Cerebral hemorrhage and edema following brain biopsy in rats: significance of mean arterial blood pressure

2000 ◽  
Vol 92 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Helene Benveniste ◽  
Katie R. Kim ◽  
Laurence W. Hedlund ◽  
John W. Kim ◽  
Allan H. Friedman

Object. It is taken for granted that patients with hypertension are at greater risk for intracerebral hemorrhage during neurosurgical procedures than patients with normal blood pressure. The anesthesiologist, therefore, maintains mean arterial blood pressure (MABP) near the lower end of the autoregulation curve, which in patients with preexisting hypertension can be as high as 110 to 130 mm Hg. Whether patients with long-standing hypertension experience more hemorrhage than normotensive patients after brain surgery if their blood pressure is maintained at the presurgical hypertensive level is currently unknown. The authors tested this hypothesis experimentally in a rodent model.Methods. Hemorrhage and edema in the brain after needle biopsy was measured in vivo by using three-dimensional magnetic resonance (MR) microscopy in the following groups: WKY rats, acutely hypertensive WKY rats, spontaneously hypertensive rats (SHR strain), and SHR rats treated with either sodium nitroprusside or nicardipine. Group differences were compared using Tukey's studentized range test followed by individual pairwise comparisons of groups and adjusted for multiple comparisons.There were no differences in PaCO2, pH, and body temperature among the groups. The findings in this study indicated that only acutely hypertensive WKY rats had larger volumes of hemorrhage. Chronically hypertensive SHR rats with MABPs of 130 mm Hg did not have larger hemorrhages than normotensive rats. There were no differences in edema volumes among groups.Conclusions. The brains of SHR rats with elevated systemic MABPs are probably protected against excessive hemorrhage during surgery because of greater resistance in the larger cerebral arteries and, thus, reduced cerebral intravascular pressures.

1982 ◽  
Vol 57 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Bjørn Magnaes

✓ When an intraspinal expanding lesion causes a spinal block, a segment of the spinal cord or cauda equina will be subjected to general pressure from the surrounding tissue. This spinal block pressure, the spinal equivalent to intracranial pressure, was measured by lumbar infusion of fluid and simultaneous recording of the volume-pressure curve caudal to the block. The point of deviation from or breakthrough of the exponential volume-pressure curve indicated the spinal block pressure. Spinal block pressure of about 500 mm H2O and more could be determined by this method, and, when it was combined with Queckenstedt's test, lower pressures could be assessed as well. In the static (thoracic) part of the spine, spinal block pressure up to the level of arterial blood pressure was recorded. In the dynamic part of the spine, however, spinal block pressure could exceed arterial blood pressure due to external compressive forces during extension of the spine. There was a general tendency for more severe neurological deficits in patients with high spinal block pressure; but the duration of the pressure, additional focal pressure, and spinal cord compared with nerve root compression seemed equally important factors. The recording has implications for diagnosis, positioning of patients for myelography and surgery, selection of high-risk patients for the most appropriate surgical procedure, and detection of postoperative hematoma. There were no complications associated with the recordings.


1974 ◽  
Vol 41 (3) ◽  
pp. 350-355 ◽  
Author(s):  
Michael E. Carey ◽  
A. Richard Vela

✓The rate of cerebrospinal fluid (CSF) production in dogs was measured by ventriculocisternal perfusion with artificial CSF containing inulin. In normotensive animals, the average CSF production was 36 ± 6 µl/min. When the mean arterial blood pressure was reduced to 62 ± 1 mm Hg, the CSF production fell to 22 ± 5 µl/min, a 39% reduction in fluid formation. The authors briefly discuss various hypotheses to explain this reduction.


