromonitoring study

2020 ◽  
pp. 0271678X2091040
Author(s):  
Alberto Addis ◽  
Maxime Gaasch ◽  
Alois J Schiefecker ◽  
Mario Kofler ◽  
Bogdan Ianosi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Function ◽  
Perfusion Pressure ◽  
Clinical Course ◽  
Brain Temperature ◽  
Cerebral Metabolism ◽  
Surrogate Marker ◽  
Poor Grade ◽  
Brain Metabolic Activity ◽  
Elevated Body Temperature

Elevated body temperature (Tcore) is associated with poor outcome after subarachnoid hemorrhage (SAH). Brain temperature (Tbrain) is usually higher than Tcore. However, the implication of this difference (Tdelta) remains unclear. We aimed to study factors associated with higher Tdelta and its association with outcome. We included 46 SAH patients undergoing multimodal neuromonitoring, for a total of 7879 h of averaged data of Tcore, Tbrain, cerebral blood flow, cerebral perfusion pressure, intracranial pressure and cerebral metabolism (CMD). Three-months good functional outcome was defined as modified Rankin Scale ≤2. Tbrain was tightly correlated with Tcore (r = 0.948, p < 0.01), and was higher in 73.7% of neuromonitoring time (Tdelta +0.18°C, IQR −0.01 – 0.37°C). A higher Tdelta was associated with better metabolic state, indicated by lower CMD-glutamate ( p = 0.003) and CMD-lactate ( p < 0.001), and lower risk of mitochondrial dysfunction (MD) (OR = 0.2, p < 0.001). During MD, Tdelta was significantly lower (0°C, IQR −0.2 – 0.1; p < 0.001). A higher Tdelta was associated with improved outcome (OR = 7.7, p = 0.002). Our study suggests that Tbrain is associated with brain metabolic activity and exceeds Tcore when mitochondrial function is preserved. Further studies are needed to understand how Tdelta may serve as a surrogate marker for brain function and predict clinical course and outcome after SAH.

scholarly journals Antivasospastic and antiinflammatory effects of caspase inhibitor in experimental subarachnoid hemorrhage

2007 ◽  
Vol 107 (1) ◽  
pp. 128-135 ◽  
Author(s):  
Keiichi Iseda ◽  
Shigeki Ono ◽  
Keisuke Onoda ◽  
Motoyoshi Satoh ◽  
Hiroaki Manabe ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Separate Experiment ◽  
Caspase Inhibitor ◽  
Caspase 1 ◽  
Delayed Cerebral Vasospasm ◽  
Experimental Subarachnoid Hemorrhage ◽  
Antiinflammatory Effects ◽  
Arterial Endothelial Cells

Object Inflammation in the subarachnoid space and apoptosis of arterial endothelial cells have been implicated in the development of delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). The authors investigated mechanisms of possible antivasospastic effects of N-benzyl-oxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK), a caspase inhibitor that can inhibit both inflammatory and apoptotic systems, in animal models of SAH. Methods Rabbits were assigned to three groups of eight animals each and were subjected to SAH by injection of blood into the cisterna magna. The experiments were performed in the following groups: SAH only, SAH + vehicle, and SAH + Z-VAD-FMK. The Z-VAD-FMK (1 mg) or vehicle (5% dimethyl sulfoxide) was intrathecally administered before SAH induction. Diameters of the basilar artery (BA) were measured on angiograms obtained before and 2 days after SAH. The BA diameter on Day 2 was expressed as a percentage of that before SAH. Interleukin (IL)–1β in the cerebrospinal fluid (CSF) was examined using Western blotting, and brains were immunohistochemically examined for caspase-1 and IL-1β. In a separate experiment, 20 rats were subjected to SAH and their brains were immunohisto-chemically assessed for caspase-1, IL-1β, and macrophages. Results In rabbits, Z-VAD-FMK significantly attenuated cerebral vasospasm (the BA diameter on Day 2 in SAH-only, SAH + vehicle, and SAH + Z-VAD-FMK groups was 66.6 ± 3.2%, 66.3 ± 3.7%, and 82.6 ± 4.9% of baseline, respectively), and suppressed IL-1β release into the CSF and also suppressed immunoreactivities of caspase-1 and IL-1β in macrophages infiltrating into the subarachnoid space. Immunoreactivities for caspase-1 and IL-1β were observed in immunohistochemically proven infiltrating macrophages in rats. Conclusions These results indicate that caspase activation may be involved in the development of SAH-induced vasospasm through inflammatory reaction.

