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• W1991626398 abstract "The aim of this study was to compare local blood flow in psoriatic plaques before and after provocations known to alter cutaneous vascular resistance, in order to determine whether plaque hyperemia is caused by a failure of normal vascular control mechanisms. Cutaneous blood flow was recorded using a laser Doppler flowmeter over plaque skin (plaque site) and clinically normal skin (nonplaque site) on the opposite arm, at least 5 cm away from the nearest plaque. It is important to note that most of the laser Doppler signal comes from the subpapillary plexus of the skin and only a small portion (2%–10%) is produced by capillary blood flow. In the psoriatic plaques the basal flux was between nine and 13 times greater than nonplaque skin. The biologic zero (a signal independent of perfusion, which also persists after complete proximal arterial occlusion) was also significantly greater at plaque sites compared with nonplaque sites. Sympathetic and local vasoconstriction in psoriatic skin was shown to be intact and responses to vasodilator tests were likewise intact, i.e., there was no failure of response to normal vascular control mechanisms, albeit some quantitative differences. Tests of vasodilatation indicated that, although basal flux is high in plaque compared with nonplaque skin, arterioles supplying plaque skin can dilate further, i.e., lesional arterioles are not normally maximally dilated but have a basal constrictor tone. Interestingly, the red cell flux at maximum dilatation in nonplaque skin is less than even the basal flux in plaque skin. This means that in plaque skin either there are more arterioles than in nonplaque skin, or there is chronic, structural widening of the existing arterioles in plaque skin. The aim of this study was to compare local blood flow in psoriatic plaques before and after provocations known to alter cutaneous vascular resistance, in order to determine whether plaque hyperemia is caused by a failure of normal vascular control mechanisms. Cutaneous blood flow was recorded using a laser Doppler flowmeter over plaque skin (plaque site) and clinically normal skin (nonplaque site) on the opposite arm, at least 5 cm away from the nearest plaque. It is important to note that most of the laser Doppler signal comes from the subpapillary plexus of the skin and only a small portion (2%–10%) is produced by capillary blood flow. In the psoriatic plaques the basal flux was between nine and 13 times greater than nonplaque skin. The biologic zero (a signal independent of perfusion, which also persists after complete proximal arterial occlusion) was also significantly greater at plaque sites compared with nonplaque sites. Sympathetic and local vasoconstriction in psoriatic skin was shown to be intact and responses to vasodilator tests were likewise intact, i.e., there was no failure of response to normal vascular control mechanisms, albeit some quantitative differences. Tests of vasodilatation indicated that, although basal flux is high in plaque compared with nonplaque skin, arterioles supplying plaque skin can dilate further, i.e., lesional arterioles are not normally maximally dilated but have a basal constrictor tone. Interestingly, the red cell flux at maximum dilatation in nonplaque skin is less than even the basal flux in plaque skin. This means that in plaque skin either there are more arterioles than in nonplaque skin, or there is chronic, structural widening of the existing arterioles in plaque skin. arm dependency biologic zero core heat load cool reflex inspiratory gasp laser Doppler flow reactive hyperemia Microvascular abnormalities are a characteristic histopathologic feature of psoriasis. Both histologic and intravital capillaroscopic studies have shown elongation and tortuosity of the capillary loop within the papillary dermis (Mordovstev and Albanova, 1989Mordovstev V.N. Albanova V.I. Morphology of skin microvasculature in psoriasis.Am J Dermatopathol. 1989; 11: 33-42Crossref PubMed Scopus (34) Google Scholar;Bull et al., 1992Bull R.H. Bates D.O. Mortimer P.S. Intravital video-capillaroscopy for the study of the microcirculation in psoriasis.Br J Dermatol. 