IMPAIRED MICROVASCULAR VASODILATOR RESERVE IN CHRONIC CIGARETTE SMOKERS : A Study of Post-occlusive Reactive Hyperemia in the Human Finger

Hashimoto, Haruhisa

doi:10.1253/jcj.58.29

Cited by 20 publications

(13 citation statements)

References 11 publications

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“…This sustained vasodilator response is mediated at least in part by nitric oxide, as it is inhibited by preventing NO formation in the skin (Kellogg et al 1999; Minson et al 2001). The finding that bretylium blocked nicotine‐induced attenuation of the sustained response suggests that this attenuation was mediated by enhanced noradrenergic neurotransmission rather than by the inhibition of endothelial NO release, a postulated mechanism in other vascular beds (Hashimoto, 1994; Habler et al 1999; Sarabi & Lind, 2000). The ability of sympathetic activity to modulate vascular axon reflex responses in skin is established (Hornyak et al 1990; Habler et al 1997).…”

Section: Discussionmentioning

confidence: 98%

“…On the other hand, prejunctional nAChRs facilitate noradrenaline (norepinephrine) release from sympathetic postganglionic nerves, a factor that could inhibit SkBF responses to local warming (Starke, 1977; Kristufek et al 1999). Nicotine may also affect the production of and responses to NO (Hashimoto, 1994; Sarabi & Lind, 2000; Gaenzer et al 2001). The effects of smoking on SkBF responses to local heating are unknown.…”

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confidence: 99%

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Nicotine increases initial blood flow responses to local heating of human non‐glabrous skin

Warner

Joyner

Charkoudian

2004

The Journal of Physiology

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Nicotine affects the regulation of skin blood flow (SkBF), but the mechanisms involved are not well understood. We tested the hypothesis that acute exposure to nicotine inhibits both the initial neurally mediated component and the later sustained component of SkBF responses to local heating of non-glabrous skin in humans. SkBF (measured by laser-Doppler) responses to local heating of forearm skin from 32 to 42• C were measured in 11 chronic smokers. Heating occurred at one site over 15 min (RAMP) and over 90 s (STEP) at another site, and was maintained for an additional 30 min. STEP heating was also applied to a site pretreated with bretylium via iontophoresis to inhibit noradrenergic neurotransmission. Responses were measured before and after acute administration of nicotine via cigarettes or nasal spray in two experimental sessions. Nicotine decreased resting skin blood flow (P < 0.05); this response was inhibited by bretylium. During RAMP, nicotine increased the initial SkBF at 42• C (by ∼12%, P < 0.05). For STEP, nicotine increased the initial peak response (by ∼25%, P < 0.05), and decreased the sustained plateau value (by ∼10%, P < 0.05). In skin pretreated with bretylium, the increase caused by nicotine in the initial peak value persisted, but the plateau value was not different from pre-nicotine. These data suggest that in abstinent cigarette smokers, nicotine augments initial responses to both gradual and rapid non-painful heating of non-glabrous skin by sensitizing the sensory nerves that mediate the axon reflex associated with rapid vasodilatation. In contrast, nicotine decreases SkBF responses to prolonged heating by activating noradrenergic nerves.

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Section: Discussionmentioning

confidence: 98%

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confidence: 99%

Nicotine increases initial blood flow responses to local heating of human non‐glabrous skin

Warner

Joyner

Charkoudian

2004

The Journal of Physiology

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“…PORH has been studied extensively in the past, and it is thought that the hyperaemic response involves endothelial, myogenic, metabolic, and physical mechanisms (Banitt et al, 1996;Beinder and Schlembach, 2001;Lombard and Duling, 1981) PORH can be used as an instrument to investigate microvascular function in a variety of vascular diseases. The method has been used to study the effect of diabetes (Yamamoto-Suganuma and Aso, 2009), heart failure (van Langen et al, 2001), peripheral vascular disease (Cheng et al, 2004), preeclampsia, (Beinder and Schlembach, 2001) and cigarette smoking (Hashimoto, 1994).…”

