The effect of increased intracranial pressure on cerebrovascular hemodynamics

1971 ◽  
Vol 34 (6) ◽  
pp. 760-769 ◽  
Author(s):  
Harry M. Lowell ◽  
Byron M. Bloor

✓ Both brain edema (increased water content) and enlargement of the vascular compartment have been implicated as being responsible for intracranial hypertension following trauma. In this study pertinent cerebrovascular hemodynamic parameters have been investigated in states of increased intracranial pressure (ICP) and graded trauma to determine whether cerebral edema or vascular factors are of major importance. Utilizing the monkey-epidural balloon experimental model, continuous measurements of the mean arterial pressure (MABP) , jugular outflow pressure (MJVP), and sagittal sinus wedge pressure (SSWP) were obtained. Shulman's observations that the sagittal sinus wedge pressure accurately reflects the intracranial pressure have been confirmed. The total cerebral blood flow (CBF) and mean transit time (t̄) were determined and the total cerebral blood volume (CBV) computed. From these data the venous (Rv), arterial (Ra), and total resistances (Rt) were calculated. Analysis of these parameters during both the acute elevation of ICP and that following graded trauma has demonstrated: 1) a progressive decrease in the total cerebral blood flow and volume and a concomitant increase in the mean transit time; 2) a progressive increase in the total resistance with a shift from the arterial to the venous side; 3) a progressive decrease in the perfusion pressure (PP = MABP-SSWP); 4) impairment of CO2 reactivity pari passu with vasomotor activity and autoregulation of flow to pressure. The findings did not support the concept that increased intracranial pressure following trauma is the result of an increase in the size of the cerebrovascular compartment.

1983 ◽  
Vol 3 (2) ◽  
pp. 246-249 ◽  
Author(s):  
A. Forster ◽  
O. Juge ◽  
D. Morel

Although it is known that hypercarbia increases and benzodiazepines decrease cerebral blood flow (CBF), the effects of benzodiazepines on CBF responsiveness to CO2 are not well documented. The influence on CBF and CBF-C02 sensitivity of placebo or midazolam, which is a new water-soluble benzodiazepine, was measured in eight healthy volunteers using the noninvasive 133Xe inhalation method for CBF determination. Under normocarbia, midazolam decreased CBF from 40.6 ± 3.2 to 27.0 ± 5.0 ml 100 g−1 min−1 (x̄ ± SD). At a later session under hypercarbia, CBF was 58.8 ± 4.4 ml 100 g−1 min−1 after administration of placebo, and 49.1 ± 10.2 ml 100 g−1 min−1 after midazolam. The mean of the slopes correlating Paco2 and CBF was significantly steeper with midazolam (2.5 ± 1.2 ml 100 g−1 min−1 mm Hg−1) than with placebo (1.5 ± 0.4 ml 100 g−1 min−1 mm Hg−1). Our results suggest that midazolam may be a safe agent to use in patients with intracranial hypertension, since it decreases CBF and thus cerebral blood volume; however, it should be administered with caution in nonventilated patients with increased intracranial pressure, since its beneficial effects on cerebrovascular tone can be readily counteracted by the increase in arterial CO2 tension induced by this drug.


1992 ◽  
Vol 262 (6) ◽  
pp. H1908-H1914 ◽  
Author(s):  
M. Ferrari ◽  
D. A. Wilson ◽  
D. F. Hanley ◽  
R. J. Traystman

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.


Stroke ◽  
1974 ◽  
Vol 5 (6) ◽  
pp. 719-724 ◽  
Author(s):  
YOSHIHIRO KURIYAMA ◽  
TAKASHI AOYAMA ◽  
KUNIHIKO TADA ◽  
SHOTARO YONEDA ◽  
TADAATSU NUKADA ◽  
...  

1980 ◽  
Vol 238 (6) ◽  
pp. H868-H875
Author(s):  
L. G. D'Alecy ◽  
C. J. Rose ◽  
S. A. Sellers ◽  
J. P. Manfredi

The single-pass extraction of sodium was measured with and without sympathetic stimulation in dogs anesthetized with alpha-chloralose. A mixture of the test (24Na) and reference ([125I]RISA) substances was injected as a bolus into the common carotid artery. Single-drop samples were taken at approximately 1-s intervals from the sagittal sinus and the temporal sinus while cerebral blood flow was continuously measured at the temporal sinus by the venous outflow technique. The extraction measurements were used to test for extracerebral contamination of venous outflow. The mean integral extraction determined from sagittal sinus samples was 2.2% during control conditions and 3.0% during sympathetic stimulation. The mean temporal sinus extraction of sodium was 6.9% during control and 2.7% during sympathetic stimulation. If true cerebral sodium extraction is assumed to be 1.4% and extracerebral sodium extraction is 60%, then these data indicate that extracerebral contamination is less than 10%.


1980 ◽  
Vol 238 (5) ◽  
pp. H745-H749 ◽  
Author(s):  
C. H. Baker ◽  
E. T. Sutton ◽  
D. L. Davis

An indicator dilution technique is described for obtaining time-concentration curves subsequent to bolus injections of sulfhemoglobin red blood cells (SH-RBC), which have a deep greenish-brown color (absorption peak 620 nm vs. 542 and 564 nm for normal red cells). The series- and parallel-coupled microvessels of cat mesentery were studied. This is accomplished by means of video microscopy with a two-window intensity-sensitive video sampler system. The relationship between SH-RBC concentration in blood and optical measurement is linear. Blood flow velocities were calculated from the difference in mean transit times between two points along a vessel. When this technique is used in association with the previously reported method for determining time-concentration curves for the plasma indicator FITC-dextran the mean transit time (t) for red blood cells was less than for plasma in arterioles. The reproducibility of t and flow velocity for both SH-RBC and FITC-dextran from successive injections were reported. The mean transit time ratio of arteriolar SH-RBC to FITC-dextran averages 0.89. Blood flow velocity calculated from SH-RBC is greater than that calculated from FITC-dextran in these same arterioles. The ratio of the velocities averages 1.29.


1987 ◽  
Vol 15 (4) ◽  
pp. 432
Author(s):  
David A. Wilson ◽  
Marco Ferrari ◽  
Daniel F. Hanley ◽  
Mark C. Rogers ◽  
Richard J. Traystman

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