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Cerebral blood flow (CBF) is the blood supply to the brain in a given period of time. [8] In an adult, CBF is typically 750 millilitres per minute or 15.8 ± 5.7% of the cardiac output. [9] This equates to an average perfusion of 50 to 54 millilitres of blood per 100 grams of brain tissue per minute. [10] [11] [12]
The dopamine neurons of the dopaminergic pathways synthesize and release the neurotransmitter dopamine. [2] [3] Enzymes tyrosine hydroxylase and dopa decarboxylase are required for dopamine synthesis. [4] These enzymes are both produced in the cell bodies of dopamine neurons. Dopamine is stored in the cytoplasm and vesicles in axon terminals.
By means of cerebral autoregulation, the body is able to deliver sufficient blood containing oxygen and nutrients to the brain tissue for this metabolic need, and remove CO 2 and other waste products. Cerebral autoregulation refers to the physiological mechanisms that maintain blood flow at an appropriate level during changes in blood pressure ...
An increase in pressure, most commonly due to head injury leading to intracranial hematoma or cerebral edema, can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause brain herniation, and restrict blood supply to the brain. [13] It is a cause of reflex bradycardia. [14]
The blood–brain barrier is formed by the brain capillary endothelium and excludes from the brain 100% of large-molecule neurotherapeutics and more than 98% of all small-molecule drugs. [28] Overcoming the difficulty of delivering therapeutic agents to specific regions of the brain presents a major challenge to treatment of most brain disorders.
Cerebral perfusion pressure, or CPP, is the net pressure gradient causing cerebral blood flow to the brain (brain perfusion).It must be maintained within narrow limits because too little pressure could cause brain tissue to become ischemic (having inadequate blood flow), and too much could raise intracranial pressure (ICP).
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The food entering the gastrointestinal tract triggers the release of these hormones, which act on the brain to produce satiety. The brain contains both CCK-A and CCK-B receptors. Glucostatic hypothesis: The activity of the satiety center in the ventromedial nuclei is probably governed by the glucose utilization in the neurons.