FA states that Cushing reaction is mediated by baroreceptors which sense the increased pressure of intracranial vessels
On the other hand, BRS says that it is mediated by chemoreceptors which sense the increased cerebral Pco2 due to cerebral ischemia.
Which one is correct? Any thoughts?
courtersy of wikipedia;
http://en.wikipedia.org/wiki/Cushing_reflex
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The Cushing reflex is complex and seemingly paradoxical.[15] The reflex begins when some event causes increased intracranial pressure (ICP). Since cerebrospinal fluid is located in an area which is surrounded by the skull, increased ICP consequently increases the pressure in the fluid itself. The pressure in the cerebral spinal fluid eventually rises to the point that it meets and gradually exceeds the mean arterial blood pressure (MABP or MAP). When the ICP exceeds the MABP, arterioles located in the brain's cerebrum become compressed. Compression then results in diminished blood supply to the brain, a condition known as cerebral ischemia.[7]
During the increase in ICP, both the sympathetic nervous system and the parasympathetic nervous system are activated. In the first stage of the reflex, sympathetic nervous system stimulation is much greater than parasympathetic stimulation.[13] The sympathetic response activates alpha-1 adrenergic receptors, causing constriction of the body's arteries.[16] This constriction raises the total resistance of blood flow, elevating blood pressure to high levels, which is known as hypertension. The body's induced hypertension is an attempt to restore blood flow to the damaged, ischemic brain. The sympathetic stimulation also increases the rate of heart contractions and cardiac output.[17] Increased heart rate is also known as tachycardia. This combined with hypertension is the first stage of the Cushing reflex.
Meanwhile, baroreceptors in the carotid arteries detect the increase in blood pressure and trigger a parasympathetic response via the Vagus cranial nerve (x). This induces bradycardia, or slowed heart rate, and signifies the second stage of the reflex.[18] Bradycardia may also be caused by increased ICP due to direct mechanical distortion of the vagus nerve. Mechanical distortion of the vagus nerve stimulates a parasympathetic response, which can in turn induce bradycardia.[citation needed] The blood pressure can be expected to stay higher than the pressure of the raised cerebral spinal fluid to continue to allow blood to flow to the brain. The pressure will rise to the point where the it overcomes the resisting pressure of the compressed artery and blood is allowed through, providing oxygen to the hypoxic area of the brain. If the increase in blood pressure is not sufficient to compensate for the compression on the artery, infarction will occur.[19]
Raised ICP, tachycardia, or some other endogenous stimulus can result in distortion and/or increased pressure on the brainstem. Since the brainstem controls involuntary breathing, changes in its homeostasis often results in irregular respiratory pattern and/or apnea.[20] This is the third and final stage of the reflex.
Commonly, in various pressor reflexes, the central chemoreceptors, which transform chemical signals into an action potentials, and the baroreceptors, which sense pressure changes, of the carotid sinuses work together to increase or decrease blood pressure. However, chemoreceptors do not play a role in the Cushing reflex. Thus, even in the presence of sympathetic stimulation from the brain, which would normally produce tachycardia, there is in fact bradycardia.[18]
