Cerebral acid-base and gas metabolism in brain injury

1970 ◽  
Vol 33 (5) ◽  
pp. 498-505 ◽  
Author(s):  
R. Zupping
Keyword(s):  
Metabolic Acidosis ◽  
Brain Injury ◽  
Brain Damage ◽  
Close Correlation ◽  
Respiratory Alkalosis ◽  
Acid Base ◽  
Content Type ◽  
Arterial Blood ◽  
Gas Metabolism ◽  
Permanent Brain Damage

✓ Acid-base and gas parameters of CSF, jugular venous and arterial blood were measured in 45 patients with brain injury in the first 12 days after trauma or operation. CSF metabolic acidosis together with respiratory alkalosis and hypoxemia in the cerebral venous and arterial blood were the most characteristic findings. A close correlation between the severity of brain damage and the intensity of the CSF metabolic acidosis and arterial hypocapnia was revealed. It was concluded that brain hypoxia and acidosis play an important role in the development of cerebral edema and permanent brain damage.

Studies on the Pathophysiology of Encephalopathy in Reye's Syndrome: Hyperammonemia in Reye's Syndrome

PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 999-1004
Author(s):  
Daniel C. Shannon ◽  
Robert De Long ◽  
Barry Bercu ◽  
Thomas Glick ◽  
John T. Herrin ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Venous Drainage ◽  
Respiratory Alkalosis ◽  
Ammonia Concentration ◽  
Reye's Syndrome ◽  
Acid Base ◽  
Arterial Blood ◽  
Cerebral Venous Drainage ◽  
Acid Base Status ◽  
The Brain

The initial acid-base status of eight survivors of Reye's syndrome was characterized by acute respiratory alkalosis (Pco2=32 mm Hg; Hco3-= 22.0 mEq/liter) while that of eight children who died was associated with metabolic acidosis as well (HCO3-=10.0 mEq/liter). Arterialinternal jugular venous ammonia concentration differences on day 1 (299 mg/100 ml) and day 2 (90 mg/ 100 ml) reflected cerebral uptake of ammonia while those on days 3 and 4 (-43 and -55 mg/100 ml) demonstrated cerebral release. Arterial blood hyperammonemia can be detoxified safely in the brain as long as the levels do not exceed approximately 300µg/100 ml. Beyond that level lactic acidosis is observed, particularly in cerebral venous drainage. Arterial blood hyperammonemia was also related to the extent of alveolar hyperventilation. These findings are very similar to those seen in experimental hyperammonemia and support the concept that neurotoxicity in children with Reye's syndrome is at least partly due to impaired oxidative metabolism secondary to hyperammonemia.

Acid-base balance and arterial and CSF lactate levels following human head injury

1974 ◽  
Vol 40 (5) ◽  
pp. 617-625 ◽  
Author(s):  
Lionel R. King ◽  
Robert L. McLaurin ◽  
Harvey C. Knowles
Keyword(s):  
Metabolic Acidosis ◽  
Head Injury ◽  
Human Head ◽  
Respiratory Alkalosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Content Type ◽  
Base Balance ◽  
Csf Lactate ◽  
Lactate Levels

✓ Sequential arterial and cerebrospinal fluid (CSF) lactate, pH, pCO2, HCO3−, and pO2 levels were determined for 4 days in 17 patients immediately following uncomplicated head injury. Lactate was initially markedly elevated in both fluids and decreased by the third day after injury. There was mild arterial metabolic acidosis and respiratory alkalosis on admission; the alkalosis continued. Arterial pO2 was below normal at all times. The CSF showed a normal pO2, and metabolic acidosis related to lactate accumulation. Blood and CSF pCO2 and HCO3− levels equilibrated well, probably because of the time factor; CSF and arterial pO2 levels were not significantly related. The clinical implications of CSF lacticacidosis after head injury are discussed.

