Autoregulation of Cerebral Blood Flow in Orthostatic Hypotension

Novak, Vera; Novák, Péter; Spies, Judith M.; Low, Phillip A.

doi:10.1161/01.str.29.1.104

Cited by 211 publications

(175 citation statements)

References 33 publications

Supporting

Mentioning

164

Contrasting

Unclassified

Order By: Relevance

“…19 Furthermore, patients with severe autonomic failure have preserved mechanical autoregulatory mechanism despite destruction of vascular autonomic fibers. 20,21 Also, ganglionic blockade and ␣ 2 -adrenoreceptor and ␣ 1 -adrenoreceptor activation did not significantly affect the mechanoregulation in healthy volunteers. 18,22 The results of this study support our aforementioned presumptions.…”

Section: Lavi Et Al Nitric Oxide and Cerebral Blood Flowmentioning

confidence: 82%

Role of Nitric Oxide in the Regulation of Cerebral Blood Flow in Humans

et al. 2003

View full text Add to dashboard Cite

Background-From animal studies it emerged that nitric oxide is important for the modulation of CO 2 -mediated cerebral blood flow (CBF chemoregulation) but not for the pressor-dependent mechanism (mechanoregulation). This hypothesis was tested in 18 healthy subjects. Methods and Results-Peak velocity (PV), diastolic velocity (DV), and mean velocity (MV) were measured by transcranial Doppler of the middle cerebral artery. Chemoregulation was assessed during normocapnia, hypocapnia, and after inhaled mixture of 95% O 2 ϩ5% CO 2 . Mechanoregulation was evaluated by incremental doses of phenylephrine. Measurements were repeated during infusion of sodium nitroprusside (SNP). Regional cerebrovascular resistance (CVR) was calculated as mean blood pressure (BP)/MV. SNP infusion decreased mean BP by 7 mm Hg and CVR decreased from 1.38Ϯ0.08 to 1.29Ϯ0.09 mm Hg/cm ⅐ s Ϫ1 ; Pϭ0.01, resulting in unaffected CBF. Phenylephrine (25 to 250 g) caused a similar increase in BP in a dose-response fashion before and during SNP infusion. Despite the increments in BP and CVR, CBF remained unaffected. During hyperventilation (end-tidal CO 2 Ϸ24 mm Hg), CVR increased by 75Ϯ3% and PV and DV decreased by 27Ϯ2% and 43Ϯ2%, respectively (PϽ0.001 for all). SNP infusion blunted the vasoconstrictive effect of hypocapnia; CVR increased only by 57Ϯ5%, and PV and DV decreased by 23Ϯ2% and 35Ϯ3%, respectively, (PϽ0.05 for all). Similarly, SNP augmented the vasodilatory effect of hypercapnia. Conclusions-Exogenous nitric oxide donor affects the basal cerebral vascular tone without affecting the CBF mechanoregulation. However, it selectively affects only the chemoregulatory mechanism (CO 2 -dependent). Thus, the CO 2 -NO axis is a cardinal pathway for CBF regulation in humans.

show abstract

Section: Lavi Et Al Nitric Oxide and Cerebral Blood Flowmentioning

confidence: 82%

Role of Nitric Oxide in the Regulation of Cerebral Blood Flow in Humans

et al. 2003

View full text Add to dashboard Cite

show abstract

“…Briefly, the ultrasound signal emitted from the Doppler probe is reflected from erythrocytes within the MCA and back to the probe. The difference in frequency between the emitted signal and the reflected signal, the Doppler shift, is used to calculate CBFV via fast Fourier transform analysis (1,28,29,31). The resultant waveform (similar to a blood pressure waveform) is produced via spectral analysis of the blood flow velocity signal (28).…”

Section: Methodsmentioning

confidence: 99%

Inspiratory resistance delays the reporting of symptoms with central hypovolemia: association with cerebral blood flow

Rickards

Ryan

Cooke

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Rickards CA, Ryan KL, Cooke WH, Lurie KG, Convertino VA. Inspiratory resistance delays the reporting of symptoms with central hypovolemia: association with cerebral blood flow. Am J Physiol Regul Integr Comp Physiol 293: R243-R250, 2007. First published May 16, 2007; doi:10.1152/ajpregu.00087.2007.-We tested the hypothesis that breathing through an inspiratory threshold device (ITD) during progressive central hypovolemia would protect cerebral perfusion and attenuate the reporting of presyncopal symptoms. Eight human subjects were exposed to lower-body negative pressure (LBNP) until the presence of symptoms while breathing through either an active ITD (Ϫ7 cmH2O impedance) or a sham ITD (0 cmH2O). Cerebral blood flow velocity (CBFV) was measured continuously via transcranial Doppler and analyzed in both time and frequency domains. Subjects were asked to report any subjective presyncopal symptoms (e.g., dizziness, nausea) at the conclusion of each LBNP exposure. Symptoms were coincident with physiological evidence of cardiovascular collapse (e.g., hypotension, bradycardia). Breathing on the active ITD increased LBNP tolerance time (mean Ϯ SE) from 2,014 Ϯ 106 s to 2,259 Ϯ 138 s (P ϭ 0.006). We compared CBFV responses at the time of symptoms during the sham ITD trial with those at the same absolute time during the active ITD trial (when there were no symptoms). While there was no difference in mean CBFV at these time points (sham, 44 Ϯ 4 cm/s vs. active, 47 Ϯ 4; P ϭ 0.587), total oscillations (sum of high-and low-frequency spectral power) of CBFV were higher (P ϭ 0.004) with the active ITD (45.6 Ϯ 10.2 cm/s 2 ) than the sham ITD (22.1 Ϯ 5.4 cm/s 2 ). We conclude that greater oscillations around the same absolute level of mean CBFV are induced by inspiratory resistance and may contribute to the delay in symptoms and cardiovascular collapse that accompany progressive central hypovolemia.inspiratory threshold device; cerebral blood flow regulation; lowerbody negative pressure THE PRESERVATION OF CEREBRAL blood flow during hypotensive stress is integral in delaying the onset of presyncopal symptoms and maintaining consciousness. Recent data reported from several investigations have demonstrated the benefits of an inspiratory impedance threshold device (ITD) in elevating cerebral perfusion pressure in animals (39, 40) and reducing the reporting of presyncopal symptoms in humans (8, 27) with reductions in central blood volume.The ITD was designed to create a greater reduction in intrathoracic pressure during inspiration, enhancing the natural vacuum within the chest (26, 37). This vacuum promotes an increase in venous return, thereby increasing ventricular preload and subsequent cardiac output (Q) and arterial blood pressure (9, 26). Breathing on the ITD also increases cerebral blood flow velocity (CBFV) in resting, supine humans (12) and in the hemorrhaging porcine model, application of negative intrathoracic pressure reduces intracranial pressure (ICP) and subsequently elevates cerebral perfusion pressure (40, 41). Th...

show abstract

“…For instance, the "mental activity" considered in [37] was to conduct simple arithmetic calculations during the orthostatic stress situation. Intimately connected with the problem of orthostatic stress are the strong autoregulatory mechanisms of cerebral blood flow which have been investigated in [60,61,63], for instance. -Reaction of the CVS/CVRS to a loss of blood volume in the CVS.…”

Section: Control Issuesmentioning

confidence: 99%