Effects of experimental intracerebral hemorrhage on blood flow, capillary permeability, and histochemistry

1987 ◽  
Vol 66 (4) ◽  
pp. 555-562 ◽  
Author(s):  
Fredrik P. Nath ◽  
Paul T. Kelly ◽  
Alistair Jenkins ◽  
A. David Mendelow ◽  
David I. Graham ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracerebral Hemorrhage ◽  
Caudate Nucleus ◽  
Brain Damage ◽  
Structural Damage ◽  
Time Course ◽  
Capillary Permeability ◽  
Autologous Blood ◽  
Ischemic Damage ◽  
Content Type

✓ Experimental intracerebral hemorrhage has been shown to cause extensive cerebral ischemia. This study was performed to ascertain the time course of these changes and also to examine the type of brain damage that may occur under such circumstances. Halothane anesthesia was induced in rats, and 25 µl autologous blood was injected into the caudate nucleus; the effects were studied with autoradiographic measurement of local cerebral blood flow and capillary permeability, and also by light microscopy and histochemical techniques. Blood flow returned to normal or to slightly increased levels within the first 3 hours, and ischemic levels of flow were found to persist only to a marginal degree beyond 10 minutes after the lesions were made. Capillary permeability was maximum during the first 30 minutes after the hemorrhage and diminished with time. Structural evidence of ischemic damage was localized to the cortex overlying the hemorrhage, but was not seen in the caudate nucleus. Nevertheless, histochemical investigation did reveal an area of disturbed enzyme function in the striatum. This finding of biochemical disturbance without structural evidence of ischemic damage reveals that there is an area around the hematoma that, although demonstrating disturbed function, does not show structural damage, and the milieu of this partially injured brain may be implicated in the delayed development of the ischemic brain damage that follows intracerebral hemorrhage in man.

Early hemodynamic changes in experimental intracerebral hemorrhage

1986 ◽  
Vol 65 (5) ◽  
pp. 697-703 ◽  
Author(s):  
Fredrik P. Nath ◽  
Alistair Jenkins ◽  
A. David Mendelow ◽  
David I. Graham ◽  
Graham M. Teasdale
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracerebral Hemorrhage ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Autologous Blood ◽  
Local Cerebral Blood Flow ◽  
Hemodynamic Changes ◽  
Content Type ◽  
Pressure Changes

✓ A model of experimental intracerebral hemorrhage is described in which carefully controlled volumes of autologous blood were injected at arterial pressure into the caudate nucleus of the rat. A comparison of intracranial pressure changes and local cerebral blood flow (CBF) was made between three groups of rats, each receiving different injection volumes, and sham-operated control rats by monitoring intraventricular pressure and by obtaining quantitative autoradiographic measurements of CBF within 1 minute of the experimental hemorrhage. Cerebral blood flow was reduced both around the hematoma and in the surrounding brain. This change was strongly volume-dependent and was not accompanied by significant alterations in cerebral perfusion pressure. This finding suggests that the degree of ischemia at the time of an intracerebral bleed depends on the size of the lesion, and implicates local squeezing of the microcirculation by the hematoma, rather than a generalized alteration in perfusion pressure, as the cause of ischemia.

Experimental intracerebral hemorrhage: effects of a temporary mass lesion

1987 ◽  
Vol 66 (4) ◽  
pp. 568-576 ◽  
Author(s):  
E. J. Sinar ◽  
A. David Mendelow ◽  
David I. Graham ◽  
Graham M. Teasdale
Keyword(s):  
Intracerebral Hemorrhage ◽  
Caudate Nucleus ◽  
Treated Group ◽  
Control Group ◽  
Ischemic Damage ◽  
Balloon Inflation ◽  
Content Type ◽  
Carbon 14 ◽  
The Mean ◽  
Hydrogen Clearance

✓ Late pathophysiological events after the production and subsequent removal of an intracerebral mass were investigated using a mechanical microballoon model to simulate intracerebral hemorrhage. Immediately following balloon inflation in the caudate nucleus of rats, there was a significant increase in intracranial pressure to 14 ± 1 mm Hg (mean ± standard error of the mean), accompanied by a reduction in cerebral blood flow (CBF) in the ipsilateral frontal cortex, as measured by the hydrogen-clearance technique. Carbon-14-iodoantipyrine autoradiography revealed a significant reduction in the CBF of the ipsilateral caudate nucleus 4 hours after balloon inflation: 31% of the caudate nucleus had a CBF of less than 20 ml ⋅ 100 gm−1 ⋅ min−1 compared to only 1% in the sham-treated control group (balloon insertion without inflation). The rats with an intracerebral mass exhibited a significant increase in the volume of ischemic damage in the ipsilateral caudate nucleus (17.1% of total volume) compared to only 1.7% in the sham-treated group; however, there was no evidence of cerebral edema. Ischemic damage and reduced CBF persisted for 4 hours after transient inflation of a microballoon in the caudate nucleus. This suggests that ischemic damage occurs at the time of formation of the lesion and is not prevented by its early removal.

