Effect of Torasemide on Intracranial Pressure, Mean Systemic Arterial Pressure, and Cerebral Perfusion Pressure in Experimental Brain Edema of the Rat

1994 ◽  
pp. 519-520
Author(s):  
Clemens A. Plangger
Keyword(s):  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Brain Edema ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Systemic Arterial Pressure ◽  
Experimental Brain Edema

Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs

1993 ◽  
Vol 265 (5) ◽  
pp. H1557-H1563 ◽  
Author(s):  
M. L. Kearney ◽  
J. E. Backofen ◽  
R. C. Koehler ◽  
M. D. Jones ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cardiovascular Response ◽  
Fetal Sheep ◽  
Peripheral Vasoconstriction ◽  
Significant Difference

Large increases in intracranial pressure in fetal sheep result in more potent peripheral vasoconstriction and better maintenance of cerebral O2 consumption (CMRO2) than in postnatal sheep. The fetus is exposed to a lower PO2. We tested the hypothesis that low PO2 in postnatal lambs potentiates peripheral vasoconstriction and better maintains cerebral perfusion pressure and CMRO2. Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O2 mixture to reduce arterial O2 saturation to 50% (n = 7). Elevation of intracranial pressure to within 3-5 mmHg of baseline mean arterial pressure for 30 min by ventricular fluid infusion initially caused a similar increase in arterial pressure in the normoxic [11 +/- 3 (SE) mmHg] and hypoxic (14 +/- 2 mmHg) groups. Plasma catecholamines increased more rapidly in the hypoxic group. However, plasma vasopressin levels were substantially elevated by hypoxia alone and failed to increase further with elevated intracranial pressure. Moreover, there was no significant difference between groups in the steady-state increase in arterial pressure, and microsphere-determined blood flow to intestines, kidney, skin, and muscle did not decrease in either group. Consequently, cerebral perfusion pressure, regional cerebral blood flow, and CMRO2 were reduced similarly in both groups. Therefore, hypoxemia failed to potentiate the postnatal pressor response. Low PO2 is unlikely to be the major mechanism for the potent Cushing response in the fetus.

Elicitation of theoretically predicted feedback oscillation in arterial pressure

1962 ◽  
Vol 203 (1) ◽  
pp. 141-146 ◽  
Author(s):  
Kiichi Sagawa ◽  
Oliver Carrier ◽  
Arthur C. Guyton
Keyword(s):  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Systemic Arterial Pressure ◽  
Time Dependent ◽  
Response Mechanism ◽  
Cerebral Ischemic ◽  
Pressure Changes

In a preceding servoanalytic study of the cerebral ischemic pressor response, the authors predicted that, under certain conditions, this emergency mechanism would go into a feedback oscillation and vasomotor waves would appear. The predicted conditions were a) that the cerebral perfusion pressure be as low as 30–10 mm Hg and b) that the time-dependent variable components of the systemic arterial pressure be transferred to the perfusion pressure with the same magnitude. The present experiment was conducted for the purpose of confirming such a theoretical prediction. The transfer of the systemic arterial pressure changes to the cerebral perfusion pressure was accomplished by a special coupling apparatus, and in all of the 11 experiments the cerebral ischemic response mechanism lapsed into feedback oscillation, and intense vasomotor waves were brought about. The period of these waves coincided almost exactly with those predicted by the servoanalysis of the cerebral ischemic response in individual dogs.

scholarly journals Dynamics of intracranial pressure, mean arterial pressure and cerebral perfusion pressure at change of head-of-bad position for patients with non-traumatic intracranial hemorrhages

2016 ◽  
Vol 15 (1) ◽  
pp. 27-32
Author(s):  
V. I. Gorbachev ◽  
N. V. Likholetova ◽  
S. V. Gorbachev
Keyword(s):  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Hemorrhagic Stroke ◽  
Perfusion Pressure ◽  
Simple Method ◽  
Bed Changes ◽  
Bed Position ◽  
Subarachnoid Hemorrhages