1992; 126: 436-445Crossref PubMed Scopus (80) Google Scholar). Morphometric analysis of the vascular changes in psoriasis has shown that there is an increase in the capillary mass, compared with normal skin, along with structural expansion of the capillaries within psoriatic lesions and to a lesser extent in clinically uninvolved skin in the same patients (Barton et al., 1992Barton S.P. Abdullah M.S. Marks R. Quantification of microvascular changes in the skin in patients with psoriasis.Br J Dermatol. 1992; 126: 569-574Crossref PubMed Scopus (62) Google Scholar). Other studies have demonstrated that the structural expansion and increased tortuosity of the dermal capillary loops occurs early in the progression of a lesion, before epidermal hyperplasia can be detected histologically or clinically (Pinkus and Mehregan, 1961Pinkus H. Mehregan A.H. The primary histologic lesion of seborrheic dermatitis and psoriasis.J Invest Dermatol. 1961; 46: 109-116Google Scholar;Telner and Fekete, 1961Telner P. Fekete Z. The capillary responses in psoriatic skin.J Invest Dermatol. 1961; 36: 225-230Abstract Full Text PDF PubMed Scopus (83) Google Scholar;Speight et al., 1993Speight E.L. Essex T.J.H. Farr P.M. The study of plaques of psoriasis using a scanning laser-Doppler velocimeter.Br J Dermatol. 1993; 128: 519-524Crossref Scopus (51) Google Scholar). Furthermore, when these structurally expanded capillaries are selectively destroyed with yellow light lasers, the psoriatic plaque clears. Patients responding to treatment with a pulsed dye laser can remain in remission for up to 13 mo at treatment sites (Zelickson and Mehregan, 1996Zelickson B.D. Mehregan D.A. Wendelschfer-Crabb G, Ruppman D, Cook A, O’Connell P, Kennedy WR. Clinical and histological evaluation of psoriatic plaques treated with a flashlamp pulsed dye laser.J Am Acad Dermatol. 1996; 35: 64-68Abstract Full Text PDF PubMed Scopus (72) Google Scholar). The tortuous, widened, elongated capillaries therefore play a central role in the pathogenesis of psoriasis and indeed they form one of the pathologic criteria for diagnosis. The expanded capillary bed in psoriasis has an increased blood flow. Blood flow is principally determined, however, by feeding resistance vessels (arterioles and terminal arteries), concerning which little is known in psoriasis. Our aim was to compare blood flow before and after provocations that alter cutaneous vascular resistance, in order to test whether the increased flow was caused by a failure of normal vascular control processes in plaque skin. Clinically uninvolved skin in the same subject served as a control. Vascular control was investigated by applying a range of provocations previously shown in our laboratory to produce reliable alterations in cutaneous vascular resistance in healthy subjects (Stanton et al., 1995Stanton A.W.B. Levick J.R. Mortimer P.S. Assessment of noninvasive tests of cutaneous vascular control in the forearm using a laser Doppler meter and a Finapres blood pressure monitor.Clin Autonomis Res. 1995; 5: 37-47Crossref PubMed Scopus (21) Google Scholar). These tests have also been used to assess the control of blood flow in the arms of women with chronic postmastectomy edema (Stanton et al., 1996Stanton A.W.B. Levick J.R. Mortimer P.S. Cutaneous vascular control in the arms of women with postmastectomy oedema.Exp Physiol. 1996; 81: 447-464Crossref PubMed Scopus (26) Google Scholar). The provocations and the accepted physiologic mechanisms of regulation concerned are as follows: reactive hyperemia (RH; locally mediated vasodilatation), core heat load (sympathetically mediated vasodilatation), inspiratory gasp and cool reflex (CR; both sympathetically mediated vasoconstriction), and arm dependency (AD; locally mediated vasoconstriction). Cutaneous blood flow was recorded using a laser Doppler flowmeter. The cutaneous circulation of the hand/finger (acral skin) is dominated by arteriovenous anastomoses under sympathetic vasoconstrictor control with a high degree of basal tone. The rest of the arm (nonacral skin), however, apparently lacks such anastomoses and has absent or only slight basal sympathetic vasoconstrictor tone. Therefore, as the control of the cutaneous circulation differs dramatically between these sites, our investigations were limited to the forearm and elbow. Furthermore, the original work in our laboratory to validate the provocation tests, in healthy subjects and in disease, was originally performed on the forearm (Stanton et al., 1995Stanton A.W.B. Levick J.R. Mortimer P.S. Assessment of noninvasive tests of cutaneous vascular control in the forearm using a laser Doppler meter and a Finapres blood pressure monitor.Clin Autonomis Res. 1995; 5: 37-47Crossref PubMed Scopus (21) Google Scholar;Stanton et al., 1996Stanton A.W.B. Levick J.R. Mortimer P.S. Cutaneous vascular control in the arms of women with postmastectomy oedema.Exp Physiol. 