SESSION IV
OXYGEN TRANSPORT AND ORGAN FUNCTION
Outline
Chapter 49: TISSUE OXYGENATION AND TISSUE METABOLISM IN THE BRAIN CORTEX DURING PRONOUNCED ARTERIAL HYPOCAPNIA
Chapter 50: CONTROL MECHANISMS INVOLVED IN THE REGULATION OF CEREBRAL TISSUE PRESSURE IN OXYGEN
Chapter 51: TISSUE OXYGENATION AND NORMAL AND HYPERTHERMIC CONDITIONS
Chapter 52: NAD-NADH AND VASCULAR VOLUME OSCILLATIONS IN THE CAT BRAIN CORTEX
Chapter 53: RESISTANCE TO BLOOD FLOW IN DENERVATED CANINE HINDLIMB DURING HYPOXIA
Chapter 54: OXYGEN CONSUMPTION BY DRONE PHOTORECEPTORS IN DARKNESS AND DURING REPETITIVE STIMULATION WITH LIGHT FLASHES
Chapter 55: THE DISTRIBUTION OF RBC VELOCITY IN CAPILLARIES OF RESTING SKELETAL MUSCLE
Chapter 56: REACTIVITY AND REGENERABILITY OF THE CARDIO-PULMONARY SYSTEM. THE ARTERIAL pO2 AS A DIAGNOSTIC PARAMETER
Chapter 57: PHYSIOLOGIC ADAPTION OF MYOCARDIAL CONTRACTILE STRENGTH AS DETERMINED BY DIRECT CHANGES IN MYOCARDIAL METABOLISM INDEPENDENT OF HEMODYNAMIC LOADING
Chapter 58: OXYGEN TENSION IN RELATION TO ENERGY METABOLISM IN EXERCISING HUMAN SKELETAL MUSCLE
Chapter 59: OPPOSITE CHANGES IN THE REDOX STATE OF THE BRAIN CORTEX DEPENDING ON THE LENGTH AND STRENGTH OF DIRECT CORTICAL STIMULATION
Chapter 60: OXYGEN SUPPLY OF THE BRAIN CORTEX (RAT) DURING SEVERE HYPOGLYCEMIA
Chapter 61: SKELETAL MUSCLE SURFACE OXYGEN PRESSURE FIELDS IN HUMANS
Chapter 62: TISSUE pH-DISTRIBUTION WITHIN MALIGNANT TUMORS AS MEASURED WITH ANTIMONY MICROELECTRODES
Chapter 63: INTRA-AMNIOTIC INJECTION OF AN OXYGEN CARRIER (PERFLUOROTRIBUTYLAMINE) DURING THE LAST STAGES OF THE RAT FETAL DEVELOPMENT
Chapter 64: EFFECT OF CALCIUM AND NICKEL IONS ON GLYCOLYTIC AND OXIDATIVE METABOLISM AND CONTRACTILITY OF THE RAT UTERUS
Chapter 65: BLOOD O2 DISSOCIATION CURVE AND O2 TRANSPORT TO THE ISOLATED AND PERFUSED TURTLE HEART
Chapter 66: MICROCIRCULATION AND OXYGEN AVAILABILITY IN THE BRAIN CORTEX AT DEPRESSED ELECTRICAL ACTIVITY
Chapter 67: METABOLIC STEADY STATES IN THE UTERUS
Chapter 68: EFFECT OF OXYGEN ON HISTOTOXIC HYPOXIA CAUSED BY CYANIDE
Chapter 69: THE EFFECT OF ACETAZOLAMIDE ON BRAIN O2 METABOLISM
Chapter 70: THE INFLUENCE OF TRAUMATIC TOXAEMIA ON THE CORTICOSTEROID LEVEL AND ON THE ACTIVITY OF MITOCHONDRIAL ENZYMES
Chapter 71: DISCUSSION AND SUMMARY SESSION IV OXYGEN TRANSPORT AND ORGAN FUNCTION
TISSUE OXYGENATION AND TISSUE METABOLISM IN THE BRAIN CORTEX DURING PRONOUNCED ARTERIAL HYPOCAPNIA
J. Grote, R. Schubert and K. Zimmer, Department of Applied Physiology and Department of Neurosurgery, University of Mainz, 65 Mainz, FRG
Publisher Summary
This chapter describes the tissue oxygenation and tissue metabolism in the brain cortex during pronounced arterial hypocapnia. Acute arterial hypocapnia induced by hyperventilation leads to typical reactions in the circulation and the metabolism of the brain tissue. With a lowering of arterial CO2 tension, the cerebro-vascular resistance (CVR) increases resulting in a decrease of cerebral blood flow. The changes in CVR are a consequence of decreasing hydrogen ion and potassium ion concentrations in the perivascular space of the brain arterioles. The corresponding changes in the brain metabolism are characterized by elevated concentrations of lactate and pyruvate and an increase in the lactate/pyruvate ratio as well as an increase in the NADH level and in the NADH/NAD+ ratio in the brain tissue. The effects of arterial hypocapnia on the nerve cell metabolism and electrical activity can be attributed to the decrease in tissue PCO2. In addition, there is evidence that these changes are in part a result of insufficient blood flow because of cerebral vasoconstriction occurring during hyperventilation. Previous measurements of mean tissue PO2 and metabolites suggest that arterial hypocapnia may lead to ischemic hypoxia in small dispersed areas of the brain tissue. The decrease of PaCO2 to 2.5 kPa produced a rapid reduction of cortical blood flow. At the same time, because of the blood flow changes and in minor part to the displacement of the blood O2 dissociation curve to the left, the PO2 histograms of the cortical tissue shifted to lower values.
