Effect of systemic hypotension on cerebral energy metabolism during chronic cerebral vasospasm in primates

1993 ◽  
Vol 78 (1) ◽  
pp. 112-119 ◽  
Author(s):  
Yuji Handa ◽  
Tetsuya Kubota ◽  
Akira Tsuchida ◽  
Masanori Kaneko ◽  
Hakan Caner ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cerebral Vasospasm ◽  
Mr Spectroscopy ◽  
High Energy ◽  
Cerebral Energy Metabolism ◽  
Systemic Hypotension ◽  
Arterial Blood ◽  
The Mean ◽  
The Right ◽  
Chronic Cerebral Vasospasm

✓ The influence of systemic hypotension on cerebral blood flow (CBF) and energy metabolism during chronic cerebral vasospasm after subarachnoid hemorrhage was studied in 15 monkeys. Changes in the phosphorus spectrum, as demonstrated by in vivo phosphorus-31 (31P) magnetic resonance (MR) spectroscopy, or in regional CBF were measured in the parietal cortex during graded hypotension. Sequential changes in the phosphorus spectrum were observed during moderate hypotension in the animals 7 days after the introduction of an autologous blood clot around the right middle cerebral artery (MCA). Angiograms revealed a reduction in vessel caliber by approximately 50% in the right MCA. The mean CBF in the spasm side decreased in parallel with a decrease in the mean arterial blood pressure (MABP) from 120 to 40 mm Hg, indicating the abolition of autoregulation. There were no significant differences in the mean percentage totals of inorganic phosphate (Pi), phosphocreatine (PCr), adenosine triphosphate (ATP), and pH between the hemispheres at baseline MABP before hypotension. The values of PCr, ATP, and pH decreased significantly (p < 0.05) and Pi increased significantly (p < 0.05) at an MABP of less than 60 mm Hg in the involved hemisphere. The ratio of PCr:Pi decreased in parallel with a decrease in MABP. The ATP showed a stepwise decrease during moderate hypotension (MABP 60 mm Hg) and was reduced significantly 20 minutes after the beginning of hypotension (p < 0.05). The results indicate that, during chronic vasospasm, changes in cerebral energy metabolism are coupled with changes in CBF in the state of impaired autoregulation. There exists a critical level for ischemia below which high-energy phosphorus metabolites become markedly depleted. It is suggested that 31P MR spectroscopy may be useful to evaluate the ischemic vulnerability of brain tissue in order to prevent delayed neurological deficit during cerebral vasospasm.

Impairment of Cerebral Autoregulation during the Development of Chronic Cerebral Vasospasm after Subarachnoid Hemorrhage in Primates

Neurosurgery ◽  
1991 ◽  
Vol 28 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Hiroaki Takeuchi ◽  
Yuji Handa ◽  
Hidenori Kobayashi ◽  
Ilirokazu Kawano ◽  
Minoru Hayashi
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Arterial Blood Pressure ◽  
Cerebral Vasospasm ◽  
Conduction Time ◽  
Arterial Blood ◽  
The Mean ◽  
The Right ◽  
Chronic Cerebral Vasospasm ◽  
The Brain

Abstract We studied the impairment of autoregulation of cerebral blood flow (CBF) and its effect on the electrical activity of the brain during the development of chronic cerebral vasospasm after subarachnoid hemorrhage, using a vasospasm model in primates. Fourteen animals were divided into two groups: a clot group (8) and a sham-operated group (6). To induce subarachnoid hemorrhage, all the animals underwent craniectomy, and in the clot group, the autologous blood clot was located around the arteries dissected free from the arachnoid membrane. Cerebral angiography was performed before subarachnoid hemorrhage and 7 days after (Day 7). On Day 7, regional CBF in the parietal lobe—measured by the hydrogen clearance method—and central conduction time were studied during either graded hypertension or hypotension. In the clot group, the mean vessel caliber of the cerebral arteries on the right side (clot side) of the circle of Willis showed significant (P&lt;0.01) reduction (more than 40%) as compared with the values on the contralateral, non-clot side. The values for the bilateral parietal CBF in the sham-operated group and the left parietal CBF in the clot group were fairly constant when the mean arterial blood pressure (MABP) was in the range of 60 to 160 mm Hg. In the clot group, right parietal CBF was significantly (P &lt; 0.05) smaller than that on the left side at an MABP level of 40 to 100 mm Hg, and increased at an MABP level of 180 mm Hg. The right parietal CBF increased as the arterial blood pressure increased, showing impairment of autoregulation. The central conduction time on the right side in the clot group was significantly (P&lt;0.05) prolonged at an MABP of 40 mm Hg. It is suggested that impairment of autoregulation is strongly affected by the development of cerebral vasospasm and that, in this state, a decrease in cerebral perfusion pressure easily depresses the electrical function of the brain.

