Raised intracranial pressure and cerebral blood flow: I. Cisterna magna infusion in primates

Changes in cerebral blood flow during incremental increases of intracranial pressure produced by infusion of fluid into the cisterna magna were studied in anaesthetized baboons. Cerebral blood flow remained constant at intracranial pressure levels up to approximately 50 mm Hg. At intracranial pressure levels between 50-96 mm Hg a marked increase in cerebral blood flow occurred, associated with the development of systemic hypertension and changes in cerebrovascular resistance. Further increases of intracranial pressure led to a progressive fall in cerebral blood flow. Prior section of the cervical cord prevented both the increase in cerebral blood flow and the systemic hypertension. Alteration of cerebral perfusion pressure by bleeding during the hyperaemia in a further group of animals suggested that autoregulation was at least partially preserved during this phase. After maximum hyperaemia had occurred, however, autoregulation appeared to be lost. The clinical implications of these findings are discussed.     

Impairment of cerebrovascular autoregulation by theophylline

The relationship between pressure and flow was investigated in the cerebral vascular bed during intraarterial theophylline infusion. The experiments were performed on isolated canine brains supported by a donor system, thus eliminating all secondary effects of theophylline on cerebral blood flow (i.e., changes in systemic blood pressure, respiration and extracranial blood flow). Cerebral blood flow was measured continuously as the total venous outflow of the confluence of sinuses and perfusion pressure was measured in the circle of Willis. Cerebral autoregulation was tested by varying the perfusion pressure in sudden steps. The position and shape of the pressure-flow curve during theophylline infusion differed significantly from control. Theophylline induced vasodilation and a considerable impairment of cerebral autoregulation, i.e., the independence of flow and pressure over the physiological range was lost. At a perfusion pressure of 80 mm Hg the mean decrease of cerebral resistance due to theophylline was 28%. During theophylline infusion the pressure-flow regression line of the pressure range, where control flow values remained constant, differed significantly from control regression line. Possible mechanisms of cerebral vasodilation due to theophylline are discussed with regard to the impairement of cerebral autoregulation. The ability of the brain to autoregulate therefore seems dependent upon the initial degree of vasodilation due to the myotropic action of theophylline. Metabolic effects of theophylline are probably not responsible for the impairment of cerebral autoregulation.     

Raised intracranial pressure and cerebral blood flow. 5. Effects of episodic intracranial pressure waves in primates.

The effects of episodic waves of intracranial pressure on cerebral blood flow were studied in primates. Six pressure waves each of 20 minutes' duration and ranging from 50 to 100 mmHg in magnitude were induced in baboons, at intervals of 30 minutes, in an attempt to simulate clinical plateau waves. With pressure waves up to 75 mmHg, cerebral blood flow remained at control levels despite falling cerebral perfusion pressures. Between the initial pressure waves a marked hyperaemia developed, with cerebral blood flow increasing by as much as 100%, and this appeared to be a means whereby adequate flow was maintained during pressure waves. Later pressure waves, up to 100 mmHg, eventually reduced blood flow below control levels, although moderately high flows were maintained during periods of very low perfusion pressure. Brain metabolism was affected by eht episodic pressure waves, although no consistent change was seen.     

Raised intracranial pressure and cerebral blood flow: 3. Venous outflow tract pressures and vascular resistances in experimental intracranial hypertension

Pressure changes within the venous outflow tract from the brain were studied in anaesthetized baboons. Segmental vascular resistance changes were also calculated and the results correlated with the changes in cerebral blood flow, measured by the ¹³³Xenon clearance method. Three different methods were used to raise intracranial pressure: cisterna magna infusion, a supratentorial subdural balloon, and an infratentorial subdural balloon. A close correlation was found between the cortical vein pressure and intracranial pressure with all methods of raising intracranial pressure: the overall correlation coefficient was 0·98. In the majority of animals sagittal sinus pressure showed little change through a wide range of intracranial pressure. In three of the six animals in the cisterna magna infusion group, however, sagittal sinus pressure increased to levels approaching the intracranial pressure during the later stages of intracranial hypertension. Jugular venous pressure showed little change with increasing intracranial pressure. The relationship between cerebral prefusion pressure and cerebral blood flow differed according to the method of increasing intracranial pressure. This was due to differing patterns of change in prevenous vascular resistance as venous resistance increased progressively with increasing pressure in all three groups. The present results confirm, therefore, the validity of the current definition of cerebral perfusion pressure—that is, cerebral perfusion pressure is equal to mean arterial pressure minus mean intracranial pressure—by demonstrating that intracranial pressure does represent the effective cerebral venous outflow pressure.     