1996; 81: 447-464Crossref PubMed Scopus (26) Google Scholar). Forearm plaques were also selected for comfort and convenience. Nine white, European patients (four men and five women), aged 25–67 y (mean 45 y), with mild to moderate plaque psoriasis participated in this study. Approval was obtained from our Local Ethics Committee and informed consent given. Topical therapies were stopped 3 wk prior to the investigation. Phototherapy (psoralen ultraviolet A and ultraviolet B) had been discontinued for at least 3 mo prior to the study and none of the patients was on systemic therapy. No descaling treatment was applied prior to measurements. The use of simple emollients was permitted throughout. All the patients were otherwise healthy and normotensive. Subjects emptied their bladders and sat with their arms and legs exposed in a temperature-controlled laboratory (25.0 ± 0.6°C; mean ± SD). The forearms were supported by armrests at heart level and subjects acclimatized for 20 min while the probes were attached. Laser Doppler red cell flux (LDF, Moor Instruments MBF3D, Axminster, Devon, U.K.) was recorded from psoriatic plaques on the forearm or elbow (plaque site) and from clinically uninvolved skin at an equivalent site on the opposite limb (nonplaque site). Non-plaque skin sites were selected for study at least 5 cm from the edge of the nearest plaque. LDF output was set at 100 arbitrary units (AU) equivalent to 2.5 V. The time constant was 1.0 s. Before the start of each experiment, the laser Doppler probes (P1) were placed on a white plastic surface and the instrumental zero recorded. This was 0.03 AU and was ignored when recording LDF. Skin temperatures (Tsk) were recorded from each forearm (Tele-thermometer, Yellow Springs Instruments, OH). Core temperature (Tc) was recorded sublingually using a clinical thermometer. In the previous studies by our group (Stanton et al., 1995Stanton A.W.B. Levick J.R. Mortimer P.S. Assessment of noninvasive tests of cutaneous vascular control in the forearm using a laser Doppler meter and a Finapres blood pressure monitor.Clin Autonomis Res. 1995; 5: 37-47Crossref PubMed Scopus (21) Google Scholar, Stanton et al., 1996Stanton A.W.B. Levick J.R. Mortimer P.S. Cutaneous vascular control in the arms of women with postmastectomy oedema.Exp Physiol. 1996; 81: 447-464Crossref PubMed Scopus (26) Google Scholar), local vascular resistance was calculated as digital blood pressure/red cell flux. Although small, transient changes in blood pressure were evoked by some of the tests, the red cell flux and resistance changed in parallel. In this study therefore changes in red cell flux are taken to reflect changes in local vascular resistance. Tests were performed in sequence as outlined below (see Table 1). The basal flux was recorded for 20 s before each test.Table 1Summary of the tests of forearm and elbow cutaneous vascular control in the sequence in which they were performedTestsProposed mechanismReference1 and 6. BZNon-flow related signalColantuoni et al., 1993Colantuoni A. Bertuglia S. Intaglietta M. Biological zero of laser Doppler fluxmetry: microcirculatory correlates in the hamster cheek pouch during flow and no flow conditions.Int J Microcirc. 1993; 13: 125-136PubMed Google Scholar,Wahlberg et al., 1992Wahlberg E. Olofsson L. Swedenborg J. Fagrell B. Effects of local hyperemia and edema on the biological zero in laser Doppler fluxmetry.Int J Microcirc: Clin Exp. 1992; 11: 157-165PubMed Google ScholarRHMyogenic and/or local vasodilator chemical factorsShepherd, 1963Shepherd J.T. Physiology of the Circulation in Human Limbs in Health and Disease. W.B. Saunders, Philadelphia. PA1963: 127-138Google Scholar2. IGIncreased sympathetic vasoconstrictor nerve activityBrowse and Hardwick, 1969Browse N.L. Hardwick P.J. The deep breath–venoconstriction reflex.Clin Sci. 1969; 37: 125-135PubMed Google Scholar3. ADLocally derived vasoconstriction mediated by a myogenic or local axon reflexHassan and Tooke, 1988Hassan A.A.K. Tooke J.E. Mechanism of the postural vasoconstrictor response in the human foot.Clin Sci. 1988; 75: 379-387Crossref PubMed Scopus (106) Google Scholar,Levick and Michel, 1978Levick J.R. Michel C.C. The effects of position and skin temperature on the capillary pressures in the fingers and toes.J Physiol. 