Time course of the impairment of cerebral autoregulation during chronic cerebral vasospasm after subarachnoid hemorrhage in primates

1992 ◽  
Vol 76 (3) ◽  
pp. 493-501 ◽  
Author(s):  
Yuji Handa ◽  
Minoru Hayashi ◽  
Hiroaki Takeuchi ◽  
Tetsuya Kubota ◽  
Hidenori Kobayashi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Cerebral Autoregulation ◽  
Time Course ◽  
Blood Clot ◽  
Autologous Blood ◽  
Conduction Time ◽  
Arterial Blood ◽  
The Right ◽  
Chronic Cerebral Vasospasm

✓ The time course of the impairment of cerebral autoregulation during chronic cerebral vasospasm after subarachnoid hemorrhage was studied in 18 monkeys. Changes in cerebral blood flow (CBF) at the regional level and central conduction times during either graded hypo- or hypertension were evaluated in these animals at three stages (3, 7, and 14 days) following the introduction of an autologous blood clot around the right middle cerebral artery (MCA). Angiograms revealed a reduction in vessel caliber (compared to the baseline level in the involved MCA) of 30% at 3 days, 50% at 7 days, and 10% at 14 days. At all stages, CBF remained constant at mean arterial blood pressures (MABP) of 60 to 160 mm Hg in the noninvolved hemisphere. In contrast, at the 3- and 7-day stages, there was an impairment of autoregulation in the involved hemisphere at MABP of 40 to 180 mm Hg. The right hemispheric CBF was significantly (p < 0.05) lower than that in the left throughout the period of investigation at MABP below 120 mm Hg, but rose to exceed the left CBF at MABP above 180 mm Hg at the 7-day stage and 160 mm Hg at the 14-day stage. The right-sided central conduction time showed significant (p < 0.05) prolongation at MABP below 60 mm Hg at the 3-day stage and 40 mm Hg at the 7-day stage. It is suggested that these results may help to develop guidelines for hemodynamic therapy for vasospasm in its various stages.

Reversal and prevention of cerebral vasospasm by intracarotid infusions of nitric oxide donors in a primate model of subarachnoid hemorrhage

1997 ◽  
Vol 87 (5) ◽  
pp. 746-751 ◽  
Author(s):  
Ryszard M. Pluta ◽  
Edward H. Oldfield ◽  
Robert J. Boock
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Arterial Blood Pressure ◽  
Cerebral Vasospasm ◽  
Primate Model ◽  
Arterial Blood ◽  
Infusion Experiment ◽  
The Mean ◽  
The Right

