Short-Term Cardiovascular Effects of E-Cigarettes: Influence of Device Power

Author(s):  
2010 ◽  
Vol 298 (2) ◽  
pp. H406-H414 ◽  
Author(s):  
D. M. Sartor ◽  
A. J. M. Verberne

Gastric-derived leptin affects satiety and gastrointestinal function via vagal mechanisms and has been shown to interact with the gut hormone cholecystokinin (CCK). CCK selectively inhibits splanchnic sympathetic nerve discharge (SND) and the activity of a subset of presympathetic vasomotor neurons in the rostroventrolateral medulla (RVLM). The present study sought to examine the effects of gastric leptin on arterial pressure (AP), heart rate (HR), SND, and RVLM neuronal activity to determine whether its effects on cardiovascular regulation are dependent on CCK1 receptors and vagal afferent transmission. To mimic gastric leptin, leptin (15–30 μg/kg) was administered close to the coeliac artery in anesthetized, artificially ventilated Sprague-Dawley rats. Within 5 min, leptin selectively decreased the activity of RVLM neurons also inhibited by CCK (−27 ± 4%; P < 0.001; n = 15); these inhibitory effects were abolished following administration of the CCK1 receptor antagonist lorglumide. Leptin significantly decreased AP and HR (−10 ± 2 mmHg, P < 0.001; and −8 ± 2 beats/min, P < 0.01; n = 35) compared with saline (−1 ± 2 mmHg, 3 ± 2 beats/min; n = 30). In separate experiments, leptin inhibited splanchnic SND compared with saline (−9 ± 2% vs. 2 ± 3%, P < 0.01; n = 8). Bilateral cervical vagotomy abolished the sympathoinhibitory, hypotensive, and bradycardic effects of leptin ( P < 0.05; n = 6). Our results suggest that gastric leptin may exert acute sympathoinhibitory and cardiovascular effects via vagal transmission and CCK1 receptor activation and may play a separate role to adipose leptin in short-term cardiovascular regulation.


2018 ◽  
Vol 4 (4) ◽  
Author(s):  
Gunther Neumayr ◽  
Peter Lechleitner

2004 ◽  
Vol 20 (4) ◽  
pp. 203-208 ◽  
Author(s):  
Bruno Baldaro ◽  
Giovanni Tuozzi ◽  
Maurizio Codispoti ◽  
Ornella Montebarocci ◽  
Francesco Barbagli ◽  
...  

2015 ◽  
Vol 35 (2) ◽  
pp. 829-840 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Priya Yuvaraju ◽  
Sumaya Beegam ◽  
Badreldin H Ali

Background/Aim: Water-pipe smoking (WPS) has acquired worldwide popularity, and is disseminating particularly rapidly in Europe and North America. However, little is known about the short-term cardiovascular effects of WPS. Methods: Presently, we assessed the short-term cardiovascular effects of nose-only exposure to mainstream WPS in BALB/c mice for 30 min/day for 5 consecutive days. Control mice were exposed to air. At the end of the exposure period, several cardiovascular endpoints were measured. Results: WPS did not affect the number of leukocytes and the plasma concentrations of C-reactive protein, tumor necrosis factor α (TNFα) and interleukin-6 (IL-6). Likewise, plasma levels of lipid peroxidation (LPO), reduced glutathione (GSH) and catalase were not affected by WPS. By contrast, WPS aggravated in vivo thrombosis by shortening the thrombotic occlusion time in pial arterioles and venules. The number of circulating platelets was reduced by WPS suggesting the occurrence of platelet aggregation in vivo. Elevated concentrations of fibrinogen and plasminogen activator inhibitor-1 were seen after the exposure to WPS. Blood samples taken from mice exposed to WPS and exposed to adenosine diphosphate showed more platelet aggregation. The heart concentrations of IL-6 and TNFα were augmented by WPS. Likewise, heart levels of LPO, reactive oxygen species and the antioxidants catalase and GSH were increased by WPS. However, the systolic blood pressure and heart rate were not affected by WPS. Conclusion: It can be concluded that short-term exposure to WPS exerts procoagulatory effects and induce cardiac inflammation and oxidative stress. At the time point investigated, there was no evidence for blood inflammation or oxidative stress.


