doi: 10.1161/01.STR.0000182257.27380.1a
(Stroke. 2005;36:2066.)
© 2005 American Heart Association, Inc.
Letters to the Editor |
What Causes the Acute Blood Pressure Elevation After Stroke?
Department of Physiology, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry 605006, India.
To the Editor:
In an insightful editorial1 to a recently published paper by Mattle et al,2 Lindsberg raises a central question as to why blood pressure increases in the acute phase of stroke. The Cushing reflex is suggested as a possible mechanism because it results in sympathetic nervous system activation; however, this reflex is typically described as occurring in the face of raised intracranial tension.3 The purpose of this letter is to suggest that the central nervous system (CNS) ischemic response may be responsible for the marked sympathoexcitation leading to marked blood pressure elevation in acute stroke. This reflex leads to marked activation of the sympathetic nervous system and serves to eventually optimize cerebral perfusion.3 Fundamentally, the Cushing reflex and the CNS ischemic response are the same in that they are both triggered by cerebral ischemia. Cushing reflex is a variant of the CNS ischemic response because raised intracranial tension diminishes blood flow to brain cells.3 Hypoxia has been demonstrated to excite vasomotor neurons raising sympathetic outflow to blood vessels.4 Although chemoreceptors typically are described as being located in the carotid and aortic bodies and in the brain stem, there is increasing evidence that all cells are capable of metering oxygen tension and eliciting appropriate responses to optimize the supply-demand relationship that is inextricably linked to homeostasis.5
References
1. Lindsberg PJ. High blood pressure after acute cerebrovascular occlusion: risk or risk marker? Stroke. 2005; 36: 268–269.
2. Mattle HP, Kappeler L, Arnold M, Fischer U, Nedeltchev K, Remonda L, Jakob SM, Schroth G. Blood pressure and vessel recanalization in the first hours after ischemic stroke. Stroke. 2005; 36: 267–272.
3. Guyton AC. Circulatory Physiology III. Arterial pressure and hypertension. Philadelphia, PA: Saunders, 1980.
4. Sun MK, and Reis DJ. Hypoxia selectively excites vasomotor neurons of the rostral ventrolateral medulla in rats. Am J Physiol Regul Integ Comp Physiol. 1994; 266: R245–R256.
5. Semenza GL. Hydroxylation of HIF-1: Oxygen sensing at the molecular level. Physiology. 2004; 19: 176–182.
Response:
Department of Neurology,, Helsinki University Central Hospital, Neuroscience Program, Biomedicum Helsinki, Helsinki, Finland
I thank the authors Prakash and Madanmohan for an interesting remark. The physiological reason for immediate hypertension in acute stroke is intriguing. Although hypoxia, increase of intracranial pressure, and very low systemic arterial pressure are known to stimulate the cerebral ischemic response (CIR) by activating the neurons of the vasomotor center located within the ventrolateral medulla,1 occlusion of a single cerebral artery causes focal ischemia that generally does not rapidly induce any of these stimuli to the medullary vasomotor center. Experimental studies in animals related to cerebral ischemia and the CIR have used experimental setups that cause global cerebral ischemia or systemic hypoxia,1–3 which directly influence those medullary oxygen sensing neurons. Translation of results from experiments in anesthesized animals into the clinical situation in conscious humans may be tricky. Furthermore, acute stroke does not reproduce CIR in its entirety; what is missing are bradypnea and bradycardia as found in classical Cushing reaction. This supports that higher cerebral centers, probably those influencing the rostral parts of the reticular formation such as hypothalamus, cingulate or other cortices, stimulate the vasomotor center4 and produce CIR during focal cerebral ischemia only for its one component, hypertension. Clamping of one common carotid artery in anesthetized dogs causes only 6 to 10 mm Hg increase in blood pressure, which quickly normalizes after release of the clamp,2 and the same holds true for humans during carotid endarterectomy, indicating functioning carotid sinus baroreceptor reflex to the vasomotor center.5 This procedure does not normally cause significant cerebral ischemia. However, if in awake patients undergoing carotid endarterectomy blood pressure paradoxically falls even moderately to clearly nonhypotensive levels, and a sudden neurological deficit develops to indicate cerebral ischemia, the deficit is completely corrected by fast-acting hypertensive drugs.6 Therefore, the immediate hypertension after occlusion of a cerebral artery would indeed seem to serve a meaningful function for brain protection. I agree that it is the increased sympathetic vasomotor excitation that most likely transmits this obviously very important hemodynamic response.
References
1. Sun M-K, Reis DJ. Hypoxia selectively excites vasomotor neurons of rostral ventrolateral medulla in rats. Am J Physiol (Regul Integr Comp Physiol 35). 1994; 266: R245–R256.
2. Guyton AC. Acute hypertension in dogs with cerebral ischemia. Am J Physiol. 1948; 154: 45–54.
3. Dampney RAL, Moon EA. Role of ventrolateral medulla in vasomotor response to cerebral ischemia. Am J Physiol (Heart Circ Physiol 8). 1980; 239: H349–H358.
4. Guyton AC, Hall JE. Nervous Regulation of the Circulation, and Rapid Control of Arterial Pressure. Textbook of Medical Physiology. Saunders, Philadelphia; 2000. 184–194.
5. Sigaudo-Roussel D, Evans DH, Naylor AR, Panerai RB, London NL, Bell P, Gaunt ME. Deterioration in carotid baroreflex during carotid endarterectomy. J Vasc Surg. 2002; 36: 793–798.[Medline] [Order article via Infotrieve]
6. Stoneham MD, Warner O. Blood pressure manipulation during awake carotid surgery to reverse neurological deficit after carotid cross-clamping. Br J Anaesth. 2001; 87: 641–644.
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