baroreceptor fibers, pass through Hering's nerves and the vagus nerves into the vasomotor center of the brain stem.
Each carotid or aortic body is supplied with an abundant blood flow through a small nutrient artery, so that the chemoreceptors are always in close contact with arterial blood. Whenever the arterial pressure falls below a critical level, the chemoreceptors become stimulated because diminished blood flow causes decreased oxygen as well as excess buildup of carbon dioxide and hydrogen ions that are not removed by the slowly flowing blood.
The signals transmitted from the chemoreceptors excite the vasomotor center, and this elevates the arterial pressure back toward normal. However, this chemo-receptor reflex is not a powerful arterial pressure controller until the arterial pressure falls below 80 mm Hg. Therefore, it is at the lower pressures that this reflex becomes important to help prevent still further fall in pressure.
The chemoreceptors are discussed in much more detail in Chapter 41 in relation to respiratory control, in which they play a far more important role than in pressure control.
Atrial and Pulmonary Artery Reflexes That Help Regulate Arterial Pressure and Other Circulatory Factors. Both the atria and the pulmonary arteries have in their walls stretch receptors called low-pressure receptors. They are similar to the baroreceptor stretch receptors of the large systemic arteries. These low-pressure receptors play an important role, especially in minimizing arterial pressure changes in response to changes in blood volume. To give an example, if 300 milliliters of blood suddenly are infused into a dog with allreceptors intact, the arterial pressure rises only about 15 mm Hg. With the arterial barorecep-tors denervated, the pressure rises about 40 mm Hg. If the low-pressure receptors also are denervated, the pressure rises about 100 mm Hg.
Thus, one can see that even though the low-pressure receptors in the pulmonary artery and in the atria cannot detect the systemic arterial pressure, they do detect simultaneous increases in pressure in the low-pressure areas of the circulation caused by increase in volume, and they elicit reflexes parallel to the barore-ceptor reflexes to make the total reflex system more potent for control of arterial pressure.
Atrial Reflexes That Activate the Kidneys—The "Volume Reflex."
Stretch of the atria also causes significant reflex dilation of the afferent arterioles in the kidneys. And still other signals are transmitted simultaneously from the atria to the hypothalamus to decrease secretion of antidiuretic hormone. The decreased afferent arteriolar resistance in the kidneys causes the glomerular capillary pressure to rise, with resultant increase in filtration of fluid into the kidney tubules. The diminution of antidi-uretic hormone diminishes the reabsorption of water from the tubules. Combination of these two effects— increase in glomerular filtration and decrease in reabsorption of the fluid—increases fluid loss by the kidneys and reduces an increased blood volume back toward normal. (We will also see in Chapter 19 that atrial stretch caused by increased blood volume also elicits a hormonal effect on the kidneys—release of atrial natri-uretic peptide that adds still further to the excretion of fluid in the urine and return of blood volume toward normal.)
All these mechanisms that tend to return the blood volume back toward normal after a volume overload act indirectly as pressure controllers as well as blood volume controllers because excess volume drives the heart to greater cardiac output and leads, therefore, to greater arterial pressure. This volume reflex mechanism is discussed again in Chapter 29, along with other mechanisms of blood volume control.
Atrial Reflex Control of Heart Rate (the Bainbridge Reflex). An increase in atrial pressure also causes an increase in heart rate, sometimes increasing the heart rate as much as 75 per cent. A small part of this increase is caused by a direct effect of the increased atrial volume to stretch the sinus node: it was pointed out in Chapter 10 that such direct stretch can increase the heart rate as much as 15 per cent. An additional 40 to 60 per cent increase in rate is caused by a nervous reflex called the Bainbridge reflex. The stretch receptors of the atria that elicit the Bainbridge reflex transmit their afferent signals through the vagus nerves to the medulla of the brain. Then efferent signals are transmitted back through vagal and sympathetic nerves to increase heart rate and strength of heart contraction. Thus, this reflex helps prevent damming of blood in the veins, atria, and pulmonary circulation.
Central Nervous System Ischemic Response—Control of Arterial Pressure by the Brain's Vasomotor Center in Response to Diminished Brain Blood Flow
Most nervous control of blood pressure is achieved by reflexes that originate in the baroreceptors, the chemoreceptors, and the low-pressure receptors, all of which are located in the peripheral circulation outside the brain. However, when blood flow to the vasomotor center in the lower brain stem becomes decreased severely enough to cause nutritional deficiency—that is, to cause cerebral ischemia—the vasoconstrictor and cardioaccelerator neurons in the vasomotor center respond directly to the ischemia and become strongly excited. When this occurs, the systemic arterial pressure often rises to a level as high as the heart can possibly pump. This effect is believed to be caused by failure of the slowly flowing blood to carry carbon dioxide away from the brain stem vasomotor center: at low levels of blood flow to the vasomotor center, the local concentration of carbon dioxide increases greatly and has an extremely potent effect in stimulating the sympathetic vasomotor nervous control areas in the brain's medulla.