1986 ◽  
Vol 251 (1) ◽  
pp. R82-R90 ◽  
Author(s):  
J. W. Hubbard ◽  
R. H. Cox ◽  
B. J. Sanders ◽  
J. E. Lawler

Normotensive Wistar-Kyoto (WKY) rats and borderline hypertensive rats (BHR) were exposed to aversive classical conditioning procedures and chronically instrumented with arterial catheters and electromagnetic flow probes around the ascending aorta. After postoperative recovery, hemodynamic measurements and blood samples were obtained from conscious animals at rest and during aversive conditioning. The cardiovascular response to the behavioral stress consisted of a significant increase in mean arterial blood pressure, total peripheral resistance index, cardiac index, heart rate, and aortic dP/dt for both strains. However, the elevated vascular resistance seen in the BHR resulted in a significantly greater increase in mean arterial blood pressure (21 mmHg) compared with the WKY rats (14 mmHg). In addition, the BHR showed a significantly (P less than 0.05) greater plasma norepinephrine concentration (760 +/- 99 pg/ml) in response to the stress than did the WKY rats (559 +/- 53 pg/ml). These data suggest that an increase in cardiac output, elevated vascular resistance, and increased sympathetic drive may contribute to the development of stress-induced hypertension in this animal model.


1999 ◽  
Vol 90 (4) ◽  
pp. 752-759 ◽  
Author(s):  
Marek Czosnyka ◽  
Hugh K. Richards ◽  
Zofia Czosnyka ◽  
Stefan Piechnik ◽  
John D. Pickard

Object. The aim of the study was to assess how cerebrospinal fluid (CSF) pressure—volume compensation depends on cerebrovascular tone.Methods. In 26 New Zealand White rabbits, intracranial pressure (ICP), arterial blood pressure, and basilar artery blood flow velocity were measured continuously. Saline was infused into the cranial subarachnoid space to assess CSF compensatory parameters: the resistance to CSF outflow, the elastance coefficient, and the amplitude of the ICP pulsatile waveform. Infusions were repeated on two different levels of CO2 concentration in the arterial blood (PaCO2), at normotension and hypotension, and after the death of the animal.An increase in PaCO2 from a mean of 27 to 48 mm Hg was accompanied by an 18% increase in the resistance to CSF outflow (p < 0.005) and a 64% increase (p < 0.05) in the elastance coefficient. A decrease in arterial blood pressure from a mean of 100 to 51 mm Hg caused a 25% decrease in CSF outflow resistance (p < 0.01) but did not affect the elastance coefficient. Postmortem, a 23% decrease in the CSF outflow resistance was associated with a 102% decrease in the elastance coefficient.Conclusions. Cerebrovascular parameters have a limited but significant impact on CSF infusion studies. The vascular component of ICP may be identified as a significant factor contributing to this phenomenon. During infusion studies, physiological parameters influencing vascular conditions should be maintained as stable as possible.


2007 ◽  
Vol 34 (1) ◽  
pp. 157-162 ◽  
Author(s):  
Sanjay Subramanian ◽  
Murat Yilmaz ◽  
Ahmer Rehman ◽  
Rolf D. Hubmayr ◽  
Bekele Afessa ◽  
...  

1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.


PEDIATRICS ◽  
1992 ◽  
Vol 89 (4) ◽  
pp. 643-647 ◽  
Author(s):  
Lena Hellström-Westas ◽  
Nils W. Svenningsen ◽  
Angela H. Bell ◽  
Liselotte Skov ◽  
Gorm Greisen

During surfactant treatment of respiratory distress syndrome, 23 premature newborns were investigated with continuous amplitude-integrated electroencephalography (cerebral function monitors). Simultaneously, arterial blood pressure and transcutaneous blood gas values were recorded. A short(&lt;10 minutes) but significant decrease in cerebral activity was seen in almost all neonates immediately after the surfactant instillation, in spite of an improved pulmonary function. In 21 of 23 neonates, a transient fall in mean arterial blood pressure of 9.3 mm Hg (mean) occurred coincidently with the cerebral reaction. Neonates in whom intraventricular hemorrhage developed tended to have lower presurfactant mean arterial blood pressure (P&gt; .05), but they had a significantly lower mean arterial blood pressure after surfactant instillation (P &lt; .05). No other differences were found between neonates in whom intraventricular hemorrhage developed and those without intraventricular hemorrhage. The present findings demonstrate that an acute cerebral dysfunction may occur after surfactant instillation. In some vulnerable neonates with arterial hypotension and severe pulmonary immaturity,the fall in mean arterial blood pressure may increase the risk of cerebral complications and could be related to an unchanged rate of intraventricular hemorrhage after surfactant treatment.


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