CBF) And Volume Research Articles

Toward absolute quantitation of bold functional MRI.

Blood-oxygenation level dependent (BOLD) image contrast in magnetic resonance imaging (MRI) has been widely used in the field of functional imaging to interpret changes in focal brain activity in response to stimuli. The BOLD image contrast relies on activation-induced changes in the magnetic properties of blood (Ogawa et al, 1990; 1993a; 1993b; Shulman et al., 1993; Kennan et al., 1994). The presence of paramagnetic deoxyhemoglobin in the microvasculature creates a magnetic susceptibility difference between the vessels and the surrounding tissue, thus producing a microscopic magnetic field gradient. The microscopic field gradients affect the value of R2* (i.e., apparent transverse relaxation rate of tissue water) which can be mapped by a gradient-echo MRI sequence. The equilibrium between deoxy- and oxyhemoglobin can be shifted by altering the blood oxygenation, and since deoxy- and oxyhemoglobin are para- and diamagnetic, respectively, BOLD image contrast can be created, whereby hemoglobin acts as an endogenous MRI contrast agent. A BOLD functional MRI sequence measures the changes in R2* upon activation. The quantitative change in R2* is determined by parameters which influence the microscopic field gradient such as the geometry of vessels, static magnetic field strength, and the concentration of deoxyhemoglobin within the vessels (Ogawa et al., 1993a; 1993b; Kennan et al., 1994). The concentration of deoxyhemoglobin or the local blood oxygenation fraction (Y) in the microvasculature is determined by the regional values of cerebral metabolic rates of oxygen consumption (CMRO2), cerebral blood flow (CBF), and volume (CBV) (Ogawa et al., 1993a; 1993b; Kennan et al., 1994). While geometry and morphology of microvessels are important for the basal BOLD image contrast at a particular magnetic field strength, it is only the change in concentration of deoxyhemoglobin, due to a short-lived and/or transient physiological perturbation, that is important for being able to quantitate the BOLD signal change for functional MRI (see Appendix).

Regulation of cerebral oxygen delivery.

Under normal conditions, it is generally accepted that for the adult mammalian cortex, almost all the energy required for cerebral ATP generation is supplied by oxidation of glucose through the tri-carboxylic acid cycle (Siesjo, 1978), and cerebral metabolic rates of oxygen and glucose use (i.e., CMRO2 and CMRglc, respectively) are regionally modified to fulfil metabolic needs through regulation of cerebral blood flow (CBF) and volume (CBV) (Roy and Sherrington, 1890). However, some positron emission tomography (PET) results have reported that during brain activation of awake humans CBF increases by a greater fraction than CMRO2 (Fox and Raichle, 1986; Fox et al., 1988). In the last few decades, ever since in vivo cortical measurements could be made of CBF and/or CMRO2, the mechanisms for the proportionality of changes between CBF and CMRO2 due to physiological perturbations have remained intangible, and the measured stoichiometries have varied reflecting a variety of experimental methods and/or conditions. However, regionally tight relationship between CMRO2 and CBF has been observed at rest with a ratio of about ~1:1 (Kety et al., 1947–8; Raichle et al., 1976).

Cortical spreading depression recorded from the human brain using a multiparametric monitoring system

The number of parameters (i.e., EEG or ICP-intracranial pressure) routinely monitored under clinical situations is limited. The brain function analyzer described in this paper enables simultaneous, continuous on-line monitoring of cerebral blood flow (CBF) and volume (CBV), intramitochondrial NADH redox state, extracellular K + concentrations, DC potential, electrocorticography and ICP from the cerebral cortex. Brain function of 14 patients with severe head injury (GCS ≤ 8), who were hospitalized in the neurosurgical or general intensive care unit was monitored using this analyzer. Leao cortical spreading depression (SD) has been reported in many experimental animals but not in the human cerebral cortex. In one of the patients monitored, spreading depression was observed. This is the first time that spontaneous repetitive cortical SD cycles have been recorded from the cerebral cortex of a patient suffering from severe head injury. Typical SD cycles appeared 4–5 h after the beginning of monitoring this patient. During the first 3–4 cycles the responses of this patient were very similar to the responses to SD recorded in normoxic experimental animals. Electrocorticography was depressed whereas extracellular K + levels increased. The metabolic response to spreading depression was characterized by oxidation of intramitochondrial NADH concomitant to a large increase in CBF. During brain death, an ischemic depolarization, characterized by decrease in CBF and an irreversible increase in extracellular K +, was recorded.

31 THE EFFECT OF AMINOPHYLLINE ON CEREBRAL, HADDYNAMICS ASSESSED BY NEAR INFRA-RED (NIR) SPECTROSCOPY

NIR spectroscopy was used to measure the effect of aminophylline on cerebral blood flow (CBF) and volume (CBV). Mean arterial BP, heart rate, transcutanenus (tc) pO2 and μO2 and intracerebral concentrations of oxyhaemoglobin (oxyHb), deoxyhaemoglobin, and cytochrome aa3 were continuously recorded (Hamamatsu Photonics KK, NIR1000). CBF was estimated using change in oxyHb concentration as a tracer (ret.1). Twenty CBF measurements wore made on 4 preterm infants (birthweight 739-893g. gestation 25 - 28w, age 3-18d) receiving a loading infusion of 6.2 mgs/kg aminophylline. CBF was unchanged in one infant and fell in 3. Median reduction of CBF was 23% (median 3.8 mls/100g/min, range 0 - 9.8). There was no consistent change in CBV. All infants showed a slight fall in tcpCO2 (median 0.2 KPa range 0.14 - 0.7) and a rise in mean BP (median 3mmHg, range 2 - 4). Aminophylline may have effects on CBF independent of CO2 mediated changes.