✓ Decreased endothelium-derived relaxing factor, nitric oxide (NO), in the arterial wall has been hypothesized to be a potential cause of cerebral vasospasm following subarachnoid hemorrhage (SAH). The authors sought to determine whether intracarotid infusions of newly developed NO-donating compounds (NONOates) could reverse vasospasm or prevent the occurrence of cerebral vasospasm in a primate model of SAH. Twenty-one cynomolgus monkeys were studied in two experimental settings. In an acute infusion experiment, saline or NONOate was infused intracarotidly in four normal monkeys and in four monkeys after onset of SAH. During the infusions regional cerebral blood flow (rCBF) was measured in eight animals and CBF velocity in two. In a chronic infusion experiment, saline (four animals) or NONOate (diethylamine-NO [three animals] or proli-NO [six animals]) was infused intracarotidly in monkeys for 7 days after SAH. In acute infusion experiments, 3-minute intracarotid diethylamine-NO infusions reversed arteriographically confirmed vasospasm of the right middle cerebral artery (MCA) (as viewed on anteroposterior projection, the decrease in area was 8.4 ± 4.3% in the treatment group compared with 35 ± 12% in the control group; p < 0.004), increased rCBF by 31 ± 1.9% (p < 0.002), and decreased the mean systolic CBF velocity in the right MCA. In a long-term infusion experiment, the area of the right MCA in control animals decreased by 63 ± 5%. In animals undergoing a 7-day continuous glucantime-NO intracarotid infusion, the area of the right MCA decreased by 15 ± 6.2%, and in animals undergoing a 7-day proli-NO infusion, the area of the right MCA decreased by 11 ± 2.9% (p < 0.05). The mean arterial blood pressure decreased in the glucantime-NO group from 75 ± 12 mm Hg (during saline infusion) to 57 ± 10 mm Hg (during glucantime-NO infusion; p < 0.05), but it was unchanged in animals undergoing proli-NO infusion (76 ± 12 mm Hg vs. 78 ± 12 mm Hg). Results of these experiments show that cerebral vasospasm is both reversed and completely prevented by NO replacement. However, only the use of regional infusion of the NONOate with an extremely short half-life avoided a concomitant decrease in arterial blood pressure, which could produce cerebral ischemia in patients with impaired autoregulation of CBF after the rupture of an intracranial aneurysm.

Effect of hyperventilation on dynamics of cerebral energy metabolism

1975 ◽  
Vol 228 (6) ◽  
pp. 1862-1867 ◽  
Author(s):  
K Kogure ◽  
R Busto ◽  
A Matsumoto ◽  
P Scheinberg ◽  
OM Reinmuth
Keyword(s):  
Energy Metabolism ◽  
Closed System ◽  
Energy Production ◽  
Energy Charge ◽  
High Energy ◽  
Utilization Rate ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Cerebral Energy Metabolism ◽  
Extreme Degree

Hypocapnia of moderate and extreme degree (Paco2 21.1 and 13.5 torr, respectively)was induced by hyperventilation in rats subjected to the closed system of Lowry inorder to evaluate the effects on utilization rate of cerebral energy metabolites. The tissue levels of high-energy phosphates and calculated intracellular pH did not change, whereas glucose, pyruvate, and lactate increased significantly. The La/Pyratio and NADH/NAD-+ RATIO BOTH INCREASED IN PROPORTION TO THE DEGREE OF HYPOCAPNIA.Utilization rates of glucose, glycogen, and ATP were all significantly reduced by hypocapnia, whereas the utilization rate of phosphocreatine was increased. The rate oftotal high-energy phosphate use was also diminished in proportion to the degree of hypocapnia. The constant value of the energy charge (0.94 plus or minus 0.01) indicates that the energy production rate might also be reduced by hyperventilation; thus the intermediate metabolics and substrates increased. It is concluded that extreme hypocapnia reduces the rate of cerebral energy metabolism significantly.

scholarly journals Cerebral energy metabolism in mallard ducks during apneic asphyxia: the role of oxygen conservation

1980 ◽  
Vol 239 (3) ◽  
pp. R352-R357
Author(s):  
R. M. Bryan ◽  
D. R. Jones
Keyword(s):  
Energy Metabolism ◽  
Right Hemisphere ◽  
Artificial Ventilation ◽  
Reduced Form ◽  
Cerebral Energy Metabolism ◽  
Nadh Fluorescence ◽  
Tissue Po2 ◽  
The Right ◽  
Electroencephalogram Eeg