Cerebral vasomotor reactivity testing in head injury: the link between pressure and flow

BACKGROUND: It has been suggested that a moving correlation index between mean arterial blood pressure and intracranial pressure, called PRx, can be used to monitor and quantify cerebral vasomotor reactivity in patients with head injury. OBJECTIVES: To validate this index and study its relation with cerebral blood flow velocity and cerebral autoregulation; and to identify variables associated with impairment or preservation of cerebral vasomotor reactivity. METHODS: The PRx was validated in a prospective study of 40 head injured patients. A PRx value of less than 0.3 indicates intact cerebral vasomotor reactivity, and a value of more than 0.3, impaired reactivity. Arterial blood pressure, intracranial pressure, mean cerebral perfusion pressure, and cerebral blood flow velocity, measured bilaterally with transcranial Doppler ultrasound, were recorded. Dynamic cerebrovascular autoregulation was measured using a moving correlation coefficient between arterial blood pressure and cerebral blood flow velocity, the Mx, for each cerebral hemisphere. All variables were compared in patients with intact and impaired cerebral vasomotor reactivity. RESULTS: No correlation between arterial blood pressure or cerebral perfusion pressure and cerebral blood flow velocity was seen in 19 patients with intact cerebral vasomotor reactivity. In contrast, the correlation between these variables was significant in 21 patients with impaired cerebral vasomotor reactivity, whose cerebral autoregulation was reduced. There was no correlation with intracranial pressure, arterial blood pressure, cerebral perfusion pressure, or interhemispheric cerebral autoregulation differences, but the values for these indices were largely within normal limits. CONCLUSIONS: The PRx is valid for monitoring and quantifying cerebral vasomotor reactivity in patients with head injury. This intracranial pressure based index reflects changes in cerebral blood flow and cerebral autoregulatory capacity, suggesting a close link between blood flow and intracranial pressure in head injured patients. This explains why increases in arterial blood pressure and cerebral perfusion pressure may be useful for reducing intracranial pressure in selected head injured patients (those with intact cerebral vasomotor reactivity).     

颅高压时脑脊液脉动压与脑灌注压相互关系的实验研究

目的　研究颅高压时脑脊液脉动压与脑灌注压的相互变化关系。方法　 14条狗安置硬膜外球囊并注液制成颅高压模型。通过改变球囊内液体量改变颅高压程度和颅内容积。通过压力传感器持续记录脑室内压力、腰椎管内压力及体动脉压。结果　随着颅内压的持续增高 ,脑灌注压逐渐下降 ,脑脊液脉动压相应增高。脑脊液脉动压与颅内压的变化趋势呈现正性线性关系 (r=0 732 2 ,P <0 0 5 ) ,而与脑灌注压的变化趋势呈现负性线性关系 (r=- 0 6 879,P <0 0 5 )。结论　在实验性颅高压中 ,脑脊液脉动压随着脑灌注压的下降而增大 ,两者间呈现负性线性关系。在脑血管自动调节机制受损的情况下 ,脑脊液脉动压的变化可能提供脑血流量改变的信息。     

Effects of increased arterial pressure on blood flow in the damaged brain.

The effect of induced arterial hypertension on cerebral blood flow and intracranial pressure was measured before and after the production of a standard cryogenic brain lesion in 10 anaesthetized, ventilated baboons. Before injury the animals were divided into a group with intact autoregulation, having more than 20% increase in cerebrovascular resistance during arterial hypertension, and a group with impaired autoregulation, in which the change in cerebrovascular resistance was much less. The cryogenic injury produced a rapid rise in intracranial pressure and a reduction of cerebral blood flow in the affected hemisphere. Despite this, there was an increase in cerebrovascular resistance during arterial hypertension in all animals after brain injury, accompanied by a further significant rise in intracranial pressure. It is suggested that this response is unlikely to represent normal physiological autoregulation and caution should be exercised in interpreting it as such in the course of studies of cerebral blood flow in patients with acute brain damage.     

