scholarly journals Perfusion Pressure-Dependent Recovery of Cortical Spreading Depression is Independent of Tissue Oxygenation over a Wide Physiologic Range

2010 ◽  
Vol 30 (6) ◽  
pp. 1168-1177 ◽  
Author(s):  
Inna Sukhotinsky ◽  
Mohammad A Yaseen ◽  
Sava Sakadžić ◽  
Svetlana Ruvinskaya ◽  
John R Sims ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Spreading Depression ◽  
Tissue Oxygenation ◽  
Perfusion Pressure ◽  
Tissue Perfusion ◽  
Systemic Blood Pressure ◽  
Critical Determinant ◽  
Wide Range ◽  
Glial Depolarization

Spreading depression (SD) is a slowly propagating wave of transient neuronal and glial depolarization that develops after stroke, trauma and subarachnoid hemorrhage. In compromised tissue, repetitive SD-like injury depolarizations reduce tissue viability by worsening the mismatch between blood flow and metabolism. Although the mechanism remains unknown, SDs show delayed electrophysiological recovery within the ischemic penumbra. Here, we tested the hypothesis that the recovery rate of SD can be varied by modulating tissue perfusion pressure and oxygenation. Systemic blood pressure and arterial pO2 were simultaneously manipulated in anesthetized rats under full physiologic monitoring. We found that arterial hypotension doubled the SD duration, whereas hypertension reduced it by a third compared with normoxic normotensive rats. Hyperoxia failed to shorten the prolonged SD durations in hypotensive rats, despite restoring tissue pO2. Indeed, varying arterial pO2 (40 to 400 mm Hg) alone did not significantly influence SD duration, whereas blood pressure (40 to 160 mm Hg) was inversely related to SD duration in compromised tissue. These data suggest that cerebral perfusion pressure is a critical determinant of SD duration independent of tissue oxygenation over a wide range of arterial pO2 levels, and that hypotension may be detrimental in stroke and subarachnoid hemorrhage, where SD-like injury depolarizations have been observed.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

Contralateral Natriuresis During Reduced Renal Artery Perfusion Pressure in "Renin-Depleted" Dogs

1972 ◽  
Vol 50 (3) ◽  
pp. 215-227
Author(s):  
L. J. Belleau ◽  
D. Mailhot
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Renal Perfusion ◽  
Systemic Blood ◽  
Renal Perfusion Pressure

The mechanism of contralateral natriuresis subsequent to reduction of renal perfusion pressure was studied. In control dogs a drop in the renal perfusion pressure caused a very significant increase in the arterial and renal venous plasma renin activity, as well as a significant contralateral natriuresis. Systemic blood pressure increased along with contralateral intrarenal resistance. Glomerular filtration rate and renal blood flow did not change in the opposite kidney.In "renin-depleted" dogs a comparable drop in the renal perfusion pressure failed to stimulate renal venous and arterial plasma renin activity. Contralateral natriuresis increased significantly as well as the systemic blood pressure. In the absence of renin, intrarenal resistance of the opposite kidney did not change. Contralateral glomerular filtration rate and renal blood flow remained unchanged.During reduction of renal perfusion pressure, the most significant findings were: (1) absence of renin release despite the stimulation in renin-depleted dogs, (2) increase in contralateral resistance explained by the renin–angiotensin system, (3) systemic blood pressure increment despite renin release inhibition, and (4) the renin–angiotensin system not directly responsible for the contralateral natriuresis following a reduction in the renal perfusion pressure.Contralateral natriuresis cannot be explained by changes in glomerular filtration, renal blood flow, or intrarenal resistance. It is suggested that the rise in blood pressure or another factor, possibly neural or humoral, could explain the contralateral natriuresis.

scholarly journals Time-Course of Cerebral Perfusion and Tissue Oxygenation in the First 6 h after Experimental Subarachnoid Hemorrhage in Rats

2009 ◽  
Vol 29 (4) ◽  
pp. 771-779 ◽  
Author(s):  
Thomas Westermaier ◽  
Alina Jauss ◽  
Jörg Eriskat ◽  
Ekkehard Kunze ◽  
Klaus Roosen
Keyword(s):  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Tissue Oxygenation ◽  
Perfusion Pressure ◽  
Oxygen Utilization ◽  
Cortical Blood Flow ◽  
Local Cortical Blood Flow

