Study of neurovascular coupling during cold pressor test in patients with migraine.

BACKGROUND: Altered neurovascular coupling in migraineurs could be a consequence of impaired function of modulatory brainstem nuclei. The cold pressor test (CPT) should activate brainstem structures. We measured visually evoked cerebral blood flow velocity response (VEFR) to CPT in migraine. METHODS: Twenty-three healthy volunteers and 29 migraineurs participated in the study. We measured arterial blood pressure, end-tidal CO2, heart rate and cerebral blood flow velocity in posterior and middle cerebral artery using transcranial Doppler. VEFR was calculated as cerebrovascular reactivity to photic stimulation before, during and after CPT. RESULTS: In healthy individuals, there was a significant decrease in peak systolic VEFR from CPT phase to recovery phase (p < 0.05). There was an increase in mean VEFR from basal to CPT phase and a decrease from CPT to recovery phase, both significant (p < 0.05). End-diastolic VEFR increased from basal to CPT phase and decreased in recovery phase below the basal phase values, all changes significant (p < 0.05). In migraine, no statistically significant changes in peak systolic, mean or end-diastolic VEFRs were observed between phases (p > 0.05). The differences in phases in mean and end-diastolic VEFRs between the basal phase and the CPT phase and between the CPT phase and the recovery phase were significantly higher in healthy individuals (p < 0.05). CONCLUSIONS: The absence of the effect of CPT on VEFR in migraine is likely to be a consequence of impaired subcortical modulation of neurovascular coupling.

Cognitive and autonomic dysfunction in presymptomatic and early Huntington's disease.

Huntington's disease is characterized by disorders of movement, cognition and behavior. Individuals with Huntington's disease display aberrant changes in the autonomic nervous system that are detected even before the onset of other symptoms. Subtle cognitive dysfunction may start before other clinical manifestations. The aim of the present study was to investigate the autonomic nervous system response to mental arithmetic and the relationship between the autonomic and cognitive/motor function in presymptomatic and early Huntington's disease. We examined 15 presymptomatic Huntington's disease gene carriers (PHD), 15 early Huntington's disease patients (EHD) and 30 healthy controls. PHD and EHD groups were determined according to Unified Huntington's Disease Rating Scale (UHDRS) motor score. ECG, heart rate, systolic and diastolic blood pressure, and cutaneous laser Doppler flux were measured during rest and during a simple mental arithmetic test. UHDRS cognitive test battery was applied to determine cognitive dysfunction. During mental arithmetic, the heart rate of PHD/EHD increased significantly less than that of controls. Decreased microvascular response to mental arithmetic was found in EHD. Significant correlations for the PHD/EHD group were found between laser Doppler flux response and Symbol Digit Modalities Test score, and between laser Doppler flux response and UHDRS motor score. It seems that central autonomic dysregulation of cardiovascular system in Huntington's disease goes along with the degeneration of other central neuronal systems. This finding is relevant as it could enable simple and noninvasive testing of disease progression.

Microcirculation response to local cooling in patients with Huntington's disease.

Altered autonomic nervous system (ANS) functioning in early stages of Huntington's disease (HD) has been suggested, presumably due to distorted high-order autonomic control. ANS functioning in the early stages of HD was further investigated. Laser-Doppler (LD) flux in the skin of the fingertips, heart rate (HR), HR variability, systolic and diastolic blood pressure were measured during rest and during a 6 min cooling of one hand at 15°C. Data of 15 presymptomatic gene mutation carriers (PHD), 15 early symptomatic HD patients (EHD), and two groups of 15 age- and sex-matched controls were compared. The area under the low frequency (LF) and high frequency (HF) bands of the HR variability spectrum were calculated. An augmented reduction of cutaneous LD flux was found in response to the direct cooling in the PHD group (37.5 ± 8.5% of resting value) compared to the PHD controls (67.27 ± 8.4%) (p < 0.05). In addition, the PHD group had higher (LF/(LF + HF) index of primary sympathetic modulation of the HR at rest (53.6 ± 3.3) compared to the EHD patients (39.7 ± 4.2) (p < 0.05). In the EHD group, a significantly smaller change of HR during cooling (100.26 ± 1.2%) was found compared to the EHD controls (95.9 ± 1.0%) (p < 0.05). The results are in line with the hypothesis that ANS dysfunction occurs even in PHD subjects. Further, they support the hypothesis that dysfunction of the high-order autonomic centres are involved in HD.