Section: Introductionmentioning

confidence: 99%

“…The techniques that have been used include those commonly used with isolated arteries, such as myography (Rogers and Sheriff, 2005) and intravital microscopy (Toth et al, 2007). In human studies, PORH has been measured by plethysmography techniques (Acree et al, 2007;Faizi et al, 2009), ultrasound (van Langen et al, 2001) and laser Doppler flowmetry (Beinder and Schlembach, 2001;Hashimoto, 1994;Thorfinn et al, 2007;Yamamoto-Suganuma and Aso, 2009). …”

Section: Introductionmentioning

confidence: 99%

Hyperaemic changes in forearm skin perfusion and RBC concentration after increasing occlusion times

Farnebo

Thorfinn

Henricson

et al. 2010

Microvascular Research

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“…The Speedwell Collaborative Heart Disease Study classified elevated fibrinogen and viscosity as high‐risk factors for smokers [13–15], but other authors found no such connection [6]. The more recent Edinburgh Artery Study confirmed increased viscosity, resulting from raised haematocrit and fibrinogen levels, to be the initiating factor in ischaemic heart disease and stroke [2, 16, 17]. The Edinburgh Artery Study [2] also stressed the need for controlled studies in the field of microcirculation.…”

Section: Introductionmentioning

confidence: 99%

Effects of cigarette smoking or nicotine replacement on cardiovascular risk factors and parameters of haemorheology

Haustein¹,

Krause²,

Haustein³

et al. 2002

Journal of Internal Medicine

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Objectives. Cigarette smoking causes cardiovascular (CV) disease, but the relative roles of nicotine and other components of tobacco smoke remain unclear. We investigated the effect of stopping smoking, by using nicotine replacement therapy (NRT), on haemorheology parameters. Design. Open, parallel-group trial (intervention group and control smokers). Setting. Clinic within university department of pharmacology. Subjects. One hundred and ninety-seven males, aged 25-45 years, smoking >20 cigarettes per day. Interventions. One hundred and sixty-four subjects were instructed to stop smoking and received NRT for 12 weeks and 33 acted as controls. After 12 weeks, NRT was discontinued, and all subjects were followed-up at 26 weeks. At the end of the study, the NRT group was divided into abstainers (self-reported, verified by exhaled carbon monoxide <10 ppm) and relapsers, who were unable to remain abstinent. Main outcome measures. Plasma viscosity, fibrinogen, erythrocyte deformability, reactive capillary blood flow, transcutaneous partial oxygen tension (tcpO 2 ) and haematocrit, assessed at 4, 8, 12, and 26 weeks. Results. After 6 months, plasma fibrinogen (9.95 vs. 8.24 lmol L -1 at baseline; P < 0.003), reactive capillary flow (t-p max : 9.3 vs. 11.2 s at baseline; P < 0.005), and tcpO 2 (50.4 vs. 34.9 mmHg at baseline; P < 0.0001) were significantly improved in abstainers, but changes in plasma viscosity and erythrocyte deformability were inconclusive. Other CV risk factors, such as haematocrit and white blood cell count, decreased to a greater extent in abstainers than in relapsers. Expired carbon monoxide concentrations reflected the changes in smoking and decreased in abstainers from 30.4 ppm at baseline to 4.2 ppm; P < 0.0001). Conclusions. Smoking cessation improved CV parameters, and use of nicotine medications did not negate these improvements.

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IMPAIRED MICROVASCULAR VASODILATOR RESERVE IN CHRONIC CIGARETTE SMOKERS : A Study of Post-occlusive Reactive Hyperemia in the Human Finger

Cited by 20 publications

References 11 publications

Nicotine increases initial blood flow responses to local heating of human non‐glabrous skin

Nicotine increases initial blood flow responses to local heating of human non‐glabrous skin

Hyperaemic changes in forearm skin perfusion and RBC concentration after increasing occlusion times

Effects of cigarette smoking or nicotine replacement on cardiovascular risk factors and parameters of haemorheology

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