Arterial blood acid-base regulation during exercise in rats

1984 ◽  
Vol 57 (2) ◽  
pp. 396-402 ◽  
Author(s):  
R. F. Fregosi ◽  
J. A. Dempsey
Keyword(s):  
Metabolic Acidosis ◽  
Lactate Concentration ◽  
Blood Gases ◽  
Fold Increase ◽  
Respiratory Alkalosis ◽  
Male Rats ◽  
Co2 Production ◽  
Acid Base ◽  
Arterial Blood ◽  
Exercise Induced

For the first time in the rat, we described the effects of exercise on arterial acid-base status and examined the role of chemical stimuli as determinants of the hyperventilatory response in this species. O2 consumption (VO2), CO2 production (VCO2), arterial blood gases, arterial lactate concentration ([LA-]a), and rectal temperature (Tre) were measured in non-trained male rats at rest and during 10 min of treadmill exercise at various intensities. During mild exercise (2.5-fold increase in VCO2), PaCO2 fell 5.5 +/- 0.6 Torr, and despite a small but significant increase in [LA-]a, respiratory alkalosis prevailed [change in arterial pH (delta pHa) = 0.034 +/- 0.006]. Arterial PO2 (PaO2) increased 4.1 +/- 1.5 Torr and Tre increased 0.6 +/- 0.1 degrees C. A progressive hyperventilation occurred from mild to heavy exercise. This response was not attributable to arterial hypoxemia or acidosis and it was not affected by preventing the exercise-induced increase in body temperature. During maximal exercise, VO2 increased 3.4-fold (72 +/- 1.50 ml X kg-1 X min-1) and VCO2 increased 4.5-fold (74 +/- 1.90 ml X kg-1 X min-1), resulting in a 9-fold increase in [LA-]a and a severe metabolic acidosis (pHa 7.31 +/- 0.02). A marked hyperventilation [arterial PCO2 (PaCO2) 28.5 +/- 1.4 Torr] resulted in partial compensation of pHa, but almost all of this hyperventilation occurred before the onset of metabolic acidosis, [i.e., at less than 65% maximum VO2 (VO2max)], and the increased [H+]a with further elevations in VO2 produced no further hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral metabolism in patients with intracranial tumors

1972 ◽  
Vol 36 (4) ◽  
pp. 451-462 ◽  
Author(s):  
Rein Zupping
Keyword(s):  
Metabolic Acidosis ◽  
Cerebral Metabolism ◽  
Brain Lesion ◽  
Clinical Signs ◽  
Sodium Concentration ◽  
Respiratory Alkalosis ◽  
Intracranial Tumors ◽  
Acid Base ◽  
Content Type ◽  
Close Relationship

✓ In a series of 64 patients with various intracranial tumors the cerebrospinal fluid (CSF), arterial and jugular venous acid-base, gas, and electrolyte values were measured before surgery and during the first 8 postoperative days. Before operation, patients without clinical signs of increased intracranial pressure had almost normal CSF acid-base status and cerebral gas exchange. The patients with signs of intracranial hypertension had CSF metabolic acidosis, arterial and jugular venous respiratory alkalosis, and mild arterial and jugular hypoxemia. Following surgery a remarkable increase in CSF metabolic acidosis, arterial and jugular hypocapnia, and hypoxemia occurred. A slight decrease of CSF potassium concentration was also revealed but the CSF sodium concentration was found to be elevated only in fatal cases or in patients with impaired consciousness. A close relationship was found between the severity of brain damage and the degree of CSF metabolic acidosis and arterial hypocapnia. Cerebral venous hypoxemia was not related to the severity of the brain lesion. It is suggested that cerebral acidosis may contribute to the development of brain edema and pulmonary hyperventilation in patients with intracranial tumors.

ERRATA

PEDIATRICS ◽  
1980 ◽  
Vol 65 (5) ◽  
pp. 1006-1006
Keyword(s):  
Metabolic Acidosis ◽  
Diagnostic Approach ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
P 351 ◽  
Normal Acid

In the article "A Diagnostic Approach to Metabolic Acidosis in Children" by Kappy and Morrow (Pediatrics 65:351-356, 1980) on p 351 under "Normal Acid-Base Physiology" the normal arterial blood pH is maintained at 7.40 (H+ = 39.8 nEq/liter not mEq/liter.