The effect of the cold pressor test on a visually evoked cerebral blood flow velocity response.

We investigated the hypothesis that during tonic pain stimulus, neurovascular coupling (NVC) decreases, measuring visually evoked cerebral blood flow velocity response (VEFR) during cold pressor test (CPT) in healthy human subjects as a test. VEFR was calculated as a relative increase in blood flow velocity in the posterior cerebral artery from average values during the last 5 s of the stimulus-OFF period to average values during the last 10 s of the stimulus-ON period. Three consecutive experimental phases were compared: basal, CPT and recovery. During CPT, end-diastolic and mean VEFR increased from 20.2 to 23.6% (p < 0.05) and from 17.5 to 20.0% (p < 0.05), respectively. In recovery phase, end-diastolic and mean VEFR decreased to 17.7% and 15.5%, respectively. Both values were statistically significantly different from CPT phase (p < 0.05). Compared with the basal phase, only end-diastolic VEFR was statistically significantly different in the recovery phase (p < 0.05). Our results are consistent with the assumption that there is a change in the activity of NVC during CPT because of the modulatory influence of subcortical structures activated during tonic pain. Contrary to our expectations, the combined effect of such influences increases rather than decreases NVC.

Regular physical activity alters the postocclusive reactive hyperemia of the cutaneous microcirculation.

Regular physical activity leads to increased endothelium-dependent vasodilatation. Postocclusive reactive hyperemia (PRH) is a transient increase of blood flow after the release of an arterial occlusion and has been used as a clinical tool to estimate endothelial function. The aim of our study was to assess the potential effect of regular physical training on PRH of skin microcirculation. Skin blood flux was estimated by laser-Doppler fluxmetry (LDF) in two groups of subjects: 12 highly trained athletes and 12 age-matched sedentary controls. LDF was measured on two specific skin sites: volar aspect of the forearm (nonglabrous area) and finger pulp of the middle finger (glabrous area). After the release of a 3-min occlusion of the brachial artery, we determined the following indices of PRH: the time to peak (tpeak), the maximal LDF (LDFpeak), the recovery time (trec), the area under the PRH curve (AUC). Baseline LDF did not differ between the trained and sedentary subjects in either site. On the forearm, we found no significant differences in either PRH parameter. On the contrary, on the finger pulp, there were statistically significant differences in the tpeak and the AUC (p < or = 0.05). The results show an altered PRH response of skin microcirculation in the finger pulp in the trained subjects. We may speculate that this could be the result of an increased endothelial vasodilator capacity. Further, the potential adaptations of the endothelium differ between the glabrous and nonglabrous skin sites.

Alteration of skin laser-Doppler flux response to local cooling in gestational hypertension.

PURPOSE: The pathophysiology of the pregnancy-induced hypertension is still poorly understood, especially with regard to the central autonomic nervous system control and peripheral vascular factors. METHODS: Our study therefore aimed to investigate simultaneously the responses of blood pressure, heart rate, heart rate variability (HRV), and laser-Doppler (LD) flux to local cooling in healthy non-pregnant women (N = 12), in pregnant women with normal pregnancy (N = 16) and in women with gestational hypertension (N = 10). RESULTS: The direct and indirect LD flux responses to local cold exposure were diminished in normotensive pregnant females (Dunnett's test, p < 0.05) when compared to non-pregnant females with normal menstrual cycle, but not in females with pregnancy-induced hypertension. In addition, blood pressure increased and heart rate decreased during cold exposure only in normotensive pregnant females, but not in pregnant hypertensive females (paired t test, p < 0.05). Simultaneously calculated heart rate variability total power of HRV and LF power values typically increased during local cold provocation test in non-pregnant females and in normotensive pregnant females (paired t test, p < 0.05). In hypertensive pregnant females HRV indices remained unchanged. CONCLUSION: Our results indicate that the cardiovascular reactivity adaptation seen in normal pregnancy is absent in gestational hypertension.

