Acute effect of cigarette smoking on the coronary circulation: Constriction of epicardial and resistance vessels

Quillen, James E.; Rossen, James D.; Oskarsson, Helgi; Minor, Robert L.; López, J. Antonio G.; Winniford, Michael D.

doi:10.1016/0735-1097(93)90170-6

Cited by 184 publications

(76 citation statements)

References 36 publications

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“…The present study was conducted under wellcontrolled in vitro conditions, excluding platelet-related phenomena as well as CNS-mediated e ects of nicotine. There was a tendency for an increase in coronary vascular resistance by nicotine in reperfused ischaemic hearts but not in nonischaemic preparations, con®rming in vivo data on increase in coronary vessel tone by nicotine in patients su ering from coronary artery disease (Quillen et al, 1993).…”

Section: Discussionmentioning

confidence: 58%

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Schrör

Zimmermann

Tannhäuser

1998

British J Pharmacology

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1 To study the e ect of nicotine on the severity of experimental myocardial ischaemia, Langendor hearts of rabbits (n=7 ± 12 per group) were subjected to 2 h of low-¯ow ischaemia followed by 1 h of reperfusion. 2 Infusion of nicotine (100 ng ml 71 ) caused only minor changes in non-ischaemic conditions but a signi®cant (P50.05) increase in end-diastolic pressure (LVEDP), loss of creatine kinase (CK) and troponin (TnT) as well as increase in noradrenaline (NA) over¯ow in reperfused ischaemic hearts. 3 RT ± PCR was done on total RNA for mRNA expression of the constitutive (COX-1) and inducible cyclooxygenase (COX-2). There was no COX-2 in non-ischaemic hearts but a signi®cant expression in ischaemia (n=5) which was further increased by nicotine. These data were con®rmed at the protein level by Western blotting and additionally shown that COX-1 remained unchanged. 4 There was a marked increase in prostacyclin (PGI 2 ) and a 2 fold increase in NA over¯ow which were both stimulated by nicotine. 5 The aggravating e ects of nicotine on myocardial ischaemia (CK release) as well as the expression of COX-2 mRNA were prevented by pretreatment with the b-blocker pindolol (1 mM). 6 The data demonstrate marked deleterious actions of nicotine in reperfused ischaemic hearts. These actions are probably related to the increase in catecholamine over¯ow, are b-receptor-mediated and involve enhanced gene expression of COX-2.

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Section: Discussionmentioning

confidence: 58%

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Schrör

Zimmermann

Tannhäuser

1998

British J Pharmacology

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“…35 There are many potential mechanisms by which chronic cigarette smoke may influence choroidal vasculature. Cigarette smoke contains a myriad of potential toxic and systemic vasoconstrictive substances [36][37][38] including nicotine. 39,40 Experimental evidence indicates that smoking induces multiple acute influences on cerebral vasculature, with vasoconstriction predominating during chronic Figure 2 Comparison of mean macular choroidal thickness (CT) among smoking categories.…”

Section: Discussionmentioning

confidence: 99%

Smoking and choroidal thickness in patients over 65 with early-atrophic age-related macular degeneration and normals

Sigler

Randolph

Calzada

et al. 2014

Eye

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Objective To compare macular choroidal thickness between cigarette smokers, those with a history of smoking, and nonsmokers in patients over 65 years of age with earlyatrophic age-related macular degeneration (AMD) and normals. Methods Prospective, consecutive, observational case series. Enhanced depth imaging spectral domain optical coherence tomography 12-line radial scans were performed and choroidal thickness manually quantified at 84 points in the central 3 mm of the macula. Data of normals, soft drusen alone, and soft drusen with additional features of early AMD were compared. A multivariate analysis of variance (MANOVA) model, controlling for age, was constructed to evaluate the effect of smoking history and AMD features on choroidal thickness. Results A history of smoking was significantly associated with a thinner choroid across all patients via logistic regression (P ¼ 0.004; O.R. ¼ 12.4). Mean macular choroidal thickness was thinner for smokers (148±63 mm) than for nonsmokers (181±65 mm) among all diagnosis categories (P ¼ 0.003). Subgroup analysis of patients with AMD features revealed a similar decreased choroidal thickness in smokers (121 ± 41 mm) compared with nonsmokers (146 ± 46 mm, P ¼ 0.006). Bivariate analysis revealed an association between increased pack-years of smoking and a thin choroid across all patients (Po0.001) and among patients with features of early AMD (Po0.001). Both the presence of features of macular degeneration (Po0.001) and a history of smoking (P ¼ 0.024) were associated with decreased choroidal thickness in a MANOVA model. ConclusionChronic cigarette smoke exposure may be associated with decreased choroidal thickness. There may be an anatomic sequelae to chronic tobacco smoke exposure that underlies previously reported AMD risk.

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“…6) Habitual cigarette smoking is one of the risk factors for cardiovascular diseases, cerebral stroke, vasospasm after subarachnoid hemorrhage, and so on. 21,24) Smoking also seems to be a prospective risk factor for incident cognitive impairment. 2) The mechanism by which smoking contributes to such diseases is not clearly understood.…”

Section: Introductionmentioning

confidence: 99%

Effects of Habitual Cigarette Smoking on Higher Cortical Function in Patients With Unruptured Cerebral Aneurysms.

Fukunaga¹,

Kawase²,

Kashima

et al. 2002

Neurol. Med. Chir.(Tokyo)

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Postoperative changes in higher cortical function and cerebral blood flow (CBF) were investigated in patients with unruptured cerebral aneurysms to assess the effect of habitual smoking on the known transient changes after aneurysm surgery. Fifty-six adults with unruptured cerebral aneurysms, including 11 heavy smokers (smoking index »600) and 45 non-smokers, were evaluated using three neuropsychological examinations, the Mini-Mental State Examination, the Maze test, and the Kana-hiroi test, and single photon emission computed tomography to measure CBF before and after surgery. Neuropsychological changes were assessed by reliable change indices to take into account the practice effects. The scores of at least one examination decreased in 15 of 56 patients 1 month after surgery. On the Maze test, five of 11 heavy smokers and five of 45 non-smokers deteriorated after surgery, showing a significant difference (p ＝ 0.018). The CBF in heavy smokers often decreased after surgery, but there was no statistically significant difference in logistic regression. Three months after surgery, the neuropsychological scores of 13 of the 15 deteriorated patients recovered to the preoperative level. Higher cortical function in heavy smokers with unruptured cerebral aneurysms often decreases transiently after operation, compared to non-smokers. Therefore, surgery planning for heavy smokers with unruptured cerebral aneurysms should consider this outcome.

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Acute effect of cigarette smoking on the coronary circulation: Constriction of epicardial and resistance vessels

Cited by 184 publications

References 36 publications

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Smoking and choroidal thickness in patients over 65 with early-atrophic age-related macular degeneration and normals

Effects of Habitual Cigarette Smoking on Higher Cortical Function in Patients With Unruptured Cerebral Aneurysms.

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