Acute arterial hypocapnia induced by hyperventilation leads to typical reactions in the circulation and the metabolism of the brain tissue. With a lowering of arterial CO2 tension the cerebro-vascular resistance (CVR) increases resulting in a decrease of cerebral blood flow (CBF). The Changes in CVR are a consequence of decreasing hydrogen ion and potassium ion concentrations in the perivascular space of the brain arterioles (see reviews by: Betz, 1972; Edvinsson and MacKenzie, 1977; Kuschinsky and Wahl, 1978). The corresponding changes in the brain metabolism are characterized by elevated concentrations of lactate and pyruvate and an increase in the lactate/pyruvate ratio, as well as an increase in the NADH level and in the NADH/NAD+ ratio in the brain tissue (Leusen and Demeester, 1966; Plum and Posner, 1967; Hohorst et al., 1968; Granholm and Siesjö, 1969, 1971; Granholm et al., 1969; Betz, 1972; Rubio et al., 1975).
Additionally, with the changes in CBF and brain metabolism high voltage slow waves in the EEG are observed (e. g. Meyer and Gotoh, 1960; Alexander et al., 1965).
The effects of arterial hypocapnia on the nerve cell metabolism and electrical activity can be attributed to the decrease in tissue PCO2,(s. Granholm and Siesjö, 1969). In addition, there is evidence that these changes are in part a result of insufficient blood flow due to cerebral vasoconstriction occuring during hyperventilation. Previous measurements of mean tissue PO2 and metabolites suggest that arterial hypocapnia may lead to ischemic hypoxia in small dispersed areas of the brain tissue (Meyer and Gotoh, 1960; Alexander et al., 1965; Hohorst et al., 1968; Granholm and Siesjö, 1969, 1971; Pickeroth, 1971; Betz, 1972; Rubio et al., 1975). It was assumed that the increase of the lactate/pyruvate ratio and the NADH/NAD+ ratio may reflect the insufficient oxygen supply state of the brain cortex. However, since at the same time the tissue concentrations of PCr and ATP were found to be normal, this assumption could not be made with certainty. In order to insure that tissue hypoxia at very low PaCO2 is present, a determination of the brain tissue oxygen tension distribution or the demonstration of depleted tissue stores of energy-rich phosphates is necessary. The present experiments were designed to study the influence of a pronounced arterial hypocapnia on regional blood flow, tissue PO2 distribution and tissue metabolism in the brain cortex of cats.
METHODS
Thirteen cats of both sexes, weighing 2.8 to 4.5 kg, were premedicated with Ketanest (10 − 20 mg•kg−1) and anaesthetized with sodium pentobarbital (Nembutal; 25 mg-kg−1 i. v.). The tracheotomized animals after immobilization with Imbetril (1.6 − 2.0 mg initially and during the experiments 0.2 − 0.3 mg every 30 min) were ventilated with a Starling type respirator. At the beginning of each experiment the output from the respiratory pump was adjusted to produce arterial normoxia and normocapnia during which the control values for regional cortical blood flow and tissue PO2 were determined. After completion of the initial measurements the animals were hyperventilated to reach constant arterial CO2 tensions of about 2.7 kPa (20 mmHg) and 1.6 kPa (12 mmHg) at normal arterial oxygen tension. Both hypocapnia levels were maintained for 45 − 60 min. In order to ass...