Effect of subarachnoid hemorrhage on the extracellular microenvironment

1982 ◽  
Vol 56 (2) ◽  
pp. 216-221 ◽  
Author(s):  
Otakar R. Hubschmann ◽  
David Kornhauser
Keyword(s):  
Cerebral Cortex ◽  
Subarachnoid Hemorrhage ◽  
Cellular Response ◽  
Extracellular Potassium ◽  
Muscular Layer ◽  
Content Type ◽  
Experimental Subarachnoid Hemorrhage ◽  
Extracellular Microenvironment ◽  
Vascular Spasm ◽  
Fine Print

✓ Local experimental subarachnoid hemorrhage (SAH) was produced over the cerebral cortex in 15 cats. The cellular response was monitored using ion-specific electrodes for extracellular potassium (K+) and calcium (Ca++) activity, DC cortical potential, and electrocorticogram. The response was characterized by a profound cellular depolarization and extracellular calcium (Ca++) depletion which accompanied extracellular potassium (K+) accumulation. The prehemorrhage baseline calcium levels measured 1.14 ± 0.11 mM, and were lowered to 0.4 to 0.7 mM/liter in different experiments. The K+ accumulation reached levels between 16 and 31 mM from a baseline of 3.17 ± 0.52 mM and were cleared to normal or nearly normal within 5 minutes. The Ca++ levels also returned to normal within 5 minutes, but remained depressed for the duration of the experiment in two animals. These results confirm that blood extravasated into the subarachnoid space has a direct effect on parenchymal elements. The combination of transient K+ elevations and calcium depression may play an important role in the development of vascular spasm by inducing or facilitating a contraction in the muscular layer in the wall of major intracranial vessels.

Responses to experimental subarachnoid hemorrhage in the spontaneously breathing primate

1980 ◽  
Vol 52 (3) ◽  
pp. 302-308 ◽  
Author(s):  
Charles Rothberg ◽  
Bryce Weir ◽  
Thomas Overton ◽  
Michael Grace
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Respiratory Pattern ◽  
Content Type ◽  
Cynomolgus Monkeys ◽  
Experimental Subarachnoid Hemorrhage ◽  
Subarachnoid Blood ◽  
Spontaneously Breathing ◽  
Fine Print

✓ The pathophysiological responses to experimental subarachnoid hemorrhage (SAH) were investigated in 20 spontaneously breathing cynomolgus monkeys. Four different volumes of fresh autogenous blood were used: 1.0, 1.33, 1.67, and 2.0 cc/kg. Five other animals had injection of 1.67 cc/kg of mock cerebrospinal fluid. Cerebral blood flow (CBF) was measured using the xenon-133 clearance technique. Respiratory rate and tidal volume were monitored by way of a Vertek pneumotach. The reduction of CBF after the SAH became more pronounced with increasing volumes of subarachnoid blood. The CBF remained reduced despite a return to normal of the cerebral perfusion pressure. Increasing SAH volumes were associated with greater abnormalities in the respiratory pattern, consisting of apnea and hyperventilation. These larger volumes were also associated with hypoxemia. Morbidity and mortality increased with increasing volumes of SAH, and are believed to be the result of a combination of decreased CBF, respiratory center disturbances, and pulmonary diffusion defects.

The blood-brain barrier following experimental subarachnoid hemorrhage

1983 ◽  
Vol 58 (3) ◽  
pp. 338-344 ◽  
Author(s):  
Eric W. Peterson ◽  
Erico R. Cardoso
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Arterial Hypertension ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Hemodynamic Variable ◽  
Content Type ◽  
Blood Brain ◽  
Intracisternal Injection ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓ In three groups of cats, the authors studied the effect of subarachnoid hemorrhage (SAH) on the permeability of the blood-brain barrier (BBB) to the penetration of Evans blue-protein complex. One group received arterial hypertension alone, one group SAH alone, and one group SAH followed by arterial hypertension. Animals subjected to arterial hypertension alone showed areas of BBB breakdown. However, when cats were rendered hypertensive after SAH, there were no demonstrable BBB lesions. The SAH was produced by intracisternal injection of whole blood and hypertension by the intravenous injection of metaraminol. The preservation of the BBB after SAH is discussed. Vasospasm is considered as a possible hemodynamic variable responsible for the protection of the BBB from hypertensive damage. The need for a new model is proposed to further investigate the state of the BBB after SAH.