The effect of alpha-adrenoceptor agonists and L-NMMA on cutaneous postocclusive reactive hyperemia.

Postocclusive reactive hyperemia (PRH) is considered to be a locally mediated vascular reaction independent of sympathetic activity. However, experiments on animal vascular preparations have shown that alpha(2)-adrenoceptor activity interferes with the production of endothelium-derived nitric oxide (NO) that has been found to play an important role in the PRH response. We attempted to elucidate the role of endothelium-derived NO in the cutaneous PRH response. Especially, we aimed to clarify the interference of the alpha-adrenoceptor activity with NO mechanism in cutaneous microcirculation. We studied the effect of intradermal microinjection of the NO synthase inhibitor L-NMMA alone, alpha(1)-agonist phenylephrine alone, alpha(2)-agonist clonidine alone and L-NMMA in combination with each alpha-agonist. The effect of the saline solution injection was used as a reference value. Laser-Doppler flux was monitored in 11 healthy volunteers before and after a 4-minute and an 8-minute occlusion of digital arteries. The application of L-NMMA significantly reduced resting LD-flux (p<0.05) only in combination with alpha(2)-agonist but not alpha(1)-agonist. The application of L-NMMA alone changed the time in which LD flux reached half of the preocclusive value during the PRH response (T/2) only after 4-minute (p<0.05) but not after an 8-minute occlusion. Phenylephrine (alpha(1)-agonist) alone shortened (p<0.05), while clonidine (alpha(2)-agonist) alone prolonged T/2 (p<0.05) of 8-minute PRH. The combined application of L-NMMA and clonidine abolished the effect of clonidine alone on 8-minute PRH. In contrast, the combination of L-NMMA and phenylephrine did not cause any change of the PRH response when compared to the injection of phenylephrine alone. Our finding is consistent with the hypothesis that alpha(2)-adrenoceptor activity (in the condition of maximal agonist stimulation) could interfere with NO mechanisms in cutaneous microcirculation, probably by increasing NO production.

The effect of glibenclamide on acetylcholine and sodium nitroprusside induced vasodilatation in human cutaneous microcirculation.

OBJECTIVE: K(ATP) channels have an important regulatory role in resting vascular tone and during hypoxia. Their role in endothelium dependent and independent vasodilatation in human skin microcirculation is less known. METHODS: We monitored the laser-Doppler (LD) response in 14 healthy male volunteers on the skin of the forearm. In the case of endothelium dependent vasodilatation [acetylcholine (ACh) induced], a saline solution (used as control) or a solution of glibenclamide (K(ATP) channel blocker) were randomly injected each into a distinct measurement site on different forearms followed by the iontophoresis of ACh. In the case of endothelium dependent vasodilatation with the inhibition of prostaglandin production, diclofenac (cyclooxygenase inhibitor) or the combination of diclofenac and glibenclamide were randomly injected each into a distinct measurement site on different forearms followed by the iontophoresis of ACh. In the case of endothelium independent vasodilatation [sodium nitroprusside (SNP) induced], a saline solution or glibenclamide were randomly injected each into a distinct measurement site on different forearms, iontophoresis of SNP followed. RESULTS: Glibenclamide alone, diclofenac alone or the combination of glibenclamide and diclofenac reduced the LD flux values during rest and after ACh application (P<0.05). The reduction of LD flux in ACh mediated vasodilatation was greatest when using the combination of glibenclamide and diclofenac. In the case of SNP application, there was also a significantly lower LD flux rise for glibenclamide in comparison with the saline solution (P<0.05). CONCLUSIONS: K(ATP) channels play an important role in human cutaneous vasodilatation induced by ACh and SNP.