Cerebral energy metabolism during apneic asphyxia was studied in ducks. Fluctuations in the reduced form of respiratory chain nicotinamide adenine dinucleotide (NADH) were monitored from the left cerebral hemisphere and used as an indicator of mitochondrial hypoxia. Electroencephalogram (EEG) and surface PO2 were recorded from the right hemisphere. Forced dives of 4- to 7-min duration on restrained ducks were characterized by bradycardia and an accumulation of NADH, which increased throughout the diving period. NADH returned to the preasphyxic level when breathing was resumed. In later experiments, asphyxia was produced by stopping artificial ventilation in paralyzed ducks. Asphyxia produced by this means caused similar changes in the measured variables (heart rate, blood pressure, and NADH fluorescence) to those obtained in forced submergence of nonparalyzed ducks. The inhibition of cardiovascular adjustments by atropine caused NADH to increase faster and tissue PO2 to decrease faster during apneic asphyxia than in nonatropinized ducks. We conclude that the oxygen-conserving cardiovascular adjustments play a key role in the increased cerebral tolerance to apneic asphyxia in ducks.

Effects of ML-9 on experimental delayed cerebral vasospasm

1989 ◽  
Vol 71 (6) ◽  
pp. 916-922 ◽  
Author(s):  
Kiyokazu Kokubu ◽  
Eiichi Tani ◽  
Masaru Nakano ◽  
Nobutaka Minami ◽  
Hideki Shindo
Keyword(s):  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Canine Model ◽  
Neurological Deficits ◽  
Content Type ◽  
Delayed Cerebral Vasospasm ◽  
Arterial Blood ◽  
Complete Reversal ◽  
The Mean ◽  
Dose Dependent

✓ Experimental delayed cerebral vasospasm was produced in a two-hemorrhage canine model. The spastic basilar artery was exposed via the transclival route under a surgical microscope, and was dilated by the topical application of 1-(5-chloronaphthalenesulfonyl)-1H-hexa-hydro-1,4-diazepine(ML-9), a selective antagonist of myosin light chain kinase. Dilation was dose-dependent, with a median effective dose (± standard deviation) of 51.4 ± 6.9 µM. In addition, 50 µM of ML-9 was injected into the cisterna magna until the intracranial pressure (ICP) reached 200 mm H2O for 30 minutes, including a complete reversal of angiographic delayed vasospasm in three of seven dogs; in contrast, 150 µM of ML-9 was infused at 1.52 ml/min into the vertebral artery for 30 minutes, producing little dilation of the spastic basilar artery. In another study, the intracisternal perfusion of 50 µM of ML-9 at 1.48 ml/min for 30 minutes in dogs with an ICP of less than 200 mm H2O produced no serious electroencephalographic abnormalities, and the mean arterial blood pressure and pulse rate remained normal; no neurological deficits or significant histological abnormalities ascribable to the intracisternal ML-9 were found.

scholarly journals Cerebral Energy Metabolism in Phenylketonuria: Findings by Quantitative In Vivo 31P MR Spectroscopy

2003 ◽  
Vol 53 (4) ◽  
pp. 654-662 ◽  
Author(s):  
Joachim Pietz ◽  
André Rupp ◽  
Friedrich Ebinger ◽  
Dietz Rating ◽  
Ertan Mayatepek ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Mr Spectroscopy ◽  
Cerebral Energy Metabolism ◽  
31P Mr Spectroscopy

scholarly journals Captopril Partially Decreases the Effect of H2S on Rat Blood Pressure and Inhibits H2S-Induced Nitric Oxide Release From S-Nitrosoglutathione

2015 ◽  
pp. 479-486 ◽  
Author(s):  
M. DROBNÁ ◽  
A. MISAK ◽  
T. HOLLAND ◽  
F. KRISTEK ◽  
M. GRMAN ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Biological Activities ◽  
Renin Angiotensin System ◽  
Bolus Administration ◽  
Angiotensin System ◽  
Nitric Oxide Release ◽  
Arterial Blood ◽  
Biphasic Effect ◽  
The Mean ◽  
The Right