Introduction and purpose. Change of the «head-of-bed» position is a routine and simple method of correction of intracranial hypertension. There is still no consensus what exactly situation most effectively reduces intracranial pressure and doesn't compromise a cerebral blood flow. The purpose of the conducted research was the assessment influence of positioning on intracranial pressure and system hemodynamic at patients with a hemorrhagic stroke. Methods. 80 patients with a hemorrhagic stroke entered research. All of the patient carried out continuous monitoring of intracranial and system arterial pressure, transcranial doppler was daily carried out. To each patient was carried out «head-of-bed position» test (30°-0°-60°). Results. Despite various mechanism of hemorrhage in two studied groups in the first three days from the beginning of a disease similar tendencies to the progressing increase of intracranial pressure and decrease in mean arterial and cerebral perfusion pressure were observed. Only for the fifth days there were essential distinctions of the studied indicators. At consecutive «head-of-bed» changes are received the essential distinctions in the studied groups which aren't allowing to apply to them uniform algorithm of positioning. Conclusions. Positioning of patients with subarachnoid hemorrhages has no essential impact on the studied parameters. For patients with parenchymatous hemorrhages is preferable «head-of-bed» situation 30° and 60° the first and third day and 30° for the second and fifth day. Thus even short stay in horizontal position (0°) leads to the expressed growth of intracranial pressure and critical decrease in cerebral perfusion.

scholarly journals Intracranial pressure influences the level of sympathetic tone

2018 ◽  
Vol 315 (5) ◽  
pp. R1049-R1053 ◽  
Author(s):  
Sarah-Jane Guild ◽  
Utkarsh A. Saxena ◽  
Fiona D. McBryde ◽  
Simon C. Malpas ◽  
Rohit Ramchandra
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Nervous System ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

Sympathetic overdrive is associated with many diseases, but its origin remains an enigma. An emerging hypothesis in the development of cardiovascular disease is that the brain puts the utmost priority on maintaining its own blood supply; even if this comes at the “cost” of high blood pressure to the rest of the body. A critical step in making a causative link between reduced brain blood flow and cardiovascular disease is how changes in cerebral perfusion affect the sympathetic nervous system. A direct link between decreases in cerebral perfusion pressure and sympathetic tone generation in a conscious large animal has not been shown. We hypothesized that there is a novel control pathway between physiological levels of intracranial pressure (ICP) and blood pressure via the sympathetic nervous system. Intracerebroventricular infusion of saline produced a ramped increase in ICP of up to 20 mmHg over a 30-min infusion period (baseline 4.0 ± 1.1 mmHg). The ICP increase was matched by an increase in mean arterial pressure such that cerebral perfusion pressure remained constant. Direct recordings of renal sympathetic nerve activity indicated that sympathetic drive increased with increasing ICP. Ganglionic blockade, by hexamethonium, preventing sympathetic transmission, abolished the increase in arterial pressure in response to increased ICP and was associated with a significant decrease in cerebral perfusion pressure. This is the first study to show that physiological elevations in ICP regulate renal sympathetic activity in conscious animals. We have demonstrated a novel physiological mechanism linking ICP levels with sympathetic discharge via a possible novel intracranial baroreflex.

Cerebral blood flow regulation during experimental brain compression

1973 ◽  
Vol 39 (2) ◽  
pp. 186-196 ◽  
Author(s):  
J. Douglas Miller ◽  
Albert E. Stanek ◽  
Thomas W. Langfitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Raised Intracranial Pressure ◽  
Content Type ◽  
Brain Compression

✓ The effect of brain compression on cerebral blood flow was measured in 13 anesthetized, ventilated dogs by inflation of extradural balloons. The effects of the raised intracranial pressure, so produced, were correlated with the presence or absence of autoregulation of cerebral blood flow to induced changes of arterial pressure, which was tested immediately prior to each episode of inflation of the balloon. Cerebral blood flow was measured by a venous outflow method and monitored continuously, together with arterial and supratentorial intracranial pressure; arterial pCO2 and body temperature were held constant. Three stages were identified. When autoregulation to a change of arterial pressure was intact, initial inflation of the balloon did not reduce cerebral blood flow until the difference between arterial and intracranial pressure (which was taken to represent cerebral perfusion pressure) was less than 40 mm Hg. When autoregulation was impaired, which occurred after the first inflation of the balloon or was due to preceding arterial hypotension, raised intracranial pressure caused an immediate reduction of cerebral blood flow. At this stage of impaired autoregulation there was a tendency for hyperemia to develop on deflation of the balloon. Finally, after repeated inflation and deflation of the balloon, when brain swelling supervened, cerebral blood flow decreased steadily and failed to increase despite induced increases of arterial pressure and cerebral perfusion pressure.

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