1978; 274: 97-109Crossref PubMed Scopus (164) Google Scholar,Henriksen, 1976Henriksen O. Local nervous mechanism in regulation of blood flow in human subcutaneous tissue.Acta Physiol Scand. 1976; 97: 385-391Crossref PubMed Scopus (56) Google Scholar4. CRIncreased sympathetic vasoconstrictor nerve activityPickering, 1933Pickering G.W. The vasomotor regulation of heat loss from the human skin in relation to external temperature.Heart. 1933; 16: 115-135Google Scholar5. CHLIncreased sympathetic vasodilator nerve activityPickering, 1933Pickering G.W. The vasomotor regulation of heat loss from the human skin in relation to external temperature.Heart. 1933; 16: 115-135Google Scholar Open table in a new tab The BZ flux signal is the signal that persists after complete proximal arterial occlusion. It is not related to tissue perfusion (Colantuoni et al., 1993Colantuoni A. Bertuglia S. Intaglietta M. Biological zero of laser Doppler fluxmetry: microcirculatory correlates in the hamster cheek pouch during flow and no flow conditions.Int J Microcirc. 1993; 13: 125-136PubMed Google Scholar) and its origin remains obscure. BZ flux was subtracted from all flux readings as recommended by others (Wahlberg et al., 1992Wahlberg E. Olofsson L. Swedenborg J. Fagrell B. Effects of local hyperemia and edema on the biological zero in laser Doppler fluxmetry.Int J Microcirc: Clin Exp. 1992; 11: 157-165PubMed Google Scholar;Colantuoni et al., 1993Colantuoni A. Bertuglia S. Intaglietta M. Biological zero of laser Doppler fluxmetry: microcirculatory correlates in the hamster cheek pouch during flow and no flow conditions.Int J Microcirc. 1993; 13: 125-136PubMed Google Scholar). To measure BZ, arterial blood flow into the arm was arrested for 2 min by placing a sphygmomanometer cuff around the upper arm and inflating it to 200 mmHg. The cuff was then rapidly deflated by abruptly breaking the connection and the subsequent peak RH recorded. RH is a vasodilator response mediated by myogenic and/or local chemical factors (Shepherd, 1963Shepherd J.T. Physiology of the Circulation in Human Limbs in Health and Disease. W.B. Saunders, Philadelphia. PA1963: 127-138Google Scholar). Time to reach the peak response for RH was measured from the moment the cuff was released to the mid-point of the peak response. The area under the curve was also calculated. This gives a measure of the cumulative response to the RH test as it takes into account the duration of the response along with the magnitude of the increase in LDF. The area measured was that enclosed by the flux signal recorded during the response and the baseline flux derived from that recorded prior to the BZ test. BZ and RH were performed on each arm in turn at the start (BZ1 and RH1) and end (BZ2 and RH2) of the experiment, immediately after the core heat load. Sharp, deep inspiration results in a reflex cutaneous vasoconstriction mediated by increased activity in sympathetic vasoconstrictor nerves (Browse and Hardwick, 1969Browse N.L. Hardwick P.J. The deep breath–venoconstriction reflex.Clin Sci. 1969; 37: 125-135PubMed Google Scholar). Subjects were asked to inhale deeply and rapidly, hold their breath for 5 s and then quickly exhale and breathe normally. This was performed three times, at 1 min intervals. Lowering the arm below heart level elicits the veni-arteriolar response, a locally derived vasoconstrictor response mediated by a myogenic or local axon reflex (Henriksen, 1976Henriksen O. Local nervous mechanism in regulation of blood flow in human subcutaneous tissue.Acta Physiol Scand. 1976; 97: 385-391Crossref PubMed Scopus (56) Google Scholar;Levick and Michel, 1978Levick J.R. Michel C.C. The effects of position and skin temperature on the capillary pressures in the fingers and toes.J Physiol. 