scholarly journals Alterations in Serotonin and Neuropeptide Y Content of Cerebrovascular Sympathetic Nerves following Experimental Subarachnoid Hemorrhage

1989 ◽  
Vol 9 (3) ◽  
pp. 271-279 ◽  
Author(s):  
A. Jackowski ◽  
A. Crockard ◽  
G. Burnstock ◽  
J. Lincoln
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Blood Clot ◽  
Cerebral Arteries ◽  
Immunohistochemical Analysis ◽  
Sympathetic Nerves ◽  
Nerve Fibers ◽  
Arterial Blood ◽  
Experimental Subarachnoid Hemorrhage

The effect of an experimental subarachnoid hemorrhage (SAH) upon neurotransmitter content in sympathetic nerves supplying the major cerebral arteries of the rat has been examined by immunohistochemical analysis and high performance liquid chromatography with electrochemical detection (HPLC–ECD). In particular, changes that occur in sympathetic nerve content of the vasoconstrictor agents serotonin (5-HT) and neuropeptide Y (NPY), which are colocalized with noradrenaline, were assessed. Subarachnoid hemorrhage was induced by a single injection of autologous arterial blood into the cerebrospinal fluid (CSF) space of the cisterna magna. The density of 5-HT-containing and NPY-containing perivascular nerve fibers per unit area of vessels was measured at defined intervals from 15 min to 5 days post-SAH. In addition, an HPLC study was performed to quantify the actual amounts of 5-HT and noradrenaline present in circle of Willis vessels at 3 h post-SAH. Comparison was made with sham-operated animals and animals that received a cisternal injection of buffered saline in place of blood. Our results reveal a major increase in cerebrovascular sympathetic nerve content of serotonin, arising by uptake, presumably from subarachnoid blood clot, within the first 3 h post-SAH. Neuropeptide Y content, however, decreased from 3 up to 48 h posthemorrhage. By 3 days post-SAH, when the majority of subarachnoid clot had resorbed, the sympathetic nerve content of both NPY and 5-HT was restored to normal. This pattern of change was not observed in either sham-operated or saline-injected controls.

scholarly journals Interregional causal influences of brain metabolic activity reveal the spread of aging effects during normal aging

2018 ◽  
Author(s):  
Xin Di ◽  
Marie Wölfer ◽  
Mario Amend ◽  
Hans Wehrl ◽  
Tudor M. Ionescu ◽  
...  
Keyword(s):  
Metabolic Activity ◽  
Fdg Pet ◽  
Aging Process ◽  
Brain Aging ◽  
Brain Regions ◽  
Causality Analysis ◽  
Aging Effects ◽  
Activity Data ◽  
Age Related ◽  
Brain Metabolic Activity

AbstractDuring healthy brain aging, different brain regions show anatomical or functional declines at different rates, and some regions may show compensatory increases in functional activity. However, few studies have explored interregional influences of brain activity during the aging process. We proposed a causality analysis framework combining high dimensionality independent component analysis (ICA), Granger causality, and LASSO (least absolute shrinkage and selection operator) regression on longitudinal brain metabolic activity data measured by Fludeoxyglucose positron emission tomography (FDG-PET). We analyzed FDG-PET images from healthy old subjects, who were scanned for at least five sessions with an averaged intersession interval of about one year. The longitudinal data were concatenated across subjects to form a time series, and the first order autoregressive model was used to measure interregional causality among the independent sources of metabolic activity identified using ICA. Several independent sources with reduced metabolic activity in aging, including the anterior temporal lobe and orbital frontal cortex, demonstrated causal influences over many widespread brain regions. On the other hand, the influenced regions were more distributed, and had smaller age related declines or even relatively increased metabolic activity. The current data demonstrated interregional spreads of aging on metabolic activity at the scale of a year, and have identified key brain regions in the aging process that have strong influences over other regions.

