Regulation of Cerebral Blood Flow

Regulation of Cerebral Blood Flow

As in most other vascular areas of the body, cerebral blood flow is highly related to metabolism of the tissue. At least three metabolic factors have potent effects in con-trolling cerebral blood flow: (1) carbon dioxide concentration, (2) hydrogen ion con-centration, and (3) oxygen concentration.

Increase of Cerebral Blood Flow in Response to Excess Carbon Dioxide or Excess Hydrogen Ion Concentration. An increase in carbon dioxide concentration in the arterial blood per-fusing the brain greatly increases cerebral blood flow. This is demonstrated in Figure 61–1, which shows that a 70 per cent increase in arterial PCO2 approximately doubles cerebral blood flow.

        Carbon dioxide is believed to increase cerebral blood flow by combining first with water in the body fluids to form carbonic acid, with subsequent dissociation of this acid to form hydrogen ions. The hydrogen ions then cause vasodilation of the cere-bral vessels—the dilation being almost directly proportional to the increase in hydrogen ion concentration up to a blood flow limit of about twice normal.

        Any other substance that increases the acidity of the brain tissue, and therefore increases hydrogen ion concentration, will likewise increase cerebral blood flow. Such substances include lactic acid, pyruvic acid, and any other acidic material formed during the course of tissue metabolism.

Importance of Cerebral Blood Flow Control by Carbon Dioxide and Hydrogen Ions. Increasedhydrogen ion concentration greatly depresses neuronal activity. Therefore, it is for-tunate that an increase in hydrogen ion concentration also causes an increase in blood flow, which in turn carries hydrogen ions, carbon dioxide, and other acid-forming substances away from the brain tissues. Loss of carbon dioxide removes carbonic acid from the tissues; this, along with removal of other acids, reduces the hydrogen ion concentration back toward normal. Thus, this mechanism helps main-tain a constant hydrogen ion concentration in the cerebral fluids and thereby helps to maintain a normal, constant level of neuronal activity.

Oxygen Deficiency as a Regulator of Cerebral Blood Flow. Except during periods of intensebrain activity, the rate of utilization of oxygen by the brain tissue remains within narrow limits—almost exactly 3.5 (± 0.2) milliliters of oxygen per 100 grams of brain tissue per minute. 

If blood flow to the brain ever becomes insufficient to supply this needed amount of oxygen, the oxygen defi-ciency mechanism for causing vasodilation immediately causes vasodilation, returning the brain blood flow and transport of oxygen to the cerebral tissues to near normal. Thus, this local blood flow regulatory mecha-nism is almost exactly the same in the brain as in coro-nary blood vessels, in skeletal muscle, and in most other circulatory areas of the body.

Experiments have shown that a decrease in cerebral tissue PO2below about 30 mm Hg (normal value is 35 to40 mm Hg) immediately begins to increase cerebral blood flow. This is fortuitous because brain function becomes deranged at not much lower values of PO2, especially so at PO2 levels below 20 mm Hg. Even coma can result at these low levels. Thus, the oxygen mecha-nism for local regulation of cerebral blood flow is a very important protective response against diminished cere-bral neuronal activity and, therefore, against derange-ment of mental capability.

Measurement of Cerebral Blood Flow, and Effect of Brain Activ- ity on the Flow. A method has been developed to recordblood flow in as many as 256 isolated segments of the human cerebral cortex simultaneously. To do this, a radioactive substance, such as radioactive xenon, is injected into the carotid artery; then the radioactivity of each segment of the cortex is recorded as the radioac-tive substance passes through the brain tissue. For this purpose, 256 small radioactive scintillation detectors are pressed against the surface of the cortex. The rapidity of rise and decay of radioactivity in each tissue segment is a direct measure of the rate of blood flow through that segment.

Using this technique, it has become clear that blood flow in each individual segment of the brain changes as much as 100 to 150 per cent within seconds in response to changes in local neuronal activity. For instance, simply making a fist of the hand causes an immedi-ate increase in blood flow in the motor cortex of the opposite side of the brain. Reading a book increases the blood flow, especially in the visual areas of the occipital cortex and in the language perception areas of the tem-poral cortex. This measuring procedure can also be used for localizing the origin of epileptic attacks because local brain blood flow increases acutely and markedly at the focal point of each attack.

Demonstrating the effect of local neuronal activity on cerebral blood flow, Figure 61–2 shows a typical increase in occipital blood flow recorded in a cat’s brain when intense light is shined into its eyes for one-half minute.

Autoregulation of Cerebral Blood Flow When the Arterial Pressure Changes. Cerebral blood flow is “autoregulated”extremely well between arterial pressure limits of 60 and 140 mm Hg. That is, mean arterial pressure can be decreased acutely to as low as 60 mm Hg or increased to as high as 140 mm Hg without significant change in cerebral blood flow. And, in people who have hyper-tension, autoregulation of cerebral blood flow occurs even when the mean arterial pressure rises to as high as 160 to 180 mm Hg. This is demonstrated in Figure 61–3, which shows cerebral blood flow measured both in persons with normal blood pressure and in hypertensive and hypotensive patients. Note the extreme constancy of cerebral blood flow between the limits of 60 and 180 mm Hg mean arterial pressure. But, if the arterial pressure falls below 60 mm Hg, cerebral blood flow then does become severely decreased.

Role of the Sympathetic Nervous System in Controlling Cerebral Blood Flow. The cerebral circulatory system has strongsympathetic innervation that passes upward from the superior cervical sympathetic ganglia in the neck and then into the brain along with the cerebral arteries. This innervation supplies both the large brain arteries and the arteries that penetrate into the substance of the brain. However, transection of the sympathetic nerves or mild to moderate stimulation of them usually causes very little change in cerebral blood flow because the blood flow autoregulation mechanism can override the nervous effects.

When mean arterial pressure rises acutely to an exceptionally high level, such as during strenuous exercise or during other states of excessive circulatory activity, the sympathetic nervous system normally con-stricts the large- and intermediate-sized brain arteries enough to prevent the high pressure from reaching the smaller brain blood vessels. This is important in pre-venting vascular hemorrhages into the brain—that is, for preventing the occurrence of “cerebral stroke.”