Relationship between cardiovascular circulation and intracranial pressure--analyses of polygraphic recordings during cardiac surgery in congenital heart diseases

Few reports have appeared in regard to cerebral perfusion pressure (CPP) accompanying fluctuations in intracranial pressure (ICP), arterial pressure (BP) and central venous pressure (CVP) as well as autoregulation of cerebral circulation in neonates and infants. Therefore, we report here on interesting findings we obtained from monitoring ICP, BP, and CVP during operations in 30 neonates or infants with congenital heart disease as our subjects. i) ICP fluctuates depending on arterial pressure and venous pressure, but changes in the latter display a clearer effect. ii) On inducing anesthesia the amplitude of ICP pulsating waves became gradually larger, but following intubation intracranial pressure was somewhat reduced and became stable. iii) Following thoracotomy CVP rose and at the same time intracranial pressure also increased somewhat. Before thoracotomy ICP pulsating waves resembled arterial pressure wave forms, but after thoracotomy they resembled central venous pressure wave forms. iv) In cases with two-peak ICP pulsating waves, when we conducted a study by blocking venous return from the internal carotid vein during the operation by the Queckenstedt method, ICP rose by increasing its amplitude, but the pulsating wave forms lost their venous component, and changed into a single peak consisting of an arterial component. v) In order to observe the relationship between changes in arterial pressure and ICP, when we looked at changes in ICP accompanying partial blockage of the descending aorta (DAo), simultaneously with the partial blocking of the DAo both AP and CVP rose, and ICP also rose accordingly. Also, when arterial blockage was relaxed, BP, CVP, and ICP immediately recovered completely to the status quo prior to the blocking procedure. This finding indicates that by blocking of the DAo, intracranial arterial and venous blood volume abruptly rapidly increase and since CVP also rises, therefore ICP rises to maintain a balance with these. As a result, this brings about the effect of normally maintaining the cerebral perfusion volume. vi) If we look at changes in ICP brought about by partial blocking of the ascending aorta, blockage of the artery brought about a further reduction in BP, and in this case since the arterial blood flow into the cranium also fell off markedly, we found that ICP also was reduced. The above results suggest that in the normal brains of neonates and infants even when under various conditions various fluctuations in corporeal circulation develop, cerebral perfusion volume adjusts itself in response to this, and thus autoregulation of cerebral blood flow is able to act in an adequate way.     

Regional cerebral blood flow and CSF pressures during Cushing response induced by a supratentorial expanding mass

In order to delineate the critical blood flow pattern during the Cushing response in intracranial hypertension, regional cerebral blood flow was measured with radioactive microspheres in 12 anesthetized dogs at respiratory arrest caused either by expansion of an epidural supratentorial balloon or by cisternal infusion. Regional cerebrospinal fluid pressures were recorded and the local cerebral perfusion pressure calculated in various cerebrospinal compartments. In the 8 dogs of the balloon expansion group, the systemic arterial pressure was unmanipulated in 4, while it was kept at a constant low level (48 and 70 mm Hg) in 2 dogs and, in another 2 dogs, at a constant high level (150 and 160 mm Hg) induced by infusion of Aramine. At respiratory arrest, regional cerebral blood flow had a stereotyped pattern and was largely independent of the blood pressure level. In contrast, concomitant pressure gradients between the various cerebrospinal compartments varied markedly in the 3 animal groups, increasing with higher arterial pressure. Flow decreased by 85-100% supratentorially and by 70-100% in the upper brain stem down to the level of the upper pons, while changes in the lower brain stem were minor, on the average 25%. When intracranial pressure was raised by cisternal infusion in 4 dogs, the supratentorial blood flow pattern at respiratory arrest was approximately similar to the flow pattern in the balloon inflation group. However, blood flow decreased markedly (74-85%) also in the lower brain stem. The results constitute another argument in favour of the Cushing response in supratentorial expansion being caused by ischemia in the brain stem. The critical ischemic region seems to be located rostrally to the oblongate medulla, probably in the pons.     

Association between intracranial, arterial pulse pressure amplitudes and cerebral autoregulation in head injury patients

OBJECTIVE: To explore whether intracranial pulse pressure amplitudes relate to arterial pulse pressure amplitudes and whether correlations between time-related changes in intracranial and arterial pulse pressure amplitudes associate with indices of cerebral autoregulation. METHODS: A total of 257 continuous and simultaneous intracranial pressure (ICP), arterial blood pressure (ABP) and middle cerebral artery (MCA) blood velocity recordings were obtained 1-14 days after ictus in 76 traumatic head injury patients and analysed retrospectively. Clinical outcome was assessed using the Glasgow outcome scale (GOS). Pulse pressure amplitudes of corresponding single ICP and ABP waves were correlated in consecutive 200 wave pairs. Mean ICP, mean ABP and mean ICP wave amplitudes, and mean and systolic MCA blood flow velocities, were computed in consecutive 6 second time windows. The indices of cerebral autoregulation PRx (moving correlation between mean ICP and mean ABP), and Mx and Sx (moving correlation between mean and systolic MCA blood velocity and cerebral perfusion pressure) were calculated over 4 minute periods and averaged over each recording. RESULTS: Intracranial pulse pressure amplitudes were not related to arterial pulse pressure amplitudes (mean of Pearson's correlations coefficients: 0.04). Outcome was related to mean ICP, PRx and Sx (p 相似文献   