Regional blood flow and capillary permeability in the ethylnitrosourea-induced rat glioma

1981 ◽  
Vol 55 (6) ◽  
pp. 922-928 ◽  
Author(s):  
Kazuo Yamada ◽  
Toru Hayakawa ◽  
Yukitaka Ushio ◽  
Norio Arita ◽  
Amami Kato ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brain Tissue ◽  
Evans Blue ◽  
Capillary Permeability ◽  
Regional Blood Flow ◽  
Blue Staining ◽  
Content Type ◽  
Rat Glioma ◽  
Blood Flows ◽  
Diameter Reduction

✓ Regional cerebral blood flow and capillary permeability of rat brains bearing ethylnitrosourea-induced gliomas of various size were investigated with 14C-antipyrine autoradiography and Evans blue staining. In the small tumors (<2 mm in diameter), blood flow was uniformly reduced when compared to the adjacent brain. Even in tiny tumors (0.3 to 0.4 mm in diameter), reduction in blood flow was evident. In the medium (2 to 4 mm in diameter) and large (> 4 mm in diameter) tumors, the blood flow increased or decreased depending on the part of the tumor examined. The necrotic center and peripheral edge had low blood flows, whereas the viable portion adjacent to the necrotic center had high blood flows. Blood flow in the brain tissue adjacent to medium and large tumors was lower than control brain tissue, probably due to local edema. Leakage of intravenous Evans blue in the tissue was only evident in the large tumors with central necrosis. The present findings suggest that neovascularization of the tumor may occur when the tumor reaches a certain size, and leaky new vessels may be the cause of brain edema associated with tumor.

Pathophysiology of periventricular tissue changes with raised CSF pressure in cats

1983 ◽  
Vol 59 (4) ◽  
pp. 606-611 ◽  
Author(s):  
Gary A. Rosenberg ◽  
Linda Saland ◽  
Walter T. Kyner
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
White Matter ◽  
Caudate Nucleus ◽  
Clinical Symptoms ◽  
Periventricular White Matter ◽  
Content Type ◽  
Acute Hydrocephalus ◽  
Tissue Changes ◽  
Adult Cats

✓ Intraventricular pressure (IVP) is increased in the early stages of acute hydrocephalus. Pressure falls, however, when compensatory routes for cerebrospinal fluid (CSF) absorption develop. In order to better understand the pathophysiology of acute hydrocephalus, the authors performed ventriculocisternal perfusions on adult cats with outflow pressures maintained at either −5, 20, or 40 cm H2O. Cerebral blood flow (CBF) was determined by the iodoantipyrine method. Penetration of an extracellular marker, horseradish peroxidase (HRP), was visualized histologically. Capillary transfer of radiolabeled molecules from CSF to blood was measured by steady-state tissue clearance. Increased IVP had several effects: 1) significant reduction in mean CBF in the periventricular white matter; 2) penetration of the HRP into deep white matter; and 3) prolongation of steady-state tissue clearance half-time for (14C)-ethylene glycol in the caudate nucleus. Reduced blood flow to periventricular white matter and impaired molecular clearance in the caudate nucleus may contribute to the clinical symptoms in acute hydrocephalus.

Brain blood volume and blood flow in patients with plateau waves

1985 ◽  
Vol 63 (4) ◽  
pp. 556-561 ◽  
Author(s):  
Minoru Hayashi ◽  
Hidenori Kobayashi ◽  
Yuji Handa ◽  
Hirokazu Kawano ◽  
Masanori Kabuto
Keyword(s):  
Blood Flow ◽  
Caudate Nucleus ◽  
Frontal Lobe ◽  
Blood Volume ◽  
Temporal Lobe ◽  
Clinical Symptoms ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Rapid Sequence ◽  
Plateau Waves

✓ Plateau waves, characterized by acute transient rises of the intracranial pressure (ICP), are accompanied by a marked decrease of the cerebral perfusion pressure. Patients with plateau waves, however, often show no clinical symptoms of ischemia of the brain stem, such as vasopressor response or impairment of consciousness during the waves. The authors studied brain blood volume and blood flow with dynamic computerized tomography using rapid-sequence scanning in patients with plateau waves identified during continuous ICP recording. Following an intravenous bolus injection of contrast medium, density-versus-time curves were obtained for the regions of interest; that is, the frontal lobe, the temporal lobe, the caudate nucleus, the putamen, and the pons. The dynamic studies were undertaken when the ICP was high during a plateau-wave phase and when it was low during an interval phase between two plateau waves. The results indicate that, in the cerebral hemisphere (frontal lobe, temporal lobe, caudate nucleus, and putamen), plateau waves were accompanied by an increase in blood volume and, at the same time, a decrease in blood flow. In the pons, however, both the blood volume and blood flow showed little change during plateau waves as compared with the intervals between two plateau waves. These observations may explain why there is no rise in the systemic blood pressure and why patients are often alert during plateau waves.