1978; 274: 97-109Crossref PubMed Scopus (164) Google Scholar;Hassan and Tooke, 1988Hassan A.A.K. Tooke J.E. Mechanism of the postural vasoconstrictor response in the human foot.Clin Sci. 1988; 75: 379-387Crossref PubMed Scopus (106) Google Scholar). Each arm was lowered in turn and allowed to hang in the dependent position for 2 min, such that the recording site and attached laser Doppler probe was 25–30 cm below heart level. The CR is a reflex vasoconstrictor response mediated by increased activity in sympathetic vasoconstrictor nerves (Pickering, 1933Pickering G.W. The vasomotor regulation of heat loss from the human skin in relation to external temperature.Heart. 1933; 16: 115-135Google Scholar). Subjects immersed both feet in water at 15°C for 1 min. The feet were then transferred to water at 33°C (thermoneutral) for 2 min before the test was repeated. The temperature of the water for the CR test was maintained at 15°C because lower temperatures may activate pain fibers, with a resultant reflex rise in blood pressure. Indirect heating of the body results in a reflex vasodilatation in the skin mediated by increased activity of sympathetic vasodilator nerves (Pickering, 1933Pickering G.W. The vasomotor regulation of heat loss from the human skin in relation to external temperature.Heart. 1933; 16: 115-135Google Scholar). After removal of the feet from the cool water (CR2), subjects were asked to place both legs, to just below the level of the knee, into a deep container of water at 45°C. In order to minimize transient movement artifacts in the LDF recording patients were assisted with this maneuver. The temperature of the water was maintained by a Thermocirculator (Harvard Instruments, Edenbridge, Kent, U.K.). The legs were heated in this manner for 30 min. In the first five subjects, the core temperature was slow to rise. Therefore, for the last four individuals, a domestic electric blanket draped around the shoulders was used to provide additional heating (Stanton et al., 1995Stanton A.W.B. Levick J.R. Mortimer P.S. Assessment of noninvasive tests of cutaneous vascular control in the forearm using a laser Doppler meter and a Finapres blood pressure monitor.Clin Autonomis Res. 1995; 5: 37-47Crossref PubMed Scopus (21) Google Scholar). By the end of the 30 min period Tc had risen by 0.4 ± 0.2°C. Tsk had increased by 0.3 ± 0.4°C on the nonplaque forearm and by 0.6 ± 0.6°C on the plaque forearm. This difference in Tsk between the arms did not quite reach conventional significance, p = 0.06 where n = 9. Results are presented as mean ± SD. Paired analysis was performed using the Student’s t test. Where results were skewed, logarithmic transformations were calculated (denoted by an asterisk in the text when used) in order to normalize their distribution. Probability values of 0.05 or less were taken as significant differences. Unless otherwise indicated in the text, n = 9 for RH1 and AD and n = 8 for RH2, CHL, and CR1–2. After values were corrected for the BZ, the ratio of the red cell flux at the plaque site to the nonplaque site at the beginning of the protocol was 13.1 ± 10.3. The mean red cell flux in plaques was 200.5 ± 134.6 AU (n = 9) and in nonplaque sites was 18.5 ± 13.1 AU (n = 9). This difference in red cell flux between the two sites was significant, p < 0.01. When measured again at the end of the experiment the ratio of the red cell flux at the plaque site to the nonplaque site was 9.3 ± 8.4. The mean red cell flux in plaques was 121.7 ± 101.5 AU (n = 8) and in nonplaque sites was 15.1 ± 10.0 AU (n = 8). This difference in red cell flux between the two sites was also significant, p = 0.01. BZ at the nonplaque sites was 3.9 ± 0.63 AU and at the plaque sites was 5.7 ± 3.5 AU, where n = 17 (BZ1 and BZ2 combined). This difference in BZ between the two sites was significant, p = 0.04. The BZ1 was then subtracted from all the remaining results (below) as recommended by others (Wahlberg et al., 1992Wahlberg E. Olofsson L. Swedenborg J. Fagrell B. Effects of local hyperemia and edema on the biological zero in laser Doppler fluxmetry.Int J Microcirc: Clin Exp. 1992; 11: 157-165PubMed Google Scholar;Colantuoni et al., 1993Colantuoni A. Bertuglia S. Intaglietta M. Biological zero of laser Doppler fluxmetry: microcirculatory correlates in the hamster cheek pouch during flow and no flow conditions.Int J Microcirc. 