The role of arterial and venous pressure for volume regulation of an organ enclosed in a rigid compartment with application to the injured brain

• Published in: Acta anaesthesiologica Scandinavica 1999-05, Vol.43 (5), p.501-508
• Main Authors: Kongstad, L., Grände, P. O.
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Pressure - physiology; Brain - blood supply; Brain edema; Brain Injuries - cerebrospinal fluid; Brain Injuries - physiopathology; Capillaries - physiology; Cats; cerebral circulation; Cerebrospinal Fluid Pressure - physiology; Cerebrovascular Circulation - physiology; compartment syndrome; Electrolytes - metabolism; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Homeostasis - drug effects; intracranial pressure; Intracranial Pressure - physiology; Medical sciences; Muscle, Skeletal - blood supply; Muscle, Skeletal - physiology; Nervous system (semeiology, syndromes); Neurology; Papaverine - pharmacology; perfusion pressure; Permeability; Plethysmography, Impedance; Shock - physiopathology; skeletal muscle; Skull - physiology; tissue pressure; Vascular Resistance - physiology; Vasodilator Agents - pharmacology; venous pressure; Venous Pressure - physiology
• ISSN: 0001-5172; 1399-6576
• DOI: 10.1034/j.1399-6576.1999.430503.x

Background: Treatment of increased intracranial pressure often includes an active change in arterial and venous pressure, sometimes with draining of cerebrospinal fluid. We evaluated tissue and perfusion pressure during corresponding interventions in an organ enclosed in a rigid compartment with capillaries permeable for electrolytes and impaired autoregulation, conditions comparable to those present in the injured brain. Method: An isolated cat skeletal muscle enclosed in a closed fluid‐filled plethysmograph served as a model for the injured brain surrounded by cerebrospinal fluid and the cranium. Tissue pressure and blood flow were measured during variation in arterial and venous pressures and in intraplethysmographic fluid volume. Autoregulation was depressed by papaverine. Results: 1) Tissue pressure was not influenced by the venous pressure when this was below the tissue pressure, hereby generating venous collapse and a venous outflow resistance. When venous pressure was higher than the tissue pressure (no venous outflow resistance), these two parameters changed in parallel. 2) A change in arterial pressure induced a similar large change in tissue pressure at steady state, whereas blood flow remained unchanged. 3) Variation in tissue pressure induced by a change in the intraplethysmographic fluid volume was transient. Conclusions: If applicable to the injured brain, the results indicate that 1) a venous pressure change has a small influence on the intracranial pressure when a venous outflow resistance is present, 2) brain oedema can be reduced by lowering of the arterial inflow pressure, and blood flow will be maintained, 3) the decrease in intracranial pressure obtained by draining cerebrospinal fluid will be transient.