Improvement in neurological outcome after administration of atorvastatin following experimental intracerebral hemorrhage in rats

2004 ◽  
Vol 101 (1) ◽  
pp. 104-107 ◽  
Author(s):  
Donald Seyfried ◽  
Yuxia Han ◽  
Dunyue LU ◽  
Jieli Chen ◽  
Ali Bydon ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Functional Outcome ◽  
Autologous Blood ◽  
Cell Loss ◽  
Study Data ◽  
Content Type ◽  
Ipsilateral Striatum ◽  
The Right ◽  
Higher Doses ◽  
Fine Print

Object. Atorvastatin, a β-hydroxy-β-methylglutaryl coenzyme A reductase inhibitor, improves neurological functional outcome, reduces cerebral cell loss, and promotes regional cellular plasticity when administered after intracerebral hemorrhage (ICH) in rats. Methods. Autologous blood was stereotactically injected into the right striatum in rats, and atorvastatin was administered orally beginning 24 hours after ICH and continued daily for 1 week. At a dose of 2 mg/kg, atorvastatin significantly reduced the severity of neurological deficit from 2 to 4 weeks after ICH. The area of cell loss in the ipsilateral striatum was also significantly reduced in these animals. Consistent with previous study data, higher doses of atorvastatin (8 mg/kg) did not improve functional outcome or reduce the extent of injury. Histochemical stains for markers of synaptogenesis, immature neurons, and neuronal migration revealed increased labeling in the region of hemorrhage in the atorvastatin-treated rats. Conclusions. Analysis of the data in this study indicates that atorvastatin improves neurological recovery after experimental ICH and may do so in part by increasing neuronal plasticity.

Longitudinal time course of reversible and irreversible components of chronic cerebrovasospasm of the rabbit basilar artery

1991 ◽  
Vol 74 (6) ◽  
pp. 951-955 ◽  
Author(s):  
Peter Vorkapic ◽  
Rosemary D. Bevan ◽  
John A. Bevan
Keyword(s):  
Basilar Artery ◽  
Time Course ◽  
Autologous Blood ◽  
Vessel Diameter ◽  
Second Phase ◽  
Total Blood ◽  
Content Type ◽  
Prepontine Cistern ◽  
Control Value ◽  
Silicone Catheter

✓ Multiple injections of autologous blood were made around the basilar artery of rabbits through a silicone catheter placed into the prepontine cistern. The total blood injected was 3 ml/kg in aliquots of 0.5 to 0.8 ml over a 4-hour period. Control angiograms were obtained 7 days before this procedure. Groups of animals were examined by angiography on each of 9 days after the injections of blood. An angiogram was obtained 15 minutes after the first injection of blood, 20 seconds after the intra-arterial injection of a maximum dilating dose of papaverine. All surviving animals showed basilar artery narrowing, which was greatest 24 hours after the hemorrhage, when the vessel diameter was reduced to 54% of the control value. The narrowing then decreased to a reduction of about 30%, which was maintained throughout the rest of the study period. A papaverine-resistant component of narrowing was not seen until the 3rd day. It increased progressively to Day 9 when it represented 63% of the total. This model has a number of features that are reminiscent of human cerebrovasospasm, including the fact that there is an initial phase of narrowing that is completely reversed by an intra-arterially administered vasodilator, and a second phase beginning on Day 3 which exhibits a progressively increasing papaverine-resistant component.

scholarly journals Fastigial Stimulation Increases Ischemic Blood Flow and Reduces Brain Damage after Focal Ischemia

1993 ◽  
Vol 13 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Fangyi Zhang ◽  
Costantino Iadecola
Keyword(s):  
Blood Flow ◽  
Brain Damage ◽  
Infarct Volume ◽  
Group Analysis ◽  
Blood Gases ◽  
Focal Ischemia ◽  
Ischemic Damage ◽  
Collateral Flow ◽  
Sprague Dawley ◽  
Mca Occlusion