The effect of nitric oxide synthase and cyclooxygenase inhibition on cutaneous microvascular reactivity.

The role of nitric oxide (NO)- and prostacyclin (PGI(2))-independent mechanism, potentially attributable to endothelium-derived hyperpolarizing factor (EDHF), has not been extensively studied in human skin microcirculation. The aim of our study was to elucidate the contribution of the NO- and PGI(2)-independent mechanism to microvascular reactivity of cutaneous microcirculation. Skin perfusion was measured on the volar aspect of the forearm in 12 healthy male subjects (mean age 25.0 +/- 1.5), using laser Doppler (LD) fluxmetry. Combined endothelial nitric oxide synthase (eNOS) and cyclooxygenase (COX) inhibition was achieved by an intradermal injection (10 microl) of the eNOS inhibitor, L(omega)-monomethyl L-arginine (L-NMMA, 10 mM) and the COX inhibitor, diclofenac (10 mM); saline was injected as a control. LD flux was assessed at rest and after an iontophoretical application of acetylcholine (ACh, 1%), an endothelial agonist and sodium nitroprusside (SNP, 1%), an endothelium-independent agonist, respectively. Combined eNOS and COX inhibition had no effect on the baseline LDF (12.5 +/- 2.3 PU (perfusion units) in control vs. 10.9 +/- 1.8 PU in the treated site). On the other hand, the ACh-stimulated increase in LDF was significantly attenuated after eNOS and COX inhibition (390.5 +/- 43.5%), compared to the control (643.7 +/- 80.3% increase, t-test, P < 0.05). Nevertheless, at least 60% of ACh-mediated vasodilatation was preserved after combined eNOS and COX inhibition. eNOS and COX inhibition had no impact on the SNP-stimulated increase in LDF (768.8 +/- 70.5% in control vs. 733.5 +/- 54.6% in the treated site). These findings indicate that NO- and PGI(2)-independent mechanism plays an important role in the regulation of blood flow in the human skin microcirculation.

The effect of glibenclamide on cutaneous laser-Doppler flux.

The K(ATP) channels play a crucial role in regulation of vascular tone in conditions of hypoxia. Whether they contribute to peripheral blood flow regulation in human cutaneous microcirculation during a non-hypoxic state is the matter of conflicting in vivo studies that have used plethysmographic method. Our aim was therefore to elucidate the role of K(ATP) channels in human skin microcirculation in three different conditions that evoke different interplays of vascular mechanisms; during resting conditions, during the postocclusive vasodilatation and in the vasoconstriction response to local cold exposure. The laser-Doppler (LD) skin response was monitored in 12 healthy volunteers on the skin of the fingertips of both hands at rest, after the release of an 8-min digital arteries occlusion, and during local cooling of one hand at 15 degrees C. We compared the direct (at the measuring site) and the indirect (at the contralateral non-cooled hand) LD flux response after intradermal microinjection of saline solution (1 mul) and after a microinjection of the K(ATP) channel blocker glibenclamide (8 muM saturated solution) at the measuring site after obtaining the dose-dependent effect of glibenclamide. The effect of the saline solution was used as a reference value. There was a statistically significant lower resting LD flux after the microinjection of glibenclamide 273.6+/-36 PU when compared to the values obtained after the application of the saline solution 375.8+/-31 PU (paired t-test, p=0.016). Glibenclamide also significantly reduced the relative area under the LD flux curve during the PRH response 14551+/-2508 PU*s vs. 6402+/-1476 PU*s (paired t-test, p=0.01) and increased the principal frequency of postocclusive PRH oscillations 0.0931+/-0.01 Hz vs. 0.1309+/-0.02 Hz (p=0.01). In addition, glibenclamide significantly decreased the LD flux during both the direct and indirect response to local cold exposure when compared to the application of saline solution (paired t-test, p<0.01). Our results support the conjecture that ATP sensitive K(+) channels are importantly involved in blood flow regulation of human skin microcirculation in PRH response, in resting conditions as well as in microvascular local cold response.