Influence of blood pressure and cardiac output on cerebral blood flow and autoregulation in acute stroke measured by TCD

Although the dependence of cerebral perfusion on blood pressure has been well studied, little data is available about the effect cardiac output has on cerebral flow velocity and autoregulation, particularly during acute stroke. To improve cerebral perfusion, we treated 10 patients who suffered from an acute ischemic stroke of the middle cerebral artery with a hypervolemic hemodilution combined with dopamine-dobutamine. The influence of blood pressure and cardiac output on the blood flow velocity in the middle cerebral artery was measured using transcranial doppler sonography (TCD). Under the therapy, a dosage-dependent increase of 12% in blood pressure (BP) and 53% increase in cardiac output was observed. There was a significant (p > 0.01) correlation between TCD-mean flow velocity (V_m) and cardiac output (r = 0.33) as well as between V_m and blood pressure (r = 0.52) on the affected side. The unaffected side showed no correlation between V_m and cardiac output (r = 0.01), or between V_m and blood pressure (r = 0.03). Systolic flow velocity increased significantly in both hemispheres. As an expression of increasing cerebral vascular resistance, the pulsating index (PI) increased significantly (p > 0.01) in the affected hemisphere as well as in the unaffected hemisphere. This suggests that during acute stroke blood flow velocity and autoregulation in the affected vascular region depend not only on cerebral perfusion pressure but also on CO levels.     

The effect of indomethacin on intracranial pressure, cerebral perfusion and extracellular lactate and glutamate concentrations in patients with fulminant hepatic failure.

Uncontrolled increase in intracranial pressure (ICP) continues to be one of the most significant causes of early death in patients with acute liver failure (ALF). In this study, we aimed to determine the effects of indomethacin on ICP and cerebral perfusion pressure in twelve patients with ALF and brain edema (9 females/3 males, median age 49,5 (range 21 to 64) yrs.). Also changes in cerebral perfusion determined by transcranial Doppler technique (Vmean) and jugular bulb oxygen saturation (SvjO2) were measured, as well as brain content of lactate and glutamate by microdialysis technique. Finally, we determined the cerebral blood flow autoregulation before and after indomethacin injection. We found that indomethacin reduced ICP from 30 (7 to 53) to 12 (4 to 33) mmHg (P < 0.05). The cerebral perfusion pressure increased from 48 (0 to 119) to 65 (42 to 129) mmHg (P < 0.05), while Vmean and SvjO2 on average remained unchanged at 68 (34 to 126) cm/s and 67 (28 to 82) %, respectively. The lactate and glutamate in the brain tissue were not altered (2.1 (1.8 to 7.8) mmol/l and 34 (2 to 268) micromol/l, respectively) after injection of indomethacin. Cerebral blood flow autoregulation was impaired in all patients before injection of indomethacin, but was not restored after administration of indomethacin. We conclude that a bolus injection of indomethacin reduces ICP and increases cerebral perfusion pressure without compromising cerebral perfusion or oxidative metabolism in patients with ALF. This finding indicates that indomethacin may be valuable as rescue treatment of uncontrolled intracranial hypertension in fulminant hepatic failure.     

Assessment of cerebrovascular and cardiovascular responses to lower body negative pressure as a test of cerebral autoregulation

The aim of this study was to determine whether lower body negative pressure (LBNP), combined with noninvasive methods of assessing changes in systemic and cerebral vascular resistance, is suitable as a method for assessing cerebral autoregulation.In 13 subjects we continuously assessed heart rate, blood pressure, cerebral blood flow velocity (CBFV) and cardiac output during graded levels of LBNP from 0 to -50 mm Hg. With increasing levels of LBNP, cardiac output declined significantly (to 55.8+/-4.5% of baseline value) but there was no overall change in mean arterial pressure. CBFV also fell at higher levels of LBNP (to 81.4+/-3.2% of baseline) but the percentage CBFV change was significantly less than that in cardiac output (P<0.01). The maximum increase in cerebrovascular resistance (pulsatility ratio) was significantly less than that in total peripheral resistance (17+/-6% vs. 105+/-16%, P<0.01). Spectral analysis showed that the power of low-frequency oscillations in mean arterial pressure, but not CBFV, increased significantly at the -50 mm Hg level of LBNP.These results show that, even during high levels of orthostatic stress, cerebral autoregulation is preserved and continues to protect the cerebral circulation from changes in the systemic circulation. Furthermore, assessment of cardiovascular and cerebrovascular parameters during LBNP may provide a useful clinical test of cerebral autoregulation.     