It is possible that other factors, such as buildup of lactic acid and other acidic substances in the vasomotor center, also contribute to the marked stimulation and elevation in arterial pressure. This arterial pressure elevation in response to cerebral ischemia is known as the central nervous system ischemic response, or simply CNS ischemic response.
The magnitude of the ischemic effect on vasomotor activity is tremendous: it can elevate the mean arterial pressure for as long as 10 minutes sometimes to as high as 250 mmHg. The degree of sympathetic vasoconstriction caused by intense cerebral ischemia is often so great that some of the peripheral vessels become totally or almost totally occluded. The kidneys, for instance, often
"Cushing reaction," showing a rapid rise in arterial pressure resulting from increased cerebrospinal fluid (CSF) pressure.
CSF pressure CSF pressure raised reduced
CSF pressure CSF pressure raised reduced
Connector to subarachnoid space pressure transducer
Connector to subarachnoid space pressure transducer entirely cease their production of urine because of renal arteriolar constriction in response to the sympathetic discharge. Therefore, the CNS ischemic response is one of the most powerful of all the activators of the sympathetic vasoconstrictor system.
Importance of the CNS Ischemic Response as a Regulator of Arterial Pressure. Despite the powerful nature of the CNS ischemic response, it does not become significant until the arterial pressure falls far below normal, down to 60 mm Hg and below, reaching its greatest degree of stimulation at a pressure of 15 to 20 mm Hg. Therefore, it is not one of the normal mechanisms for regulating arterial pressure. Instead, it operates principally as an emergency pressure control system that acts rapidly and very powerfully to prevent further decrease in arterial pressure whenever blood flow to the brain decreases dangerously close to the lethal level. It is sometimes called the "last ditch stand" pressure control mechanism.
Cushing Reaction. The so-called Cushing reaction is a special type of CNS ischemic response that results from increased pressure of the cerebrospinal fluid around the brain in the cranial vault. For instance, when the cerebrospinal fluid pressure rises to equal the arterial pressure, it compresses the whole brain as well as the arteries in the brain and cuts off the blood supply to the brain. This initiates a CNS ischemic response that causes the arterial pressure to rise. When the arterial pressure has risen to a level higher than the cerebrospinal fluid pressure, blood will flow once again into the vessels of the brain to relieve the brain ischemia. Ordinarily, the blood pressure comes to a new equilibrium level slightly higher than the cerebrospinal fluid pressure, thus allowing blood to begin again to flow through the brain. A typical Cushing reaction is shown in Figure 18-10, caused in this instance by pumping fluid under pressure into the cranial vault around the brain. The Cushing reaction helps protect the vital centers of the brain from loss of nutrition if ever the cerebrospinal fluid pressure rises high enough to compress the cerebral arteries.
Special Features of Nervous Control of Arterial Pressure
Role of the Skeletal Nerves and Skeletal Muscles in Increasing Cardiac Output and Arterial Pressure
Although most rapidly acting nervous control of the circulation is effected through the autonomic nervous system, at least two conditions in which the skeletal nerves and muscles also play major roles in circulatory responses are the following.
Abdominal Compression Reflex. When a baroreceptor or chemoreceptor reflex is elicited, nerve signals are transmitted simultaneously through skeletal nerves to skeletal muscles of the body, particularly to the abdominal muscles. This compresses all the venous reservoirs of the abdomen, helping to translocate blood out of the abdominal vascular reservoirs toward the heart. As a result, increased quantities of blood are made available for the heart to pump. This overall response is called the abdominal compression reflex. The resulting effect on the circulation is the same as that caused by sympathetic vasoconstrictor impulses when they constrict the veins: an increase in both cardiac output and arterial pressure. The abdominal compression reflex is probably much more important than has been realized in the past because it is well known that people whose skeletal muscles have been paralyzed are considerably more prone to hypotensive episodes than are people with normal skeletal muscles.