Age-related changes in the relationship between visual evoked potentials and visually evoked cerebral blood flow velocity response.

We evaluated neurovascular coupling during normal aging using visual evoked potentials (VEPs) and visually evoked cerebral blood flow velocity responses (VEFRs). The recordings were made from a group of healthy younger and older subjects. The stimulus was a black and white checkerboard with visual contrasts of 1%, 10% and 100%. The VEFRs were measured in the posterior cerebral artery using transcranial Doppler simultaneously with VEPs from occipital leads. A significant increase in the VEFRs and VEPs in response to graded visual contrasts (p<0.01) was found in both groups. Linear regression analysis showed a significant positive association between the VEPs and the VEFRs in the younger (r=0.66, p<0.01) and older subjects (r=0.74, p<0.01). We also found significant differences in neurovascular coupling index (VEFR/VEP) between both groups at each visual contrast (p<0.01). We conclude that simultaneous recording of VEFRs and VEPs at graded visual contrasts indicated attenuated neurovascular coupling in older subjects.

The influence of visual contrast on visually evoked cerebral blood flow responses.

Transcranial Doppler (TCD) could be used to evaluate the visually evoked cerebral blood flow responses (VEFRs) during graded visual cortex activity. The purpose of the study was to evaluate the effects of visual contrasts on VEFR. The records were made from 30 healthy volunteers aged 38.0 +/- 9.6 years. The stimulus was a black-and-white checkerboard with visual contrasts of 1%, 10% and 100%. The VEFRs were measured in the posterior cerebral artery using TCD. We found that the VEFRs at 100% visual contrast were 36% higher than those at 10% visual contrast (p < 0.01). The VEFRs at 10% visual contrast were 81% higher than those at 1% visual contrast (p < 0.01). The linear regression showed significant relationships between the visual contrast and the VEFR (r = 0.61, p < 0.01). We have concluded that TCD monitoring of VEFR detects the changes of the blood flow in the visual cortex and that TCD could allow an assessment of neurovascular coupling.

The relationship between visually evoked cerebral blood flow velocity responses and visual-evoked potentials.

A noninvasive assessment of neurovascular coupling would be of great importance. For this reason, we simultaneously studied graded responses of visually evoked cerebral blood flow (CBF) velocity responses (VEFR) and visual-evoked potentials (VEP) to visual contrasts. The records were made from 30 healthy volunteers aged 38.0 +/- 9.6 years. The stimulus was a black-and-white checkerboard with visual contrasts (VC) of 1%, 10%, and 100%. The VEFR were measured in the posterior cerebral artery using transcranial Doppler, and the VEP were recoded from the scalp from occipital leads. To test the relationship between the VEFR and the VEP, a linear regression analysis was performed. We found that the VEFR at 100% VC were 36% higher than those at 10% VC (P < 0.01). The VEFR at 10% VC were 81% higher than those at 1% VC (P < 0.01). The VEP at 100% VC were 76% higher than those at 10% VC (P < 0.01). The VEP at 10% VC were 184% higher than those at 1% VC (P < 0.01). The linear regression showed a significant, moderate association between the VEP and the VEFR (r = 0.66, P < 0.01). The analysis of the regression slopes (b = 0.48 in older subjects vs. b = 0.58 in younger subjects) between two different age subgroups (P < 0.01) did not show any significant difference (P = 0.035). We concluded that a simultaneous recording of VEFR and VEP to graded visual contrasts could allow an assessment of neurovascular coupling.

Autonomic nervous system and microvascular alterations in normotensives with a family history of hypertension.