An in vitro comparative study of conducting vessels and penetrating arterioles after experimental subarachnoid hemorrhage in the rabbit

1992 ◽  
Vol 77 (1) ◽  
pp. 113-119 ◽  
Author(s):  
Dennis G. Vollmer ◽  
Masakazu Takayasu ◽  
Ralph G. Dacey
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Isometric Tension ◽  
Channel Blockers ◽  
Cerebral Microvessels ◽  
Content Type ◽  
Large Arteries ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓ The reactivity of rabbit basilar artery and penetrating arteriolar microvessels was studied in vitro using an isometric-tension measurement technique and an isolated perfused arteriole preparation, respectively. Comparisons were made between reactivities of normal vessels and those obtained from animals subjected to experimental subarachnoid hemorrhage (SAH) 3 days prior to examination. Subarachnoid hemorrhage produced significant increases in basilar artery contraction in response to increasing concentrations of serotonin (5-hydroxytryptamine) (10−9 to 10−5 M) and prostaglandin F2α (10−9 to 10−5 M) when compared to normal arteries. In addition, SAH attenuated the relaxing effect of acetylcholine following serotonin-induced contraction and of adenosine triphosphate after KCl-induced basilar artery contractions. In contrast to the changes observed in large arteries, cerebral microvessels did not demonstrate significant differences in spontaneous tone or in reactivity to a number of vasoactive stimuli including application of calcium, serotonin, and acetylcholine. On the other hand, small but significant changes in arteriolar responsiveness to changes in extraluminal pH and to application of KCl were noted. Findings from this study suggest that intracerebral resistance vessels of the cerebral microcirculation are not greatly affected by the presence of subarachnoid clot, in contrast to the large arteries in the basal subarachnoid space. The small changes that do occur are qualitatively different from those observed for large arteries. These findings are consistent with the observation of significant therapeutic benefit with the use of calcium channel blockers without changes in angiographically visible vasospasm in large vessels. It is likely, therefore, that calcium antagonists may act to decrease total cerebrovascular resistance at the level of the relatively unaffected microcirculation after SAH without changing large vessel diameter.

Does administration of recombinant human erythropoietin attenuate the increase of S-100 protein observed in cerebrospinal fluid after experimental subarachnoid hemorrhage?

2002 ◽  
Vol 96 (3) ◽  
pp. 565-570 ◽  
Author(s):  
Giovanni Grasso ◽  
Marcello Passalacqua ◽  
Alessandra Sfacteria ◽  
Alfredo Conti ◽  
Antonio Morabito ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Protein Level ◽  
Neurological Outcome ◽  
Content Type ◽  
Protein Levels ◽  
Group 4 ◽  
S 100 ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

Object. Results of recent studies indicate that erythropoietin (EPO) produces a neuroprotective effect on experimental subarachnoid hemorrhage (SAH). It has been reported that S-100 protein levels increase in cerebrospinal fluid (CSF) after SAH, providing a highly prognostic indication of unfavorable outcome. This study was conducted to validate further the findings of S-100 protein as an index of brain damage and to assess whether treatment with recombinant human EPO (rhEPO) would limit the increase of S-100 protein level in CSF following experimental SAH. Methods. Thirty-two rabbits were each assigned to one of four groups: Group 1, control; Group 2, SAH; Group 3, SAH plus placebo; and Group 4, SAH plus rhEPO (each group consisted of eight rabbits). The rhEPO and placebo were administered to the rabbits after SAH had been induced, and S-100 protein levels in the CSF of these animals were measured at 24, 48, and 72 hours after the experimental procedure. In each group of animals levels of S-100 protein were compared with the mortality rate, neurological outcome, and neuronal ischemic damage. High S-100 protein levels were found in rabbits in Groups 2 and 3, which exhibited poor neurological status and harbored a high number of damaged cortical neurons. Favorable neurological outcome and significant reductions in total numbers of damaged neurons were observed in animals in Group 4 in which there were significantly lower S-100 protein concentrations compared with animals in Groups 2 and 3 (p < 0.001). Conclusions. The results of this study support the concept that determination of the S-100 protein level in CSF has prognostic value after SAH. The findings also confirm that rhEPO acts as a neuroprotective agent during experimental SAH.