We studied the effects of the H2S donor Na2S on the mean arterial blood pressure (MAP) and heart and breathing rates of anesthetized Wistar rats in the presence and absence of captopril. Bolus administration of Na2S (1-4 µmol/kg) into the right jugular vein transiently decreased heart and increased breathing rates; at 8-30 µmol/kg, Na2S had a biphasic effect, transiently decreasing and increasing MAP, while transiently decreasing heart rate and increasing and decreasing breathing rate. These results may indicate independent mechanisms by which H2S influences MAP and heart and breathing rates. The effect of Na2S in decreasing MAP was less pronounced in the presence of captopril (2 µmol/l), which may indicate that the renin-angiotensin system is partially involved in the Na2S effect. Captopril decreased H2S-induced NO release from S-nitrosoglutathione, which may be related to some biological activities of H2S. These results contribute to the understanding of the effects of H2S on the cardiovascular system.

Histological studies of intracranial vessels in primates following transluminal angioplasty for vasospasm

1993 ◽  
Vol 78 (3) ◽  
pp. 481-486 ◽  
Author(s):  
Hidenori Kobayashi ◽  
Hisashi Ide ◽  
Hiroshi Aradachi ◽  
Yoshikazu Arai ◽  
Yuji Handa ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Cerebral Artery ◽  
Cell Damage ◽  
Blood Clot ◽  
Autologous Blood ◽  
Transluminal Angioplasty ◽  
Content Type ◽  
Histological Studies ◽  
The Right ◽  
Chronic Cerebral Vasospasm

✓ Percutaneous transluminal angioplasty for treatment of cerebral vasospasm was performed in primates. Chronic cerebral vasospasm was induced by placement of an autologous blood clot over the right internal carotid artery (ICA), middle cerebral artery (MCA), and anterior cerebral artery (ACA). Cerebral angiography on Day 7 showed that the diameters of the ICA, MCA, and ACA were reduced to 55.7% ± 1.3%, 55.3% ± 2.6%, and 59.6% ± 1.3%, respectively, of baseline. The angioplasty was carried out with a silicone microballoon attached to a microcatheter under somatosensory evoked potential (SEP) monitoring on Day 7. The angioplasty for ICA was performed satisfactorily; however, the balloon could be not advanced to the spastic M1 or A1 portions of the cerebral artery. Following angioplasty, the diameters of the ICA, the M1 segment, and the A1 segment were 79.6% ± 2.9% (p < 0.001), 67.6% ± 4.3% (p < 0.05), and 61.7% ± 2.2% (not significant), respectively, of baseline. Histological studies demonstrated that the vessels were well dilated and patent without endothelial cell damage.

Relationship of blood flow and myocardial Rb86 clearance in right and left ventricles

1963 ◽  
Vol 205 (2) ◽  
pp. 382-384 ◽  
Author(s):  
William D. Love ◽  
Lawrence P. O'Meallie
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Venous Blood ◽  
Percentage Error ◽  
Fick Principle ◽  
Mean Error ◽  
Arterial Blood ◽  
The Mean ◽  
The Right ◽  
Relationship Of

The rate of myocardial clearance of Rb86 from arterial blood and the rate of coronary blood flow were studied simultaneously during a 10-min period of isotope infusion in dogs. In order to measure blood flow to the right and left ventricles separately using the Fick principle, venous blood was obtained from an anterior cardiac vein and from the coronary sinus. The relationship of myocardial blood flow and Rb86 clearance was not detectably different in the right and left ventricles. The percentage error in predicting flow from clearance rose as the values increased. At rates of flow below 6 ml/g 10 min the mean error was 4.7%. From 6 to 12 ml/g 10 min the mean error was 10.0% in controls and 14.4% in a group with pulmonary embolism or obstruction of the pulmonary artery. Since the clearance technique does not require catheterization of a cardiac vein, this method can be used to study coronary blood flow under conditions approximating the undisturbed state.

Sign in / Sign up

Export Citation Format

Share Document