Autonomic nervous system and microvascular alterations at pre-hypertensive stage of hypertension have still not been fully elucidated. We aimed at addressing central and local influences on microvascular reactivity at pre-hypertensive stage of hypertension. To that end, we studied microvascular reactivity in 59 normotensives with a family history of hypertension and 46 controls. We measured laser-Doppler flow on the finger nailfold skin in the resting condition, after an 8-min occlusion of digital arteries and during local nitroglycerin application. Finger pressure, pulse and ECG were monitored by a Finapres device. Heart rate power spectral analysis was performed using Fast Fourier transformation. Baroreflex sensitivity was estimated by the sequence method. Normotensives with a family history of hypertension showed higher systolic pressure, decreased high-frequency power of the heart rate variability spectrum and reduced baroreflex sensitivity in the resting condition as well as decreased fundamental frequency of laser-Doppler flow oscillations during nitroglycerin application. We conclude that normotensives with a family history of hypertension exhibit altered sympathovagal balance with decreased parasympathetic activity at the cardiac level as well as increased myogenic microvascular reactivity.

Effects of visual contrast on visual evoked potentials and Doppler signal.

We studied visually evoked cerebral blood flow responses (VEFR) and visual evoked potentials (VEP) to different visual contrasts and analysed the relationship between them. The records were made from 35 healthy volunteers aged 38.6 +/- 10.1 years. The stimulus was a black-and-white checkerboard with visual contrasts (VC) of 1%, 10% and 100%. The VEFR were measured in the posterior cerebral artery using transcranial Doppler, and the VEP were recorded from the occipital leads. We found the relationship between visual contrast and VEFR (r = 0.79, P < 0.01) as well as between visual contrast and VEP (r = 0.71, P < 0.01). We also found moderate association between the VEP and the VEFR (r = 0.69, P < 0.01). The analysis of the regression slopes between two different age subgroups (P < 0.01) did not show a significant difference (P = 0.020). We concluded that a simultaneous recording of VEFR and VEP to visual contrasts could allow an assessment of neurovascular coupling in humans.

Effect of regular physical training on cutaneous microvascular reactivity.

PURPOSE: To investigate whether regular intense physical training induces changes in microvascular reactivity of human glabrous and nonglabrous skin. METHODS: Subjects were physically trained competitive cyclists (N = 19) and age-matched sedentary controls (N = 20). We measured cutaneous microvascular blood flow on the dorsum of the hand (nonglabrous skin) and on the finger pulp (glabrous skin) using the laser-Doppler (LD) method. Endothelium-dependent vasodilation was assessed by an iontophoretic application of acetylcholine (ACh) on the dorsum of the hand and by an induction of postocclusive reactive hyperemia (PRH) on the finger pulp. Endothelium-independent vasodilation was assessed on the dorsum of the hand by iontophoretically applied sodium-nitroprusside (SNP). RESULTS: The ACh-evoked increase in LD flux (LDF) was significantly greater in the group of cyclists (7.5-fold +/- 0.5 increase) as compared with controls (5.9-fold +/- 0.5). We found no differences in the peak LDF during PRH, whereas the recovery time of PRH was significantly longer (241.5 +/- 21.6 s in trained vs 154.6 +/- 9.3 s in sedentary group) and the area under the PRH curve significantly larger in the group of trained subjects (19,066 +/- 2,653 PU x s in trained vs 12,168 +/- 864 PU x s in sedentary). In contrast, we found a significantly smaller response to SNP in the group of cyclists (6.2-fold +/- 0.5 increase) as compared with sedentary subjects (7.8-fold +/- 0.5 increase). CONCLUSION: The results of our study point to a greater vasodilator capacity of endothelium in glabrous as well as in nonglabrous skin in the group of physically trained subjects. In addition, our results indicate that regular physical activity also modifies the reactivity of vascular smooth muscle cells.

Autonomic nervous system activity in normotensive subjects with a family history of hypertension.

