Studies on the cerebral circulation of the baboon in acutely induced hypertension.

Strandgaard, Svend; MacKenzie, Eric T.; Jones, J V; Harper, A. M.

doi:10.1161/01.str.7.3.287

Cited by 39 publications

(7 citation statements)

References 22 publications

(11 reference statements)

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“…Within a physiological range, a moderate in crease or decrease in cerebral perfusion pressure is accom panied by reciprocal changes in cerebrovas cular resistance, resulting in a constant CBF (Lassen, 1959;Purves, 1972). In spite of this "au toregulatory" mechanism, acute hemodynamic and metabolic changes under certain circumstances may temporarily or permanently alter cerebral cir culation (Harper, 1966;Freeman and Ingvar, 1968;Strandgaard et aL, 1976). Physical exercise elicits a succession of physiological reactions that are known to influence CBF, such as an increase in cardiac output and mean blood pressure and a de crease in peripheral resistance (Sture-Bevegard and Shepherd, 1967).…”

mentioning

confidence: 99%

Effect of Exercise on Cerebral Circulation

Globus

Melamed

Keren

et al. 1983

J Cereb Blood Flow Metab

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The effect of supine physical exercise on cerebral blood flow (CBF) was measured in 30 normal subjects with the 133Xe inhalation technique. The CBF measurements were correlated to changes in Pco2, heart rate, and blood pressure, and to cardiac output and right atrial pressure in 10 of the subjects who underwent Swan-Ganz catheterization. No significant change was found in CBF during physical exercise, although a marked increase in cardiac output, blood pressure, and right atrial pressure and a mild decrease in PCO2 were found. Cerebrovascular resistance increased by 38%, in contrast to a decrease of 33% in the peripheral vascular resistance. The factors that affect the mechanism of cerebrovascular autoregulation during exercise are discussed.

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mentioning

confidence: 99%

Effect of Exercise on Cerebral Circulation

Globus

Melamed

Keren

et al. 1983

J Cereb Blood Flow Metab

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“…This general similarity in the actions (both electrical and mechanical) of these 2 drugs suggests that, even if the direct action of angiotensin at lower doses is weak or negligible, the possibility of synergistic action with the norepinephrine released by the extra sympathetic activity occurring under these conditions should not be entirely overlooked. Despite earlier reports of absence of effects in vivo at very low doses, 22 - 23 angiotensin II has been found to have significant contractile effects on cerebral arteries in vitro 7 ' 8> 24t 25 and recently in vivo. 26 We believe that experiments testing physiological mechanisms in the cerebral circulation under the effects of high perfusion pressure induced by angiotensin should be interpreted viewing the cerebrovascular activity of this peptide.…”

Section: 5min I5mmhg_mentioning

confidence: 76%

Correlated electrical and mechanical responses of isolated rabbit pial arteries to some vasoactive drugs.

Lusamvuku¹,

Sercombe²,

Aubineau³

et al. 1979

Stroke

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SUMMARY Simultaneous measurements were made of spike activity and perfusion pressure (P A ) in intact segments of rabbit middle cerebral artery in vitro. The segments were mounted on a Teflon tube designed so that the perfusing solution flowed in the annular space between the tube and the artery wall, thus magnifying the P A changes occurring when the artery constricted or dilated. A widened portion of the Teflon tube immobilized 1-2 mm of the artery segment for electrical recording with fine glass microelectrodes. Spontaneous spike activity (extra-and intracellular) was regularly observed. When a steady P A and spike discharge was obtained, tests were performed by substituting for the normal perfusion liquid, solutions containing 5 ng/m\ norepinephrine, 5 Mg/ml angiotensin II or 7.5 Mg/ml isoproterenol. Norepinephrine and angiotensin each increased spike frequency (+ 293 and + 126%) and P A (+ 6.6 and + 7.9 mm Hg) whereas isoproterenol decreased spike frequency (-89%) and P A (-22.9 mm Hg). These results a) confirm the presence of receptors to these agents in pial arteries, and b) demonstrate a high degree of correlation between membrane electrical events and mechanical activity of these spontaneously-active myovascular cells. Stroke Vol 10, No 6, 1979PREVIOUS WORK in vitro on cerebral arteries has been concerned with measurements made on helical strip preparations 1 or on short whole segments in which circular tension is measured isometrically. smooth muscle are closely related to the electrical activity in many, but not necessarily all, cases, 6 and it may be that a synergistic action of several factors on the membrane potential is sufficient to elicit a mechanical change even if each factor alone is insufficient.For these reasons we have chosen to measure simultaneously mechanical and electrical activity in isolated perfused segments of rabbit cerebral arteries. This first report concerns the action of norepinephrine, isoproterenol and angiotensin II on the middle cerebral artery of the rabbit. Norepinephrine was used to allow comparison with the other (mechanical) methods for studying cerebral vessels and also with vessels from other organs, since norepinephrine has been extensively studied elsewhere. The beta-adrenergic agonist isoproterenol was used to determine whether relaxation could be obtained under the conditions of our experiment and how such action is related to the electrical activity. Our primary reason for studying angiotensin stems from its widespread use experimentally to create a

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“…Normal cerebral blood flow (CBF) remains relatively constant despite dramatic changes in systemic blood pressure. Subsequent experimental work, however, suggested that hypertensive encephalopathy results not from overregulation but underregulation or breakthrough of circulatory response, with a consequent increase in the CBF that results in cerebral edema [14]. In hypertensive encephalopathy cerebral autoregulation is deranged such that CBF may be adversely affected by severe hypertension.…”

Section: Hypertensive Encephalopathymentioning

confidence: 99%

Hypertensive Crises

Ram

Hyman

1987

J Intensive Care Med

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Hypertensive crises are a group of medical conditions in which a rapid decrease in blood pressure is necessary to prevent serious complications. Although uncommon in clinical practice, a hypertensive crisis should be recognized and treated promptly. Any form of hypertension may be associated with hypertensive crisis, the main determinant being the level of blood pressure rather than the cause of hypertension. In certain clinical situations the abruptness with which the blood pressure increases seems to be more important than the absolute level of blood pressure in causing the hypertensive crisis (e.g., toxemia of pregnancy in women and acute onset of hypertension in children with acute glomerulonephritis). In other clinical situations the absolute level of blood pressure does not affect the seriousness of hypertension so much as coexisting complications that may make even moderate hypertension dangerous (e.g., acute aortic dissection and acute left ventricular failure ).

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Studies on the cerebral circulation of the baboon in acutely induced hypertension.

Cited by 39 publications

References 22 publications

Effect of Exercise on Cerebral Circulation

Effect of Exercise on Cerebral Circulation

Correlated electrical and mechanical responses of isolated rabbit pial arteries to some vasoactive drugs.

Hypertensive Crises

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