Extracellular pH In Brain Research Articles

Extracellular Brain Ph with or without Hypoxia is a Marker of Profound Metabolic Derangement and Increased Mortality after Traumatic Brain Injury

Cerebral hypoxia and acidosis can follow traumatic brain injury (TBI) and are associated with increased mortality. This study aimed to evaluate a relationship between reduced pH(bt) and disturbances of cerebral metabolism. Prospective data from 56 patients with TBI, receiving microdialysis and Neurotrend monitoring, were analyzed. Four tissue states were defined based on pH(bt) and P(bt)O(2): 1--low P(bt)O(2)/pH(bt), 2--low pH(bt)/normal P(bt)O(2), 3--normal pH(bt)/low P(bt)O(2), and 4--normal pH(bt)/P(bt)O(2)). Microdialysis values were compared between the groups. The relationship between P(bt)O(2) and lactate/pyruvate (LP) ratio was evaluated at different pH(bt) levels. Proportional contribution of each state was evaluated against mortality. As compared with the state 4, the state 3 was not different, the state 2 exhibited higher levels of lactate, LP, and glucose and the state 1--higher LP and reduced glucose (P<0.001). A significant negative correlation between LP and P(bt)O(2) (rho=-0.159, P<0.001) was stronger at low pH(bt) (rho=-0.201, P<0.001) and nonsignificant at normal pH(bt) (P=0.993). The state 2 was a significant discriminator of mortality categories (P=0.031). Decreased pH(bt) is associated with impaired metabolism. Measuring pH(bt) with P(bt)O(2) is a more robust way of detecting metabolic derangements.

Monitoring of head injured patients

This article reviews recent advances in multimodality monitoring of patients following severe head injury during the period of 2004-2005. Whilst intracranial pressure measurement remains the cornerstone of neuromonitoring, analysis of the intracranial pressure waveform provides additional information, which may help guide treatment and predict outcome. Non-invasive detection of intracranial hypertension and assessment of cerebral perfusion pressure and autoregulation is the focus of ongoing research. Although jugular venous saturation monitoring remains a useful method for detecting global hypoperfusion its sensitivity to regional ischaemia is low. Brain tissue oxygen monitoring overcomes this deficiency and sheds new light on the pathophysiology of cerebral ischaemia following brain injury. Further studies are required to define ischaemic thresholds and their association with outcome. Extracellular brain pH has been recently linked to outcome and further studies are required to establish the role of pH regulation. Monitoring of brain metabolism using a cerebral microdialysis continues to develop its niche in clinical neuromonitoring, although it currently remains a research tool. Multimodality neuromonitoring plays an important role in managing patients with severe head injury. It helps guide treatment, provides prognostic information and explores the pathophysiology of evolving brain injury.

Extracellular Brain pH and Outcome following Severe Traumatic Brain Injury

The ability to measure brain tissue chemistry has led to valuable information regarding pathophysiological changes in patients with traumatic brain injury (TBI). Over the last few years, the focus has been on monitoring changes in brain tissue oxygen to determine thresholds of ischemia that affect outcome. However, the variability of this measurement suggests that it may not be a robust method. We have therefore investigated the relationship of brain tissue pH (pH(b)) and outcome in patients with TBI. We retrospectively analyzed prospectively collected data of 38 patients admitted to the Neurosciences Critical Care Unit with TBI between 1998 and 2003, and who had a multiparameter tissue gas sensor inserted into the brain. All patients were managed using an evidence-based protocol targeting CPP > 70 mm Hg. Physiological variables were averaged over 4 min and analyzed using a generalized least squares random effects model to determine the temporal profile of pH(b) and its association with outcome. Median (IQR) minimum pH(b) was 7.00 (6.89, 7.08), median (IQR) maximum pH(b) was 7.25 (7.18, 7.33), and median (IQR) patient averaged pH(b) was 7.13 (7.07, 7.17). pH(b) was significantly lower in those who did not survive their hospital stay compared to those that survived. In addition, those with unfavorable neurological outcome had lower pH(b) values than those with favorable neurological outcome. pH(b) differentiated between survivors and non-survivors. Measurement of pH(b) may be a useful indicator of outcome in patients with TBI.

Cooperation of peripheral and central chemosensitive mechanisms in the control of the extracellular pH in brain in non-respiratory acidosis.

The mathematical model of the respiratory control system in man of Middendorf and Loeschcke (1976 a, b) opens the possibility to stimulate the constellation of parameters in non-respiratory acidosis. Several investigators agree that the pH in CSF or in the extracellular fluid of the brain stays remarkably constant in this situation and it can be shown that this is a result of a precise control rather than the consequence of a sluggishly reacting system. Application of the model assuming constant extracellular brain pH allowed to calculate the relative sensitivities to pH changes of the central and the peripheral sensory mechanisms generating respiratory drive. Assuming air breathing and a normal critical arterial O2-pressure and otherwise normal parameters of respiration, circulation and blood composition (except diminished buffer base) the central chemosensitivity to a pH change turned out to be 25 times the peripheral. This factor is critically dependent on the ratio of the bicarbonate change in extracellular brain fluid to that in arterial blood. The coinciding data of Fencl (1971) and of Kronenberg and Cain (1968) were used for the calculation.