Balint's syndrome following eclampsia

A young female patient sustained bilateral parieto-occipital infarcts and presented with Balint's syndrome following treatment of eclampsia and caesarean section. Altered cerebral blood flow autoregulation and raised intracranial pressure due to eclampsia probably resulted in impaired cerebral perfusion and borderzone cerebral ischaemia in this patient. Careful reduction of blood pressure in patients with eclampsia is emphasized.     

Dispersion of cerebral temperature, cerebral perfusion and intracranial pressure in rabbits placed with epidural balloons

This study examines the intracranial pressure and temperature dispersion in a rabbit model after epidural balloon compression. Right and left supratentorial, intraventricular and infratentorial pressures and temperatures of the rabbits have been measured before epidural balloon was placed. Afterwards, the epidural balloon was placed in right parietal epidural area. The intracranial pressure and temperature dispersion values were recorded after inflation with 0.3 and 0.6 ml, respectively. The control values of intracranial pressure measurements of four different brain regions were found to be similar. When the balloon was inflated to 0.3 ml, the intracranial pressure distribution was found to be equal in all the fields. After the balloon was inflated up to 0.6 ml, right and left supratentorial intracranial pressure values were found to be equal. However, infratentorial pressure values were lower and intraventricular pressure values were higher when compared with the right hemisphere. Before the inflation and at two different inflation volumes, perfusion pressure and temperature dispersion were found to be similar between right hemisphere and other compartments. We conclude that, the effective mechanism in cerebral temperature regulation may be related to preserved cerebral perfusion pressure and cerebral blood flow.     

Cardiovascular and cerebrovascular responses to lower body negative pressure in type 2 diabetic patients

In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation and contribute to orthostatic intolerance. The aim of our study was to determine whether impaired cerebral autoregulation contributes to orthostatic intolerance during lower body negative pressure in diabetic patients. Thirteen patients with early-stage type 2 diabetes were studied. We continuously recorded RR-interval, mean blood pressure and mean middle cerebral artery blood flow velocity at rest and during lower body negative pressure applied at -20 and -40 mm Hg. Spectral powers of RR-interval, blood pressure and cerebral blood flow velocity were analyzed in the sympathetically mediated low (LF: 0.04-0.15 Hz) and the high (HF: 0.15-0.5 Hz) frequency ranges. Cerebral autoregulation was assessed from the transfer function gain and phase shift between LF oscillations of blood pressure and cerebral blood flow velocity. In the diabetic patients, lower body negative pressure decreased the RR-interval, i.e. increased heart rate, while blood pressure and cerebral blood flow velocity decreased. Transfer function gain and phase shift remained stable. Lower body negative pressure did not induce the normal increase in sympathetically mediated LF-powers of blood pressure and cerebral blood flow velocity in our patients indicating sympathetic dysfunction. The stable phase shift, however, suggests intact cerebral autoregulation. The dying back pathology in diabetic neuropathy may explain an earlier and greater impairment of peripheral vasomotor than cerebrovascular control, thus maintaining cerebral blood flow constant and protecting patients from symptoms of presyncope.     

Association between intracranial,arterial pulse pressure amplitudes and cerebral autoregulation in head injury patients

Abstract

Objective: To explore whether intracranial pulse pressure amplitudes relate to arterial pulse pressure amplitudes and whether correlations between time-related changes in intracranial and arterial pulse pressure amplitudes associate with indices of cerebral autoregulation.

Methods: A total of 257 continuous and simultaneous intracranial pressure (ICP), arterial blood pressure (ABP) and middle cerebral artery (MCA) blood velocity recordings were obtained 1–14 days after ictus in 76 traumatic head injury patients and analysed retrospectively. Clinical outcome was assessed using the Glasgow outcome scale (GOS). Pulse pressure amplitudes of corresponding single ICP and ABP waves were correlated in consecutive 200 wave pairs. Mean ICP, mean ABP and mean ICP wave amplitudes, and mean and systolic MCA blood flow velocities, were computed in consecutive 6 second time windows. The indices of cerebral autoregulation PRx (moving correlation between mean ICP and mean ABP), and Mx and Sx (moving correlation between mean and systolic MCA blood velocity and cerebral perfusion pressure) were calculated over 4 minute periods and averaged over each recording.