This study was designed to address alterations in autonomic nervous system activity in normotensive subjects with a family history of hypertension. We compared the autonomic nervous system activity in 59 normotensives with a family history of hypertension and 46 normotensives with no family history of hypertension. Skin blood flow was measured using laser-Doppler method on the nailfold skin in the resting condition, during systemic cooling and during upright tilting. Finger blood pressure, pulse and ECG were monitored by a finapres device. Heart rate, systolic pressure and microvascular flow power spectral analyses were performed using fast Fourier transformation. Baroreflex sensitivity was estimated with the sequence method. Compared to the control group, normotensives with a family history of hypertension showed significantly higher systolic pressure, decreased proportion and area of the high-frequency band of the heart rate variability power spectrum and reduced baroreflex sensitivity in the resting condition as well as a decreased proportion and area of the high-frequency band of the heart rate variability power spectrum during systemic cooling. We also proved a different time course of baroreflex sensitivity during upright tilting in the two groups. In contrast, we did not find any significant differences in the parameters of systolic pressure and microvascular variability power spectra between the two groups. Our results indicate that even normotensives with a family history of hypertension exhibit an increased ratio of sympathetic to parasympathetic activity at the cardiac level; however, they do not show any alteration of the vascular sympathetic reactivity.

The influence of brightness, colour and complexity on visual evoked doppler flow responses.

The purpose of this study was to evaluate specific influence of colour, brightness and complexity on visual evoked flow responses (VEFRs). A total of 31 healthy subjects aged 35.1 +/- 7.7 years participated in the study. Mean arterial velocity was measured in the right posterior cerebral artery (v(pca)) and in the left middle cerebral artery (v(mca)) by Multi-DopX4 (DWL). Simple-white (SW), red (R) and complex-checkerboard (C) stimuli were used. VEFRs were determined by the difference of the v(pca):v(mca) ratio before and after stimulation. The VEFRs of SW with brightness of 21.4 cd/m(2), 10.5 cd/m(2) and 2 cd/m(2) were 8.7 +/- 3.4%, 9.1 +/- 3.0% and 8.0 +/- 3.7%, respectively (p < 0.001). The VEFRs of R and C stimuli were 10.4 +/- 6.5% and 12.4 +/- 6.1%, respectively (p < 0.001). ANOVA for repeated measurements did not show significant variances (p = 0.295) between VEFRs of SW of different brightness, but variances between VEFRs of SW, R and C stimuli were significant (p < 0.001). We found significant differences between VEFRs of SW and of C stimuli (3.8 +/- 1.9%, p < 0.001), VEFRs of SW and of R stimuli (1.8 +/- 2.4%, p = 0.008) as well as between VEFRs of C and of R stimuli (2.0 +/- 2.5%, p = 0.010). We have concluded that SW, R and C stimuli have a specific influence on VEFRs. Brightness does not appear to affect VEFRs.

Role of alpha-adrenoceptors in the cutaneous postocclusive reactive hyperaemia.

Laser-Doppler (LD) flow measurements reveal typical flow oscillations in the descending part of the cutaneous postocclusive reactive hyperaemia (PRH). The origin of these oscillations is still poorly understood. We tested the hypothesis that the high frequency (HF) components within the frequency band 0.06-0.2 Hz are due to the local myogenic mechanism, whereas the low frequency (LF) components within frequency band 0.01-0.05 Hz reflect sympathetic vasomotor activity. LD flow was monitored on fingertips of 11 healthy volunteers before and after an 8-minute occlusion of digital arteries. We studied the effect of intradermal microinjection (1 µl) of α-antagonists (prazosine, yohimbine) and α-agonists (phenilephrine, clonidine) on PRH oscillations. We analysed the magnitude of peak flow and its duration and performed spectral power analysis to obtain fundamental HF and LF frequencies (defined as components with the highest amplitude in the part of the respective frequency band). The results (mean ± SE) for each substance were compared to the control values obtained after microinjection (1 µl) of 0.9% NaCl. The fundamental HF significantly decreased from 0.11 ± 0.008 Hz after an injection of saline solution to 0.08 ± 0.006 Hz after an application of antagonists (p<0.05). The local application of α-antagonists did not abolished HF oscillations what suggests that activity of local sympathetic nervous system is not essential in generation of these oscillations. However, the significant decrease of fundamental frequency in HF band after application of α-antagonists supports the hypothesis of their local origin and could be explained by the effect on pacemaker myogenic mechanism.