Present knowledge about hemodynamic and metabolic changes after subarachnoid hemorrhage (SAH) originates from neuromonitoring usually starting with aneurysm surgery and animal studies that have been focusing on the first 1 to 3 h after SAH. Most patients, however, are referred to treatment several hours after the insult. We examined the course of hemodynamic parameters, cerebral blood flow, and tissue oxygenation (ptiO2) in the first 6 h after experimental SAH. Sixteen Sprague–Dawley rats were subjected to SAH using the endovascular filament model or served as controls ( n = 8). Bilateral local cortical blood flow, intracranial pressure, cerebral perfusion pressure, and ptiO2 were followed for 6 h after SAH. After induction of SAH, local cortical blood flow rapidly declined to 22% of baseline and returned to 80% after 6 h. The decline of local cortical blood flow markedly exceeded the decline of cerebral perfusion pressure. ptiO2 declined to 57%, recovered after 2 h, and reached ≥140% of baseline after 6 h. Acute vasoconstriction after SAH is indicated by the marked discrepancy of cerebral perfusion pressure and local cortical blood flow. The excess tissue oxygenation several hours after SAH suggests disturbed oxygen utilization and cerebral metabolic depression. Aside from the sudden increase of intracranial pressure at the time of hemorrhage and delayed cerebral vasospasm, the occurrence of acute vasoconstriction and disturbed oxygen utilization may be additional factors contributing to secondary brain damage after SAH.

Effects of Acupuncture on Tissue-Oxygenation of the Rat Brain

1977 ◽  
Vol 05 (02) ◽  
pp. 147-154 ◽  
Author(s):  
Gregory S. Chen ◽  
Wilhelm Erdmann
Keyword(s):  
Rat Brain ◽  
Brain Tissue ◽  
Tissue Oxygenation ◽  
Perfusion Pressure ◽  
Tissue Perfusion ◽  
Albino Rats ◽  
Capillary Perfusion ◽  
Unconscious Patients ◽  
The Brain ◽  
Inspiratory Oxygen

Acupuncture has been claimed to be effective in restoring consciousness in some comatose patients. Possible mechanisms to explain alleged acupuncture-induced arousal may include vasodilatory effects caused by sympathetic stimulation which leads to an augmentation of cerebral microcirculation and thereby improves oxygen supply to the brain tissue. Experiments were performed in ten albino rats (Wistar) employing PO 2 microelectrodes which were inserted into the cortex of the animals through small burholes. Brain tissue PO 2 was continuously recorded before, during, and after acupuncture. Stimulation of certain acupuncture loci (Go-26) resulted in immediate increase of PO 2 in the frontal cortex of the rat brain. This effect was reproducible. The effect was comparable to that obtained with increase of inspiratory CO 2 known to induce arterial vasodilatation and thus capillary perfusion pressure. The effect was more significant as compared to tissue PO 2 increases obtained after increase of inspiratory oxygen concentration from 21% to 100%. It appears that acupuncture causes an increase of brain tissue perfusion which may be, at least in part, responsible for arousal of unconscious patients. Dilatation of cerebral vascular vessels and improvement of autoregulation in the brain by acupuncture stimulation may also explain the effectiveness of acupuncture in the treatment of migraine headache.

Effects of Hydroxyethyl Starch, Nimodipine, and Propylene Glycol on Cochlear Blood Flow

1991 ◽  
Vol 105 (6) ◽  
pp. 840-844 ◽  
Author(s):  
J. K. M. Coleman ◽  
H. A. Dengerink ◽  
John W. Wright
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Propylene Glycol ◽  
Perfusion Pressure ◽  
Systemic Blood Pressure ◽  
Nonaqueous Solvent ◽  
Systemic Blood ◽  
Arterial Infusion ◽  
Cochlear Blood Flow ◽  
Vascular Origin

A primary goal of pharmacologic treatment for otopathologies of vascular origin is to elevate cochlear blood flow (CoBF), thus facilitating the transport of oxygen and nutrients without compromising perfusion pressure in other tissues. In the present investigation, significant increases in CoBF were measured during intra-arterial infusion of the plasma expanding agent, hydroxyethyline starch (HES), and the vasodilator nimodipine, in anesthetized adult male guinea pigs. There were no changes in systemic blood pressure during the infusion of HES or nimodipine. Intra-arterial infusion of propylene glycol (PG), which is used as a nonaqueous solvent, produced inconsistent CoBF effects accompanied by initial decreases in systemic blood pressure with subsequent increases. It is concluded that nimodipine and HES are very promising agents for inducing increases in CoBF, whereas PG produced inconsistent effects on CoBF while elevating blood pressure, thus compromising its potential usefulness in the treatment of otopathologies.

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