Effects of Increased Intracranial Pressure on Cerebral Blood Flow and on Cerebral Venous pO2, pCO2, pH, Lactate and Pyruvate in Dogs

1969 ◽  
Vol 75 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Å. Kjällquist ◽  
B. K. Siesjö ◽  
N. Zwetnow
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.


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.


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