1993; 13: 125-136PubMed Google Scholar). Results for the RH responses are illustrated in Figure 1. Both baseline and maximal flux are greater in the plaque than the nonplaque sites. When the ratio of maximum to baseline responses are calculated, however, the nonplaque site demonstrates a greater magnitude of change (Table 2).Table 2Summary of red cell flux measured during the RH response at the beginning (RH1) and end (RH2) of the protocolaBasal flux was recorded for 20 s prior to the BZ. A blood pressure cuff was then placed around the upper arm and a pressure of 200 mmHg exerted for 2 min (BZ). The cuff was then rapidly deflated and the subsequent peak RH response recorded. Results are presented as mean ± SD and are corrected for BZ.Non-plaque (NP)Plaque (P)Ratio of P/NPp value for P versus NPRH1 Basal flux (AU)18.5 ± 13.1200.5 ± 134.613.1 ± 10.3<0.01 Maximum flux (AU)82.3 ± 35.3319.4 ± 165.04.3 ± 2.60.001 Ratio of maximum flux/basal flux5.1 ± 2.01.9 ± 0.74—<0.001bOwing to skewing of the results for ratios, these p values are calculated after logarithmic transformations (n = 9 for RH1 and n = 8 for RH2). p value for maximum versus basal response<0.001<0.001<0.001bOwing to skewing of the results for ratios, these p values are calculated after logarithmic transformations (n = 9 for RH1 and n = 8 for RH2).—RH2 Basal flux (AU)32.2 ± 47.3175.0 ± 108.59.4 ± 6.70.001 Maximum flux (AU)85.8 ± 64.0318.2 ± 200.85.3 ± 4.8<0.01 Ratio of maximum flux/basal flux4.6 ± 3.02.5 ± 1.4—0.05 bOwing to skewing of the results for ratios, these p values are calculated after logarithmic transformations (n = 9 for RH1 and n = 8 for RH2). p value for maximum versus basal response<0.010.010.05bOwing to skewing of the results for ratios, these p values are calculated after logarithmic transformations (n = 9 for RH1 and n = 8 for RH2).—a Basal flux was recorded for 20 s prior to the BZ. A blood pressure cuff was then placed around the upper arm and a pressure of 200 mmHg exerted for 2 min (BZ). The cuff was then rapidly deflated and the subsequent peak RH response recorded. Results are presented as mean ± SD and are corrected for BZ.b Owing to skewing of the results for ratios, these p values are calculated after logarithmic transformations (n = 9 for RH1 and n = 8 for RH2). Open table in a new tab Time to attain peak response at the start of the experiment was 8.8 ± 2.5 s at the nonplaque site and 22.0 ± 10.9 s at the plaque site. This difference in times between the two sites is significant, p < 0.01. Values were similar from a vasodilated baseline, namely 11.0 ± 5.2 s at the nonplaque site and 19.0 ± 5.2 s at the plaque site. Once again the difference in time to attain the peak response between the two sites is significant, p = 0.02. Therefore, plaque skin takes significantly longer to attain the peak response than nonplaque skin. At the start of the experiment the area under the hyperemia curve was 1712.7 ± 1245.5 AU s at the nonplaque site and 4659.0 ± 2224.0 AU s at the plaque site. The difference in area under the curve between the two sites is significant, p < 0.01. At the end of the protocol area under the curve at the control site was 1108.2 ± 1100.8 AU s and at the plaque site was 3685.5 ± 1201.2 AU s. Again there was a significant difference in area under the curve between the nonplaque and plaque sites, p < 0.01. Figure 2 demonstrates an RH response as recorded by the laser Doppler. All three inspirations were associated with a fall in red cell flux (Figure 3), although in all cases flux rose transiently before falling. The reduction in flux was significant for each of the three inspirations, in both the nonplaque and plaque sites. When ratios of minimum to basal flux were analyzed, the ratio was significantly smaller for nonplaque skin (0.43 ± 0.27) than plaque skin (0.59 ± 0.13) in IG1, *p = 0.04. It was not significantly different for IG2, where the ratio at the nonplaque site was 0.55 ± 0.34 and at the plaque site was 0.67 ± 0.18, *p = 0.07, or for IG3 where the ratio at the nonplaque site was 0.58 ± 0.24 and at the plaque site was 0.67 ± 0.18, *p = 0.2. When the results for all three experiments were pooled (Table 3), however, the ratio of minimum to basal flux was significantly smaller for nonplaque skin (0.52 ± 0.28) than plaque skin (0.64 ± 0.16), *p = 0.001.Table 3Summary of red cell flux measured during the inspiratory gasp responses (IG1–3)aBasal flux was recorded for 20 s prior to the