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  • 1990-1994  (2)
  • 1990  (2)
  • Cerebral vasospasm  (1)
  • cerebral circulation  (1)
  • 1
    ISSN: 0942-0940
    Keywords: Cerebral vasospasm ; haemorrhagic infarction ; intracranial aneurysm ; normovolaemic induced hypertension therapy ; subarachnoid haemorrhage ; Swan-Ganz catheter
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We showed that normovolaemic induced hypertension therapy was effective in reducing ischaemic symptoms attributed to cerebral vasospasm in 41 patients after subarachnoid haemorrhage. By inducing hypertension to 25% to 50% above normal systolic arterial blood pressure, we observed that in 17 of 24 cases (71%) neurological deficits improved. In four cases of haemorrhagic infarction, the blood pressure rose to over 50% of systolic arterial pressure, and a low density area was confirmed on computerized tomography (CT) scan prior to vasospasm. Induced hypertension was therefore not considered when a low density area was revealed on CT scan. Restriction of fluid input is usually a factor in producing hypovolaemia after a neurosurgical operation. Intravascular volume expansion has been reported effective in reversing ischaemic deficits. However, according to Poiseuille's equation, increasing blood volume to a state of hypervolaemia can not enhance flow. The cerebral blood flow (CBF) was raised by increasing perfusion pressure, reducing viscosity, or increasing blood vessel diameter. Intravascular volume expansion elevates not only systemic arterial pressure, but also pulmonary artery wedge pressure over 18 mmHg and cardiac index over 2.2. Since pulmonary oedema and congestive heart failure may develop, one should monitor haemodynamic parameters with the Swan-Ganz catheter as a preventive measure. We emphasize that normovolaemic induced hypertension, maintaining haemodynamics subset 1 of the comparable haemodynamic subsets, is effective in raising perfusion pressure of CBF.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0942-0940
    Keywords: Endothelin ; neuropeptide Y ; angiotensin II ; cerebral arteries ; cerebral circulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have studied the effect of endothelin, an endothelium-derived peptide, on isolated canine and bovine cerebral arteries in vitro and on canine vertebral blood flow (VBF) in vivo. Endothelin produced a dose-dependent contraction of canine and bovine arterial smooth muscle with ED50 values ranging from 4 to 8 nM. The response to endothelin developed slowly and persisted as a sustained contraction. Maximal contraction by endothelin required the presence of extracellular calcium and was independent of the presence of endothelium. The maximal contraction produced by endothelin was approximately 2–3 times greater than that produced by neuropeptide Y or angiotensin II. The injection of endothelin into the vertebral artery decreased vertebral blood flow (VBF) dose-dependently without affecting systemic blood pressure or heart rate. The decrease in VBF produced by endothelin was long-lasting, like that produced by neuropeptide Y, but more potent. The present data, together with our previous study demonstrating that the intracisternal injection of endothelin induces an unusually long-lasting decrease in the basilar artery diameter angiographically, suggests that endothelin may act as a long-acting vasoconstrictor in cerebral vascular disease.
    Type of Medium: Electronic Resource
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