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.

scholarly journals Changes of Subarachnoid Space after the Experimental Subarachnoid Hemorrhage in the Dog

1976 ◽  
Vol 16pt2 (4) ◽  
pp. 323-330
Author(s):  
SHIGEHARU SUZUKI ◽  
KUNIHIKO EBINA ◽  
MASAMI ISHII ◽  
TAKASHI IWABUCHI
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Experimental Subarachnoid Hemorrhage

Abstract TP418: Red Blood Cell Transfusion Increases Cerebral Oxygen Delivery After Subarachnoid Hemorrhage Regardless of Hemoglobin Level

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Rajat Dhar ◽  
Allyson Zazulia ◽  
Tom Videen ◽  
Colin P Derdeyn ◽  
Michael Diringer
Keyword(s):  
At Risk ◽  
Subarachnoid Hemorrhage ◽  
Oxygen Delivery ◽  
Delayed Cerebral Ischemia ◽  
Brain Regions ◽  
Oxygen Extraction Fraction ◽  
Red Blood Cell Transfusion ◽  
Cerebral Oxygen ◽  
Arterial Blood ◽  
Patients At Risk

Introduction: Impaired oxygen delivery (DO 2 ), as a result of reduced cerebral blood flow (CBF), is the hallmark of delayed cerebral ischemia (DCI) following subarachnoid hemorrhage (SAH). Anemia further contributes to reductions in DO 2 and places the brain at risk for infarction. Transfusion, by raising hemoglobin (Hgb) and oxygen content of arterial blood, may be able to reduce the risk of ischemia. However, it is unknown whether an Hgb threshold exists above which CBF will fall sufficient to negate any benefit of transfusion on DO 2 . In this physiologic proof-of-principle study we evaluated whether transfusion improves DO 2 and reduces brain vulnerable to ischemia across a broad range of Hgb values. Methods: 47 SAH patients with/at-risk for DCI with Hgb 7-13 g/dl were transfused 1 unit of red blood cells (RBCs). 15 O-PET imaging was used to measure CBF, DO 2 , and oxygen extraction fraction (OEF) before and after transfusion. Vulnerable brain regions were defined as those with baseline DO 2 < 4.5 ml/100g/min (equivalent to CBF of 25 ml/100g/min at low-normal Hgb). Results: Baseline Hgb was 9.7 g/dl (range 6.9-12.5) and CBF was 43±11 ml/100g/min. After transfusion, Hgb rose by 12% and global DO 2 by 10% (from 5.0 to 5.5 ml/100g/min, p=0.001), with CBF only marginally lower; response to transfusion was not dependent on Hgb level. Transfusion resulted in a greater (16%) rise in DO 2 , associated with a larger reduction in OEF, in vulnerable brain regions (p=0.005 for low vs. normal regions), even after adjusting for Hgb. Number of vulnerable regions was reduced from median 9 to 4 per patient (p=0.005). Conclusions: Transfusion of RBCs to patients at-risk for DCI improves cerebral oxygen delivery, preferentially to vulnerable regions and reduces brain at-risk for ischemia. This physiologic benefit does not appear limited to those with severe anemia but persists to Hgb as high as 13 g/dl. Our findings suggest that restrictive transfusion practices may not be appropriate in this population. Prospective trials are needed to determine if these physiologic benefits outweigh risks of transfusion and translate into clinical prevention of DCI.

Observations on the effects of intrathecal papaverine in experimental vasospasm

1973 ◽  
Vol 38 (1) ◽  
pp. 20-25 ◽  
Author(s):  
Masahiro Ogata ◽  
B. M. Marshall ◽  
W. M. Lougheed
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Subarachnoid Space ◽  
Biphasic Response ◽  
Content Type ◽  
Arterial Blood ◽  
Potent Vasodilator ◽  
Slow Infusion ◽  
Fine Print ◽  
Experimentally Induced

✓ Subarachnoid hemorrhage was produced in monkeys by injecting fresh arterial blood. Serial angiographic studies of the basilar artery then showed vasospasm, occurring as a biphasic response similar to that seen following subarachnoid hemorrhage in man. Papaverine had previously been found to be the most potent vasodilator for topical use to release spasm resulting from experimentally induced subarachnoid hemorrhage. This drug was therefore administered, in various dilutions, as a slow infusion into the subarachnoid space of these monkeys. In a concentration of 0.03%, papaverine proved to be effective in reducing the vasospasm without toxicity.

Sign in / Sign up

Export Citation Format

Share Document