Increased Cardiac Output and Arterial Pressure Caused by Skeletal Muscle Contraction During Exercise. When the skeletal muscles contract during exercise, they compress blood vessels throughout the body. Even anticipation of exercise tightens the muscles, thereby compressing the vessels in the muscles and in the abdomen. The iwwvww resulting effect is to translocate blood from the peripheral vessels into the heart and lungs and, therefore, to increase the cardiac output. This is an essential effect in helping to cause the fivefold to sevenfold increase in cardiac output that sometimes occurs in heavy exercise. The increase in cardiac output in turn is an essential ingredient in increasing the arterial pressure during exercise, an increase usually from a normal mean of 100 mm Hg up to 130 to 160 mm Hg.
Respiratory Waves in the Arterial Pressure iwwvww
With each cycle of respiration, the arterial pressure usually rises and falls 4 to 6 mm Hg in a wavelike manner, causing respiratory waves in the arterial pressure. The waves result from several different effects, some of which are reflex in nature, as follows:
1. Many of the "breathing signals" that arise in the respiratory center of the medulla "spill over" into the vasomotor center with each respiratory cycle.
2. Every time a person inspires, the pressure in the thoracic cavity becomes more negative than usual, causing the blood vessels in the chest to expand. This reduces the quantity of blood returning to the left side of the heart and thereby momentarily decreases the cardiac output and arterial pressure.
3. The pressure changes caused in the thoracic vessels by respiration can excite vascular and atrial stretch receptors.
Although it is difficult to analyze the exact relations of all these factors in causing the respiratory pressure waves, the net result during normal respiration is usually an increase in arterial pressure during the early part of expiration and a decrease in pressure during the remainder of the respiratory cycle. During deep respiration, the blood pressure can rise and fall as much as 20 mm Hg with each respiratory cycle.
Arterial Pressure "Vasomotor" Waves—Oscillation of Pressure Reflex Control Systems
Often while recording arterial pressure from an animal, in addition to the small pressure waves caused by respiration, some much larger waves are also noted—as great as 10 to 40 mm Hg at times—that rise and fall more slowly than the respiratory waves. The duration of each cycle varies from 26 seconds in the anesthetized dog to 7 to 10 seconds in the unanesthetized human. These waves are called vasomotor waves or "Mayer waves." Such records are demonstrated in Figure 18-11, showing the cyclical rise and fall in arterial pressure.
The cause of vasomotor waves is "reflex oscillation" of one or more nervous pressure control mechanisms, some of which are the following.
Oscillation of the Baroreceptor and Chemoreceptor Reflexes.
The vasomotor waves of Figure 18-115 are often seen in experimental pressure recordings, although usually much less intense than shown in the figure. They are caused mainly by oscillation of the baroreceptor reflex. That is, a high pressure excites the baroreceptors; this then inhibits the sympathetic nervous system and lowers the pressure a few seconds later. The decreased
A, Vasomotor waves caused by oscillation of the CNS ischemic response. B, Vasomotor waves caused by baroreceptor reflex oscillation.
pressure in turn reduces the baroreceptor stimulation and allows the vasomotor center to become active once again, elevating the pressure to a high value. The response is not instantaneous, and it is delayed until a few seconds later. This high pressure then initiates another cycle, and the oscillation continues on and on.
The chemoreceptor reflex can also oscillate to give the same type of waves. This reflex usually oscillates simultaneously with the baroreceptor reflex. It probably plays the major role in causing vasomotor waves when the arterial pressure is in the range of 40 to 80 mm Hg because in this low range, chemoreceptor control of the circulation becomes powerful, whereas baroreceptor control becomes weaker.
Oscillation of the CNS Ischemic Response. The record in Figure 18-11A resulted from oscillation of the CNS ischemic pressure control mechanism. In this experiment, the cerebrospinal fluid pressure was raised to 160 mm Hg, which compressed the cerebral vessels and initiated a CNS ischemic pressure response up to 200 mm Hg. When the arterial pressure rose to such a high value, the brain ischemia was relieved and the sympathetic nervous system became inactive. As a result, the arterial pressure fell rapidly back to a much lower value, causing brain ischemia once again. The ischemia then initiated another rise in pressure. Again the ischemia was relieved and again the pressure fell. This repeated itself cyclically as long as the cerebrospinal fluid pressure remained elevated.
Thus, any reflex pressure control mechanism can oscillate if the intensity of "feedback" is strong enough and if there is a delay between excitation of the pressure receptor and the subsequent pressure response. The vasomotor waves are of considerable theoretical importance because they show that the nervous reflexes that control arterial pressure obey the same principles as those applicable to mechanical and electrical control systems. For instance, if the feedback "gain" is too great in the guiding mechanism of an automatic pilot for an airplane and there is also delay in response time of the guiding mechanism, the plane will oscillate from side to side instead of following a straight course.
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.