A quantitative analysis of the contributions of the cranial and spinal compartments to the cerebrospinal fluid pressure‐volume curve was made using dogs. The curve was determined by rapid continuous injection of fluid into the cisterna magna with simultaneous measurement of the pressure. Spinal block at the C 1 level was produced by inflation of an epidural rubber balloon allowing the recording of the pressure‐volume curve for the isolated cranial system. By subtraction of the two curves obtained, the spinal pressure‐volume curve could be calculated. 70 % of the variation in volume within the system was related to the spinal section and 30 % to the cranial section. The intracranial curve represents the effects on the fluid pressure of forced alterations in the volume of the intracranial vascular bed. The spinal compartment has a quantitatively defined and probably mechanically important function as an expansion vessel for the intracranial system.
The effects of repeated subarachnoid hemorrhages have been investigated experimentally in dogs. The main objectives were to determine the tolerance to repeated hemorrhage and to study the changes occurring during the repeated bleeds, in intracranial pressure, EEG, ECG, systemic arterial pressure and respiration. The natural course of an intracranial hemorrhage was simulated by shunting blood from a femoral artery through a drop recorder into five different sites in the craniospinal system: the chiasmatic cistern, a lateral ventricle, the cisterna magna, the lumbar subarachnoid space and into the cerebral tissue of the left frontal lobe. The hemorrhage was allowed to continue until it stopped spontaneously. Each bleed resulted in a transient rise in intracranial pressure to the level of the arterial pressure, followed by a return to a steady state value. The time taken for the attainment of the steady state was increasingly prolonged. The final steady state pressure increased with each bleed. Ultimately, a stage was reached where the hemorrhage resulted in a sustained high pressure at the level of the arterial blood pressure, producing failure of vital functions and an irreversibly isoelectric electroencephalogram. The average number of bleeds necessary to produce this state in the case of hemorrhage into brain parenchyma was 3 (range 2-4), into the lateral ventricle, 4 range 3-5), and into the cisterna chiasmatica, 5 (range 2-7). After 5 hemorrhages into the cisterna magna and the spinal subarachnoid space, a local resistance at the bleeding site was built up which prevented further bleeding.
Siesjö, B. K. and N. N. Zwetnow. The effect of hypovolemic hypotension on extra‐and intracellular acid‐base parameters and energy metabolites in the rat brain. Acta physiol. scand. 1970. 79. 114–124. The influence of hypovolemic decreases in the mean arterial pressure upon intra‐ and extracellular acid‐base parameters in the brain, and upon tissue concentrations of ATP, ADP, AMP and phosphocreatine, was studied in immobilized and artificially ventilated rats. Hypotensive periods of 20 or 60 min duration did not lead to any significant changes in ATP, ADP, AMP or phosphocreatine concentrations until the mean arterial pressure was below 40 mm Hg, but there was a small gradual increase in tissue lactate concentration, and in the lactate/pyruvate ratio, even at a moderate decrease in blood pressure. The lactate and pyruvate changes were significant even after corrections for blood and CSF lactate and pyruvate contents, and similar changes were seen in the CSF. The moderate changes in extra‐ and intracellular lactate concentrations did not lead to any noticeable decreases in calculated extra‐ and intracellular pH values since even moderate reductions in blood pressure usually led to small concomitant falls in the tissue CO2 tension. Thus, if it can be assumed that the cerebral blood flow was upheld at the moderately reduced perfusion pressures, the results strongly speak against the possibility that the decrease in cerebrovascular resistance, which occurs during autoregulation of flow in hypovolemic hypotension, is related to extracellular pH changes.
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