test. Subjects were then asked to inhale deeply and rapidly, hold their breath for 5 s and then quickly exhale and breathe normally. This resulted in a fall in flux. The minimum response was taken as the lowest point of the trough generated. Results, presented as mean ± SD, are pooled from three independent experiments and are all corrected for BZ.Non-plaque (NP)Plaque (P)Ratio of P/NPp value for P versus NPBasal flux (AU)19.0 ± 13.3188.8 ± 113.212.2 ± 8.5<0.001Minimum flux (AU)8.8 ± 6.1114.1 ± 61.720.8 ± 20.8<0.001Ratio of minimum flux/basal flux0.52 ± 0.280.64 ± 0.16—0.001bOwing to skewing of the result for ratios, these p values are calculated after logarithmic transformations (n = 24).p value for minimum versus basal response<0.001<0.0010.001bOwing to skewing of the result for ratios, these p values are calculated after logarithmic transformations (n = 24).—a Basal flux was recorded for 20 s prior to the test. Subjects were then asked to inhale deeply and rapidly, hold their breath for 5 s and then quickly exhale and breathe normally. This resulted in a fall in flux. The minimum response was taken as the lowest point of the trough generated. Results, presented as mean ± SD, are pooled from three independent experiments and are all corrected for BZ.b Owing to skewing of the result for ratios, these p values are calculated after logarithmic transformations (n = 24). Open table in a new tab In all three tests, there was no significant difference in the time to attain the maximum response for nonplaque and plaque sites. For IG1 this was 8.0 ± 3.1 s at the nonplaque site and 7.9 ± 2.9 s at the plaque site, p = 0.9. For IG2 the nonplaque site took 8.1 ± 2.8 s to reach the peak response and the plaque site took 7.7 ± 2.2 s, p = 0.4. In IG3 the nonplaque site took 9.7 ± 4.6 s and the plaque site took 7.4 ± 1.9 s, p = 0.2. Following an initial, brief rise in red cell flux (a movement artifact), flux fell and stabilized at a level below baseline (Figure 4). Basal red cell flux was 17.0 ± 10.6 AU at the nonplaque site and 192.5 ± 115.9 AU at the plaque site. The reduced flux at the nonplaque site was 7.4 ± 6.0 AU and 116.0 ± 102.9 AU at the plaque site. The reduction in flux at both the nonplaque and plaque sites was significant (p < 0.01 at the nonplaque site and at the plaque site). Ratios of the reduced, dependent flux to basal flux were calculated for both nonplaque (0.42 ± 0.22) and plaque sites (0.55 ± 0.19). The ratio was significantly smaller at the nonplaque site, *p = 0.03. Initial movement artifacts were ignored. Thereafter, the CR caused a fall in the red cell flux to below baseline. The results of the response are illustrated in Figure 5. When ratios of minimum to basal flux for nonplaque and plaque sites were compared, these were not significantly different in both CR1 and CR2. For CR1, the ratio at the nonplaque site was 0.56 ± 0.29 and the plaque site was 0.63 ± 0.19, *p = 0.3. For CR2 the ratio at the nonplaque site was 0.62 ± 0.29 and the plaque site was 0.61 ± 0.19, *p = 0.4. When the results for both experiments were pooled, once again the ratio of minimum to basal flux was not significantly different between the two sites (Table 4).Table 4Summary of red cell flux measured during the CR responses (CR1–2)Non-plaque (NP)Plaque (P)Ratio of P/NPp value for P versus NPBasal flux (AU)15.9 ± 11.5160.8 ± 106.413.5 ± 11.6<0.001Minimum flux (AU)67.7 ± 5.488.4 ± 57.819.5 ± 19.1<0.001Ratio of minimum flux/basal flux0.59 ± 0.280.62 ± 0.19—0.16aOwing to skewing of the results for ratios, these p values are calculated after logarithmic transformations (n = 16).p value for minimum versus basal response0.020.0010.16aOwing to skewing of the results for ratios, these p values are calculated" @default.
• W1991626398 created "2016-06-24" @default.
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• W1991626398 date "1999-07-01" @default.
• W1991626398 modified "2023-10-09" @default.
• W1991626398 title "Control of Cutaneous Blood Vessels in Psoriatic Plaques" @default.
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• W1991626398 doi "https://doi.org/10.1046/j.1523-1747.1999.00638.x" @default.
• W1991626398 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10417631" @default.
• W1991626398 hasPublicationYear "1999" @default.
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