Stability of cerebrospinal fluid pH in chronic acid-base disturbances in blood

1965 ◽  
Vol 20 (3) ◽  
pp. 443-452 ◽  
Author(s):  
R. A. Mitchell ◽  
C. T. Carman ◽  
J. W. Severinghaus ◽  
B. W. Richardson ◽  
M. M. Singer ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Active Transport ◽  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Respiratory Alkalosis ◽  
Regulation Of Respiration ◽  
Respiratory Drive ◽  
Acid Base ◽  
Peripheral Chemoreceptors ◽  
Mean Values

In chronic acid-base disturbances, CSF pH was generally within the normal limits (7.30–7.36 units, being the range including two standard deviations of 12 normal subjects). The mean values of CSF and arterial pHH, respectively, were: 1) metabolic alkalosis, 7.337 and 7.523; 2) metabolic acidosis, 7.315 and 7.350; 3) respiratory alkalosis, 7.336 and 7.485; and 4) respiratory acidosis (untreated), 7.314 and 7.382. Other investigators report similar values. The constancy of CSF pH cannot be explained by a poorly permeable blood-CSF barrier in chronic metabolic acidosis and alkalosis, nor can it be explained by respiratory compensation. It cannot be explained by renal compensation in respiratory alkalosis (high altitude for 8 days), although it may be explained by renal compensation in respiratory acidosis. The former three states suggest that active transport regulation of CSF pH is a function of the blood-CSF barrier. Since CSF pH is constant, so also must that portion of the respiratory drive originating in the superficial medullary respiratory chemoreceptors be constant. Ventilation changes in chronic acid-base disturbances thus may result from changes in the activity of peripheral chemoreceptors, in response to changes in arterial pH, arterial PO2, and possibly in neuromuscular receptors. regulation of respiration; medullary respiratory; chemoreceptors; peripheral chemoreceptors; metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; active transport; blood-brain barrier; pregnancy Submitted on July 27, 1964

Changes in brain surface pH during acute isocapnic metabolic acidosis and alkalosis

1981 ◽  
Vol 51 (2) ◽  
pp. 276-281 ◽  
Author(s):  
S. Javaheri ◽  
A. Clendening ◽  
N. Papadakis ◽  
J. S. Brody
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Surface Ph ◽  
Brain Surface ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean ◽  
The Brain

It has been thought that the blood-brain barrier is relatively impermeable to changes in arterial blood H+ and OH- concentrations. We have measured the brain surface pH during 30 min of isocapnic metabolic acidosis or alkalosis induced by intravenous infusion of 0.2 N HCl or NaOH in anesthetized dogs. The mean brain surface pH fell significantly by 0.06 and rose by 0.04 pH units during HCl or NaOH infusion, respectively. Respective changes were also observed in the calculated cerebral interstitial fluid [HCO-3]. There were no significant changes in cisternal cerebrospinal fluid acid-base variables. It is concluded that changes in arterial blood H+ and OH- concentrations are reflected in brain surface pH relatively quickly. Such changes may contribute to acute respiratory adaptations in metabolic acidosis and alkalosis.

Platelet-activating factor and progressive brain damage following focal brain injury

1990 ◽  
Vol 73 (2) ◽  
pp. 223-233 ◽  
Author(s):  
Kai U. Frerichs ◽  
Perttu J. Lindsberg ◽  
John M. Hallenbeck ◽  
Giora Z. Feuerstein
Keyword(s):  
Brain Injury ◽  
Brain Damage ◽  
Neuronal Death ◽  
Hippocampal Neurons ◽  
Neuronal Damage ◽  
Platelet Activating Factor ◽  
Secondary Brain Damage ◽  
Content Type ◽  
Focal Brain Injury ◽  
Fine Print