Experimental cerebral vasospasm

1974 ◽  
Vol 41 (3) ◽  
pp. 285-292 ◽  
Author(s):  
Hajime Nagai ◽  
Yoshiaki Suzuki ◽  
Mitsuo Sugiura ◽  
Satoshi Noda ◽  
Hideo Mabe
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Posterior Communicating Artery ◽  
Content Type ◽  
Aneurysmal Rupture ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓The authors describe a model for making an experimental subarachnoid hemorrhage that closely simulates human aneurysmal rupture. A needle previously inserted into the posterior communicating artery is subsequently withdrawn by traction on a thread. Using this model they demonstrate biphasic spasm by measurement of cerebral blood flow and angiography after rupture of the artery; the early spasm lasted 60 minutes and the late spasm began 3 or 4 hours after subarachnoid hemorrhage and continued for several days. The authors discuss the pathogenesis of early and late spasm.

Effects of prostaglandin E1 on experimental cerebral vasospasm

1972 ◽  
Vol 36 (5) ◽  
pp. 634-639 ◽  
Author(s):  
Stanley Pelofsky ◽  
Eugene D. Jacobson ◽  
Robert G. Fisher
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Prostaglandin E1 ◽  
Prostaglandin E ◽  
Arterial Spasm ◽  
Content Type ◽  
Experimental Subarachnoid Hemorrhage ◽  
Group 2 ◽  
Fine Print ◽  
Group 1 ◽  
Carotid Flow

✓ This study reports the effects of intraarterial prostaglandin E1 (PGE1) upon intracerebral blood flow under control and vasospastic conditions. A new transorbital means of producing acute experimental subarachnoid hemorrhage with concomitant arterial spasm is presented. Two groups of animals were delineated in this investigation. Five animals (Group 1) were extremely sensitive to PGE1 and subarachnoid hemorrhage (SAH); carotid flow studies with simultaneous intracerebral angiography in this group demonstrated the ability of PGE1 to relieve vasospasm. Two other animals (Group 2) were relatively insensitive to SAH and PGE1. The study suggests an important role for PGE1 in the treatment of intracerebral vasospasm.

Structural changes of the intradural arteries following subarachnoid hemorrhage

1972 ◽  
Vol 37 (6) ◽  
pp. 715-723 ◽  
Author(s):  
Louis W. Conway ◽  
Larry W. McDonald
Keyword(s):  
Structural Change ◽  
Subarachnoid Hemorrhage ◽  
Structural Changes ◽  
Intimal Thickening ◽  
Muscular Layer ◽  
Content Type ◽  
Intracranial Arteries ◽  
Subarachnoid Blood ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ The histology of the intradural arteries was studied in 12 consecutive autopsy cases of patients dying 1 day to 15 months after their initial spontaneous subarachnoid hemorrhage. In all patients surviving 4 weeks or more and in one surviving 4 days, the lumina of the intracranial arteries were narrowed by subendothelial granulation tissue which thickened the intima. In all seven cases with structural changes in the intracranial arteries, vessels near the site of hemorrhage were involved; in four cases vessels remote from the site of hemorrhage were also involved. Changes were usually restricted to large arteries with a prominent muscular layer and confined to the subarachnoid space. The presence and degree of intimal thickening correlated with the distribution and amount of subarachnoid blood or its breakdown products. This process apparently does not represent an obliterative endarteritis involving vessels exclusively supplying infarcted brain, but is probably a reaction to mechanical or anoxic damage to the intima following vasoconstriction. It is suggested that this arterial structural change might be confused with delayed or prolonged “vasopasm.”

