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The aim of this study was to assess the influence of the handgrip test (HGT) on: (1) pial artery pulsation (cc-TQ), (2) subarachnoid space (SAS) width (sas-TQ) and (3) the relationship between peripheral blood pressure (BP), heart rate (HR), cerebral blood flow velocity (CBFV), resistive index (RI), cc-TQ and sas-TQ. The study was performed on 29 healthy volunteers (11 men and 18 women) with a mean age of 29.3 ± SE 4.0. HGT was performed in the sitting position at 30% of maximal voluntary contraction. cc-TQ and sas-TQ were registered using near-infrared transillumination/backscattering sounding (NIR-T/BSS); BP and heart rate (HR) were measured using a Finapres monitor. CBFV and RI were recorded using a transcranial Doppler. A significant reduction in cc-TQ (-34.3%, P<0.0001) and sas-TQ (-12.9%, P<0.001) were observed, while mean arterial pressure and HR increased (+34.8%, P<0.0001 and +7.9%, P<0.0001, respectively). There was no significant change in CBFV (+1.0%) while RI increased (+12.0%, P<0.05). Correlation and regression analysis did not reveal any interdependencies between the investigated variables. HGT evoked a significant increase in pial artery resistance, with a simultaneous decrease in the width of the SAS. A decrease in pial artery compliance should be seen as protective mechanism against acute BP elevation, most likely mediated by sympathetic activation. NIR-T/BSS recordings allowed for non-invasive assessments of changes in pial artery compliance, and were consistent with data from the literature and physiological knowledge.
The objective was to assess changes in the width of the subarachnoid space (SAS) and amplitude of cerebrovascular pulsation (CVP) during acute elevation of intracranial pressure (ICP) using Near Infrared Transillumination/Back Scattering Sounding (NIR-T/BSS). Changes in the width of the SAS and amplitude of CVP were observed in rabbits during experimental ICP elevation induced by: (1) quick injections of saline into the subdural space of the spinal cord, and (2) distension of a surgical catheter balloon placed intracranially in the subdural space. The amplitude of CVP was also assessed during acute elevation of blood pressure in the intracranial portion of the internal carotid artery (ICA) induced by adrenaline. Each of the injections of saline caused a transient rise in the width of the SAS and amplitude of CVP. The amplitude of the increase in CVP was dependent on changes in blood pressure in the ICA (r=-0.82, P<0.01). Distension of the intracranial balloon resulted in elimination of the respiratory oscillations in the CVP and increased its systolic-diastolic amplitude. An increase in the amplitude of CVP was evoked by adrenaline without an increase in the carotid blood flow. We demonstrated that during elevation of ICP the amplitude of CVP depends on blood pressure rather than on blood flow in large cerebral vessels. Elimination of the respiratory oscillations by a minute ("sub-critical") ICP increase may be used as an early indicator of rising ICP. The direction of changes recorded using NIR-T/BSS was consistent with changes recorded using tensometric transducers.
Background: The evidence accumulates that the response to acetazolamide test is delayed on the ipsilateral side to stenosis. However, the effect of acetazolamide beyond 30 min after acetazolamide administration remains unknown. The aim of this study was to assess the diameters of anterior cerebral arteries (ACAs), middle cerebral arteries (MCAs) and posterior cerebral arteries (PCAs) before and 60 min after the acetazolamide test. Materials and methods: Seventeen patients with carotid artery stenosis ≥ 90% on the ipsilateral side and ≤ 50% on the contralateral side were enrolled into the study. Diagnosis was based on ultrasonography examination and was confirmed using digital subtractive angiography. In all patients, two computed tomography angiography examinations were carried out; the first was performed before the acetazolamide administration, while the second one was carried out 60 min after injections. Results: In response to the acetazolamide test: PCA diameter diminished in both ipsi- and contra-lateral side to stenosis (from 1.31 to 1.24 mm and from 1.23 to 1.15 mm, respectively), ACA and MCA decreased in the contralateral side to the stenosis (from 1.33 to 1.26 mm and from 2.75 to 2.66 mm, respectively), ACA and MCA increased in the ipsilateral side to the stenosis (from 1.29 to 1.46 mm and from 2.77 to 2.96 mm, respectively). All changes were statistically significant. Conclusions: There were significant differences in reactivity to acetazolamide challenge between the internal carotid artery (ICA) and vertebrobasilar circulation in patients suffering from chronic carotid artery stenosis. Within the ICA territory, ACA and MCA responses vary in the affected and not affected side. (Folia Morphol 2017; 76, 1: 10–14)
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