It would seem likely that increased CCA(Common carotid artery) flow would be helpful immediately post stroke. Better blood flow to the brain, more oxygen delivered. But I'm not medically trained so ask your doctor if this would help. But your doctor will need to determine the EXACT AGE when you switch from young to old.
The cold pressor test is a cardiovascular test performed by immersing the hand into an ice water container, usually for one minute, and measuring changes in blood pressure and heart rate. These changes relate to vascular response and pulse excitability.
If your doctor is not doing this, what exactly is being done to increase oxygen delivery to the brain in the first days? If nothing, then you have EXTREME INCOMPETENCE IN YOUR STROKE HOSPITAL.
oxygen delivery (4 posts to January 2020)
brain blood flow (3 posts to April 2019)
Extra- and intracranial blood flow regulation during the cold pressor test: influence of age
Abstract
We determined how the extra- and intracranial circulations respond to generalized sympathetic activation evoked by a cold pressor test (CPT) and whether this is affected by healthy aging. Ten young [23 ± 2 yr (means ± SD)] and nine older (66 ± 3 yr) individuals performed a 3-min CPT by immersing the left foot into 0.8 ± 0.3°C water. Common carotid artery (CCA) and internal carotid artery (ICA) diameter, velocity, and flow were simultaneously measured (duplex ultrasound) along with middle cerebral artery and posterior cerebral artery mean blood velocity (MCAvmean and PCAvmean) and cardiorespiratory variables. The increases in heart rate (~6 beats/min) and mean arterial blood pressure (~14 mmHg) were similar in young and older groups during the CPT (P < 0.01 vs. baseline). In the young group, the CPT elicited an ~5% increase in CCA diameter (P < 0.01 vs. baseline) and a tendency for an increase in CCA flow (~12%, P = 0.08); in contrast, both diameter and flow remained unchanged in the older group. Although ICA diameter was not changed during the CPT in either group, ICA flow increased (~8%, P = 0.02) during the first minute of the CPT in both groups. Whereas the CPT elicited an increase in MCAvmean and PCAvmean in the young group (by ~20 and ~10%, respectively, P < 0.01 vs. baseline), these intracranial velocities were unchanged in the older group. Collectively, during the CPT, these findings suggest a differential mechanism(s) of regulation between the ICA compared with the CCA in young individuals and a blunting of the CCA and intracranial responses in older individuals.
NEW & NOTEWORTHY Sympathetic activation evoked by a cold pressor test elicits heterogeneous extra- and intracranial blood vessel responses in young individuals that may serve an important protective role. The extra- and intracranial responses to the cold pressor test are blunted in older individuals.
the cold pressor test (CPT) has been widely employed for the assessment of human autonomic function (13, 17), peripheral vascular reactivity (7, 45, 53, 72), and cardiovascular risk stratification (6, 38, 61). However, the cerebrovascular responses to the CPT remain poorly understood, particularly in healthy aging and chronic disease. This issue is compounded by the controversy surrounding the sympathetic regulation of the extra- and intracranial blood vessels (1, 58). During the CPT, signals from activated cutaneous thermoreceptor and nociceptor afferents are rapidly integrated within the central nervous system (principally the hypothalamic and medullary regions) and lead to the activation of cortical sites (10). This activation elevates peripheral vascular resistance, heart rate (HR), and blood pressure (23) on account of the characteristic autonomic efferent response, consisting of a robust increase in sympathetic nerve activity (SNA) (e.g., increased plasma noradrenaline (19) and muscle sympathetic nerve activity; see Ref. 65) and potentially a decrease in cardiac parasympathetic nerve activity (e.g., decreased HR variability; see Ref. 16). Cerebral blood flow may be affected by several mechanisms during the CPT, including neurovascular coupling, a hydraulic pressure effect even in the absence of a change in vascular resistance, and local autoregulatory mechanisms, and by the sympathetic modulation of extra- and intracranial blood vessels.
In animal studies, innervation of the CCA, ICA, and intracranial vasculature by postganglionic sympathetic nerve fibers has been identified (12, 37, 42); electrical stimulation of sympathetic nerves can evoke cerebral vasoconstriction (2, 66), and norepinephrine causes vasoconstriction in cerebral microvessels (36, 59). In humans, the spillover of noradrenaline from the brain into the internal jugular vein has been reported (43); clinically indicated upper thoracic sympathectomy increases ICA diameter and flow (26), and stellate ganglion blockade reportedly increases cerebral perfusion (62), although this is not been a universal finding (27). The effect of CPT-evoked sympathoexcitation on cerebral perfusion has principally been evaluated in terms of intracranial artery mean blood flow velocity and usually within the middle cerebral artery (MCAvmean). Intriguingly, both reductions (3, 41) and elevations (46, 47, 56, 73) in cerebral perfusion have been reported during the CPT, which are possibly due to differences in the partial pressure of arterial carbon dioxide (
). With respect to the regulation of extracranial blood flow during the CPT, an increase in common carotid artery (CCA) diameter by ∼8% is reported in young healthy individuals (28, 34, 53). In contrast, CCA diameter is reduced during the CPT in patients with coronary artery disease, which is possibly due to the greater sensitivity of the α-adrenergic receptors (53). Unfortunately, to date, no assessment of internal carotid artery (ICA) diameter or volumetric flow during the CPT has been made, but these are essential to understand the implications for cerebral blood flow (as opposed to blood flow to the head and scalp via the external carotid artery). It would seem unlikely that the same responses were observed in the CCA and ICA during the CPT. In accordance with Poiseuille’s Law, small changes in diameter have a major effect on flow [e.g., flow-α (diameter/2)4]. Accordingly, if the ICA were to dilate to a degree similar to that of the CCA (e.g., ∼8%), brain blood flow would increase markedly. Given that the brain seems to be particularly effective at protecting itself from overperfusion (68) and that the ICA (and vertebral arteries) are known to be integral to the regulation of cerebral blood flow through modifying vascular resistance (14, 22, 29, 39, 40), it seems reasonable to expect that different responses occur in the CCA and ICA during the CPT.
Increased age is associated with a multitude of structural, functional, and regulatory alterations throughout the cardiovascular system (30, 31), including the brain (5, 54). Age-related increases in arterial stiffness (28, 33), impairments in endothelial vasodilator function, and altered α- and β-adrenergic receptors signaling within the peripheral vasculature have been identified in humans (4, 11). However, the extent to which age modifies the cerebral blood flow responses to sympathetic stimulation remains unclear.
The purpose of this study was twofold: 1) to comprehensively describe the extra- (CCA, ICA) and intracranial (MCA) blood flow responses to the CPT and 2) to ascertain the influence of age on these cerebrovascular responses to the CPT. To achieve these goals, in both younger and older subjects, simultaneous measurements of CCA and ICA diameter, velocity, and flow were made along with MCAvmean and posterior cerebral artery mean blood flow velocity (PCAvmean) during the CPT under conditions of controlled isocapnia. We hypothesized that there would be less of an increase in ICA diameter compared with the CCA during the CPT in young individuals. In addition, we anticipated that the extra- and intracranial responses to the CPT would be blunted in older individuals.
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