Results: Intracranial pulse pressure amplitudes were not related to arterial pulse pressure amplitudes (mean of Pearson's correlations coefficients: 0.04). Outcome was related to mean ICP, PRx and Sx (p ≤ 0.04, multiple regression analysis). Correlations between intracranial and arterial pulse pressure amplitudes were weakly related to PRx (Pearson's correlation coefficient: 0.16; p=0.01), but were not related to the indices of cerebral autoregulation Mx (Pearson's correlation coefficient: 0.07) and Sx (Pearson's correlation coefficient: 0.04).

Conclusions: In this cohort of pressure recordings, we found no evidence of a correlation between intracranial and arterial blood pressure amplitudes. The correlation appeared not to be related to the state of cerebral autoregulation, although a weak correlation was found with pressure reactivity index PRx.     

Spinal cord compression and blood flow. I. The effect of raised cerebrospinal fluid pressure on spinal cord blood flow

The effect of cerebrospinal fluid pressure (CSFP) on spinal cord blood flow (SCBF), measured by the hydrogen clearance technique, was studied in dogs. CSFP was altered by the infusion of mock CSF into the lumbar subarachnoid space. Occluding snares at T-13 limited the effect of raised pressure on the brain. As the perfusion pressure was reduced when the CSFP was increased, flow remained constant up to a perfusion pressure of approximately 50 mm Hg. Below this value, flow decreased with decreasing perfusion pressure. Normal flow values could be reestablished even at a raised CSFP if the perfusion pressure was increased by raising the arterial blood pressure. Rapid reduction of CSFP was accompanied by reactive hyperemia. The autoregulation of flow down to a perfusion pressure of 50 mm Hg was due to progressive decrease in vascular resistance. Carbon dioxide-responsiveness of the vessels was decreased markedly as the perfusion pressure was reduced.     

Cerebral blood flow in experimental intracranial mass lesions. Part I: The compression phase

We have shown that a rebound of intracranial pressure (ICP) occurring after decompression of an intracranial mass lesion is a threshold phenomenon dependent upon the cerebral perfusion pressure (CPP) during compression and the duration of the compression. In the present study regional cerebral blood flow (rCBF) was measured during balloon compression of a degree critical for the development of a postdecompression rebound. The effects were compared with those of hydrostatically raised pressure which under similar conditions rarely produces a rebound of ICP. Disproportionately marked reductions in flow occurred in the hemisphere ipsilateral to the balloon, especially in white matter and in cortex adjacent to the balloon with flow values of, respectively, 1.1 +/- 0.9 and 6.4 +/- 3.4 ml 100 g-1 min-1. The differences in flow between balloon and hydrostatic compression were found to be due to an increased cerebrovascular resistance (CVR) caused by a direct compressive effect by the balloon overriding the generalized vasodilation which occurs in response to the raised ICP. Thus the increase in CVR attributable to compression by the balloon added to the reduction in CPP caused by the diffuse increase in ICP. As a consequence flow in large regions of the brain was reduced below the thresholds for structural infarction and for ischaemic damage to the blood-brain barrier.     

The effect of metabolic acidosis upon autoregulation of cerebral blood flow in newborn dogs

The radioactive microsphere technique was used in 13 newborn dogs to determine the effect of a metabolic (lactic)acidosis upon cardiac outout (CO), cerebral blood flow (CBF), and autoregulation of cerebral blood flow. The animals were mechanically ventilated with supplemental oxygen to ensure normocarbia and hyperoxia throughout the experiments. Baseline cardiac output and cerebral blood flow measurements were made, followed by a lactic acid infusion to maintain pH < 7.25. Metabolic acidosis produced a 27% fall in cardiac output and no change in cerebral blood flow (19 ml/100 g/min). Autoregulation was tested in 6 of the acidemic puppies by acute volume depletion to reduce blood pressure by 30% of baseline, followed by rapid volume re-expansion of the withdrawn blood. With volume depletion, CO decreased by 38%, and with volume re-expansion CO returned to baseline. The CBF remained at baseline levels with volume depletion but was slightly increased after rapid volume re-expansion. Five academic controls maintained CO and CBF constant with time. Thus cerebral autoregulation is preserved in the newborn dogs during metabolic acidosis, although cerebral blood flow was slightly increased following volume re-expansion.