Evaluation of the microvasculature and cerebral ischemia after experimental subarachnoid hemorrhage in dogs

2002 ◽  
Vol 97 (4) ◽  
pp. 896-904 ◽  
Author(s):  
Eddie Perkins ◽  
Hitoshi Kimura ◽  
Andrew D. Parent ◽  
John H. Zhang
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Morphological Characteristics ◽  
Ultrastructural Level ◽  
Ultrastructural Changes ◽  
Control Group ◽  
Internal Elastic Lamina ◽  
Content Type ◽  
Basilar Arteries ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

Object. Whether cerebral vasospasm occurs only in surface vessels or also in parenchymal arterioles is debatable. The present study was undertaken to evaluate comprehensively the microvasculature of the brainstem after experimental subarachnoid hemorrhage (SAH). Methods. Nine mongrel dogs of either sex, each weighing between 18 and 24 kg, underwent double blood injections spaced 48 hours apart; the injections were infused into the cisterna magna immediately after angiography of the basilar arteries (BAs). Three additional dogs assigned to a control group received no blood injections. The dogs were killed on Day 7. Axial sections obtained from the midpontine region of both control dogs and animals subjected to SAH were evaluated with respect to the morphological characteristics of vessels and neurons, and for ultrastructural changes. Severe vasospasm occurred in the BAs of all dogs subjected to SAH. Nevertheless, in these animals, the luminal areas and vessel perimeter in parenchymal arterioles, but not in parenchymal venules, were observed to have increased when compared with those of control dogs (p < 0.01, t-test). No corrugation of the internal elastic lamina was observed and smooth-muscle and endothelial cells remained normal at the ultrastructural level in the dogs with SAH. Conclusions. In this model, vasospasm of the BAs did not extend into the region of the pons to affect the intraparenchymal arterioles. Dilation of the parenchymal arterioles might serve as compensation for reduced blood flow. Thus, no neuronal ischemia or infarction resulted in the pontine region of the brain.

Cortical cellular response in acute subarachnoid hemorrhage

1980 ◽  
Vol 52 (4) ◽  
pp. 456-462 ◽  
Author(s):  
Otakar R. Hubschmann ◽  
David Kornhauser
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cellular Response ◽  
Initial Step ◽  
Cellular Level ◽  
Cortical Cells ◽  
Content Type ◽  
Acute Subarachnoid Hemorrhage ◽  
Cellular Dysfunction ◽  
K Release ◽  
Fine Print

✓ Acute subarachnoid hemorrhage (SAH) over the cerebral cortex causes single or multiple waves of cellular depolarization, which may occur in a self-propagating, reverberating fashion. This process is characterized by a massive K+ release and transient depression in electrocortical activity. The K+ levels in the extracellular space reach magnitudes known to substantially affect the membrane potentials of neurons and glia, and may cause a release of neurotransmitters from depolarized presynaptic terminals. The release of K+ may be the initial step in the development of cellular edema and, together with a multitude of other chemical and biochemical changes taking place at the cellular level, may underlie the loss of autoregulation. Cortical cells rather than blood vessels are the primary targets in the initial stages of SAH, and ischemia does not play a causal role in the pathogenesis of cellular dysfunction during this stage.

Aneurysm-induced third nerve palsy

1972 ◽  
Vol 36 (5) ◽  
pp. 548-551 ◽  
Author(s):  
Iftikhar A. Raja
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Functional Recovery ◽  
Poor Prognosis ◽  
Nerve Palsy ◽  
Nerve Function ◽  
Content Type ◽  
Third Nerve Palsy ◽  
Carotid Ligation ◽  
Third Nerve ◽  
Fine Print

✓ Forty-two patients with aneurysm-induced third nerve palsy are described. After carotid ligation, 58% showed satisfactory and 42% unsatisfactory functional recovery. In some patients the deficit continued to increase even after carotid ligation. Early ligation provided a better chance of recovery of third nerve function. Patients in whom third nerve palsy began after subarachnoid hemorrhage had a poor prognosis. No relationship was noted between the size of the aneurysm and the recovery of third nerve function.

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