Blood pressure regulation IX: cerebral autoregulation under blood pressure challenges

Tzeng, Yu‐Chieh; Ainslie, Philip N.

doi:10.1007/s00421-013-2667-y

“…Nonetheless, it is generally accepted that CA in general is mediated by the integration of metabolic, myogenic, and neurogenic factors (438,439,475). The evidence of these factors in the regulation of human CA have been recently reviewed (456 (475) (Fig. 2).…”

Section: Cerebral Autoregulationmentioning

confidence: 98%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

¹

,

Nybo

²

,

Ainslie

³

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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“…Nonetheless, the observation strongly suggests the importance of arterial stenosis in the J-curve phenomenon. Second, the J-curve phenomenon may also depend on the feature of regional circulation [4,27,28] . Coronary circulation is different from cerebral and renal circulation in blood flow regulation.…”

Section: Plausible Mechanisms Of the J-curve Phenomenonmentioning

confidence: 99%

The J-Curve Phenomenon in Hypertension

Kang¹,

Wang²

2016

Hypertension and Cardiovascular Disease

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Almost immediately after antihypertensive therapy was proven effective in preventing cardiovascular events, the J-curve issue emerged as a hot topic. The Hypertension Optimal Treatment (HOT) trial attempted to address this question (diastolic blood pressure <80, <85, and <90 mm Hg) but ended up with a post hoc analysis indicating a nadir of 138.5 mm Hg systolic and 82.6 mm Hg diastolic blood pressure. Nevertheless, this observational finding was supported by the results of observational studies in the general population and by post hoc analyses of antihypertensive treatment trials. The currently ongoing Systolic Hypertension Optimal Treatment (SHOT) trial investigates whether the relationship between systolic blood pressure and stroke recurrence is linear or J-shaped by treating systolic blood pressure to <125, <135, and <145 mm Hg in patients with a history of recent stroke. This trial may provide additional but probably inconclusive evidence, because optimal blood pressure might differ between individuals and across outcomes. Nevertheless, a universal beneficial, instead of optimal, level of blood pressure for antihypertensive treatment may exist approximating 130/80 mm Hg and should be investigated by comparing 130/80 mm Hg with 140/90 mm Hg as a target blood pressure in hypertensive patients with the simultaneous use of modern blood pressure measuring techniques, such as home and ambulatory blood pressure monitoring.

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“…Second, the J-curve phenomenon may also depend on the feature of regional circulation [4,27,28]. Coronary circulation is different from cerebral and renal circulation in blood flow regulation.…”

Section: Plausible Mechanisms Of the J-curve Phenomenonmentioning

confidence: 99%

“…In both cerebral and renal circulation, there is autoregulation mainly by adjusting the vessel diameter, but not resistance, because the peripheral resistance is generally low. For instance, the cerebral blood flow remains constant in arterial pressures ranging from approximately 60 to 160 mm Hg [28]. However, coronary circulation has high peripheral resistance.…”

Section: Plausible Mechanisms Of the J-curve Phenomenonmentioning

confidence: 99%

The J-Curve Phenomenon in Hypertension

Kang

¹

,

Wang²

2016

Pulse

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Almost immediately after antihypertensive therapy was proven effective in preventing cardiovascular events, the J-curve issue emerged as a hot topic. The Hypertension Optimal Treatment (HOT) trial attempted to address this question (diastolic blood pressure <80, <85, and <90 mm Hg) but ended up with a post hoc analysis indicating a nadir of 138.5 mm Hg systolic and 82.6 mm Hg diastolic blood pressure. Nevertheless, this observational finding was supported by the results of observational studies in the general population and by post hoc analyses of antihypertensive treatment trials. The currently ongoing Systolic Hypertension Optimal Treatment (SHOT) trial investigates whether the relationship between systolic blood pressure and stroke recurrence is linear or J-shaped by treating systolic blood pressure to <125, <135, and <145 mm Hg in patients with a history of recent stroke. This trial may provide additional but probably inconclusive evidence, because optimal blood pressure might differ between individuals and across outcomes. Nevertheless, a universal beneficial, instead of optimal, level of blood pressure for antihypertensive treatment may exist approximating 130/80 mm Hg and should be investigated by comparing 130/80 mm Hg with 140/90 mm Hg as a target blood pressure in hypertensive patients with the simultaneous use of modern blood pressure measuring techniques, such as home and ambulatory blood pressure monitoring.

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Blood pressure regulation IX: cerebral autoregulation under blood pressure challenges

Cited by 186 publications

References 107 publications

Cerebral Vascular Control and Metabolism in Heat Stress

Cerebral Vascular Control and Metabolism in Heat Stress

The J-Curve Phenomenon in Hypertension

The J-Curve Phenomenon in Hypertension

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