✓ The effects of a platelet-activating factor (PAF) antagonist on brain edema, cortical microcirculation, blood-brain barrier (BBB) disruption, and neuronal death following focal brain injury are reported. A neodymium:yttrium-aluminum-garnet (Nd:YAG) laser was used to induce highly reproducible focal cortical lesions in anesthetized rats. Secondary brain damage in this model was characterized by progressive cortical hypoperfusion, edema, and BBB disruption in the vicinity of the hemispheroid lesion occurring acutely after injury. The histopathological evolution was followed for up to 4 days. Neuronal damage in the cortex and the hippocampus (CA-1) was assessed quantitatively, revealing secondary and progressive loss of neuronal tissue within the first 24 hours following injury. Pretreatment with the PAF antagonist BN 50739 ameliorated the severe hypoperfusion in 12 rats (increasing local cerebral blood flow from a mean ± standard error of the mean of 40.5% ± 8.3% to 80.2% ± 7.8%, p < 0.01) and reduced edema by 70% in 10 rats (p < 0.05) acutely after injury. The PAF antagonist also reduced the progression of neuronal damage in the cortex and the CA-1 hippocampal neurons (decrease of neuronal death from 88.0% ± 3.9% to 49.8% ± 4.2% at 24 hours in the cortex and from 40.2 ± 5.0% to 13.2% ± 2.1% in the hippocampus in 30 rats; p < 0.05). This study provides evidence to support progressive brain damage following focal brain injury, associated with secondary loss of neuronal cells. In this latter process, PAF antagonists may provide significant therapeutic protection in arresting secondary brain damage following cerebral ischemia and neurological trauma.

Effects of fluid-percussion brain injury on regional cerebral blood flow and pial arteriolar diameter

1986 ◽  
Vol 64 (5) ◽  
pp. 787-794 ◽  
Author(s):  
Douglas S. DeWitt ◽  
Larry W. Jenkins ◽  
Enoch P. Wei ◽  
Harry Lutz ◽  
Donald P. Becker ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Pial Arterioles ◽  
High Level ◽  
Arteriolar Diameter

✓ The effects of two levels of fluid-percussion brain injury on cerebral blood flow (CBF) and pial arteriolar diameter were investigated in cats. Regional CBF was measured using the radioactive microsphere technique. Experimental brain injury resulted in changes in arterial blood pressure, CBF, and pial arteriolar diameter that were related to the severity of the injury. Low-level injury (1.88 ± 0.11 atm, mean ± standard error of the mean) resulted in a slight transient increase in CBF which had returned to preinjury levels by 30 minutes. High-level injury (2.68 ± 0.19 atm) resulted in larger, statistically significant (p < 0.01) increases in whole-brain CBF, decreases in cerebrovascular resistance, and increases in pial arteriolar diameter 1 minute postinjury. One hour after injury, CBF had returned to preinjury levels while cerebral perfusion pressure was significantly (p < 0.01) reduced. There was no evidence of reduced CBF in any region studied. Pial arterioles dilated during the posttraumatic hypertensive period and then returned to control diameters within 1 hour after injury. Changes in the diameter of pial arterioles were significantly correlated with posttraumatic changes in CBF.

Hyperoxia of cerebral venous blood and cisternal cerebrospinal fluid following arterial air embolism

1972 ◽  
Vol 37 (1) ◽  
pp. 30-35 ◽  
Author(s):  
Norval M. Simms ◽  
Don M. Long ◽  
James H. Matthews ◽  
Shelley N. Chou
Keyword(s):  
Cerebrospinal Fluid ◽  
Oxygen Tension ◽  
Venous Blood ◽  
Air Embolism ◽  
Carbon Dioxide Tension ◽  
Acid Base ◽  
Content Type ◽  
Arterial Blood ◽  
Base Parameters ◽  
The Right

✓ Oxygen tension and acid-base parameters of cerebral venous blood and cisternal cerebrospinal fluid, as well of femoral arterial blood, were studied in 14 dogs following injection of varying amounts of room air into the right vertebral artery. Acute elevations in oxygen tension were demonstrated in both cerebral venous blood and CSF, whereas hypoxemia occurred concomitantly in systemic arterial blood. Post-embolic increases in carbon dioxide tension with reciprocal diminutions in pH were evident in all sampling sites. The pathophysiological bases for these air-induced alterations are discussed.

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