Electrical stimulation of the cerebellar fastigial nucleus (FN) increases CBF and reduces brain damage after focal ischemia. We studied whether FN stimulation “protects” the brain from ischemic damage by increasing blood flow to the ischemic territory. Sprague–Dawley rats were anesthetized (halothane 1–3%) and artificially ventilated through a tracheal cannula inserted transorally. CBF was monitored by a laser-Doppler probe placed over the convexity at a site corresponding to the area spared from infarction by FN stimulation. Arterial pressure (AP), blood gases, and body temperature were controlled, and the electroencephalogram (EEG) was monitored. The stem of the middle cerebral artery (MCA) was occluded. After occlusion, the FN was stimulated for 60 min (100 μA; 50 Hz; 1 s on–1 s off) while AP was maintained at 97 ± 11 mm Hg (mean ± SD) by controlled hemorrhage. Rats were then allowed to recover, and infarct volume was determined 24 h later in thioninstained sections. In unstimulated rats ( n = 7), proximal MCA occlusion reduced CBF and the amplitude of the EEG. One day later, these rats had infarcts involving neocortex and striatum. FN stimulation after MCA occlusion ( n = 12) enhanced CBF and EEG recovery [61 ± 34 and 73 ± 43%, respectively at 60 min; p < 0.05 vs. unstimulated group; analysis of variance (ANOVA)] and reduced the volume of the cortical infarct by 48% (p < 0.05). In contrast, hypercapnia (Pco2 = 64 ± 4; n = 7) did not affect CBF and EEG recovery or infarct volume (p > 0.05). Thus, FN stimulation, unlike hypercapnia, increases CBF to the ischemic cortex, improves recovery of electrical activity, and reduces tissue damage after MCA occlusion. These findings support the hypothesis that FN stimulation reduces ischemic damage by enhancing collateral flow to the ischemic territory.

Effects of methylprednisolone on peritumoral brain edema

1983 ◽  
Vol 59 (4) ◽  
pp. 612-619 ◽  
Author(s):  
Kazuo Yamada ◽  
Yukitaka Ushio ◽  
Toru Hayakawa ◽  
Norio Arita ◽  
Noriko Yamada ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brain Edema ◽  
Capillary Permeability ◽  
Clinical Symptoms ◽  
Treated Group ◽  
Untreated Group ◽  
Content Type ◽  
Intracerebral Transplantation ◽  
Edema Fluid ◽  
Peritumoral Brain Edema

✓ Peritumoral brain edema was produced by intracerebral transplantation of Walker 256 tumor in rats. Local cerebral blood flow (LCBF), local cerebral glucose utilization (LCGU), and capillary permeability were studied in untreated and methylprednisolone-treated rats by quantitative autoradiography. In the untreated group, LCBF and LCGU were widely depressed in the cortex and deep structures of the hemisphere ipsilateral to the tumor. In the methylprednisolone-treated animals, LCBF and LCGU were significantly better than in the untreated animals. Capillary permeability was highly increased in the viable part of the tumor in the untreated animals. In the methylprednisolone-treated group, capillary permeability of the tumor was significantly lower than that in the untreated group. These results may suggest that increase in capillary permeability of the tumor is the major source for edema fluid production, and that methylprednisolone improves brain edema by decreasing capillary permeability of the tumor. Decrease in edema fluid formation may result in restoration of blood flow and glucose metabolism in the adjacent brain tissue, and may improve clinical symptoms and signs.

Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury

1978 ◽  
Vol 48 (5) ◽  
pp. 689-703 ◽  
Author(s):  
Erna M. Enevoldsen ◽  
Finn T. Jensen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Damage ◽  
Severely Injured ◽  
Content Type ◽  
Cerebrovascular Autoregulation ◽  
Decerebrate Rigidity ◽  
Arterial Blood ◽  
Fine Print

✓ Regional cerebral blood flow (rCBF), cerebral intraventricular pressure (IVP), systemic arterial blood pressure, and cerebral ventricular fluid (CSF) lactate and pH were studied repeatedly in 23 patients during the acute phase of severe brain injury lasting from 3 to 21 days after the trauma. Cerebrovascular autoregulation was tested repeatedly by means of angiotensin infusion in 21 of the patients, and CO2 response in 14 by means of passive hyperventilation. The pressure in the brain ventricles was measured continuously in all patients and kept below 45 mm Hg during the study. If the IVP increased more than 10 mm Hg during the angiotensin infusion (as in one case), the autoregulation test was considered contraindicated and the angiotensin infusion was discontinued. Dissociation between cerebrovascular autoregulation and CO2 response was a common phenomenon. Typically, autoregulation appeared preserved in the most severely injured areas of the cerebral cortex when the patient was deeply comatose, but deteriorated concomitantly with recovery; by the time the patient became alert, the autoregulation was always impaired. The CO2 response was impaired only in patients who were deeply comatose and had attacks of decerebrate rigidity; during recovery the CO2 response became normal. Thus, preserved autoregulation associated with impaired CO2 response indicated very severe brain damage, whereas impaired autoregulation associated with preserved CO2 response suggested moderate or severe brain damage in recovery. These paradoxical observations raise the question whether the preserved autoregulation seen in severely injured brain tissue is a true autoregulation caused by an active vasoconstrictor response to an increase in blood pressure.

Sign in / Sign up

Export Citation Format

Share Document