2001 ◽  
Vol 157 (2) ◽  
pp. 163-167 ◽  
Author(s):  
Scott Lukas ◽  
Elena Kouri ◽  
Christina Rhee ◽  
Alex Madrid ◽  
Perry Renshaw

2011 ◽  
Vol 301 (4) ◽  
pp. H1716-H1722 ◽  
Author(s):  
Jennifer A. Miner ◽  
Emily R. Martini ◽  
Michael M. Smith ◽  
Vienna E. Brunt ◽  
Paul F. Kaplan ◽  
...  

Very few studies have explored the cardiovascular effects of progesterone in premenopausal women. This study aimed to examine the short-term effects of oral progesterone alone, transdermal estrogen alone, and progesterone and estrogen combined on flow-mediated dilation (FMD) in healthy reproductive-aged women. We suppressed endogenous estrogens and progesterone in 17 premenopausal women for 10–12 days using a gonadotropin-releasing hormone antagonist. On day 4 (hormone suppression condition), subjects were tested ( n = 17) and were then supplemented with either 200 mg micronized progesterone ( n = 8) orally or 0.1 mg estradiol ( n = 9) transdermally per day. On day 7 (progesterone-first or estradiol-first condition), subjects were tested and began supplementation with both hormones ( n = 17) and were tested again on day 10 (combined hormone condition). FMD of the brachial artery was assessed using B-mode arterial ultrasound, combined with synchronized Doppler analysis. As a result, significant differences in FMD were observed between hormone suppression (7.85 ± 1.06%) and estrogen-first conditions (10.14 ± 1.40%; P < 0.05). The estradiol-induced increase was abolished when oral progesterone was also supplemented (6.27 ± 0.96%). In contrast, we observed a trend toward a decrease in FMD with unopposed progesterone administration, but no statistically significant differences were found between the progesterone-first (6.66 ± 1.23%), hormone suppression (7.80 ± 1.23%), and combined hormone conditions (7.40 ± 1.29%). In conclusion, these data suggest that short-term oral micronized progesterone administration antagonizes the beneficial effect of transdermal estradiol on FMD.


Author(s):  
Fatemeh Aminaei ◽  
Mohammad Javad Zare Sakhvidi ◽  
Hamideh Mihanpour ◽  
Mojtaba Moghaddasi ◽  
Mahdiyeh Shafieizadeh Bafghi

Introduction: According to the literature, Central Retinal Arteriolar Equivalent (CRAE), Central Retinal Venular Equivalent (CRVE), and Artemio Venule Ratio (AVR) are three important markers in determining the changes of retinal artery. These markers are employed as an indicator of cardiovascular effects in workers. This study aimed to evaluate the changes in retinal micro vascular responses in workers exposed to short-term exposure to particulate matters caused by occupational processes using CRAE, CRVE, and AVR markers. Materials and Methods: In this study, 96 workers exposed to job-related pollution in a tile and ceramic company were investigated. Fundus photos of these people were analyzed via ARIA software using the related protocols. The data were investigated employing Kolmogorov–Smirnov and Mann-Whitney tests as well as the correlation and regression tests. Results: No significant difference was observed in the ocular parameters of smokers and non-smokers. Cardiovascular parameters had no significant correlation with CRAE and CRVE as well as breathable and inhalable dust; however, these parameters had a direct and significant correlation with AVR, PM10, and PM2.5 particles. Conclusion: The results did not show any changes in the retinal artery in workers who were exposed to job-related pollution. Moreover, no significant relationship was found between retinal artery changes and cardiovascular parameters. However, more large-scale studies are needed to clarify the relationship of particulate air pollutants with CRAE, CRVE, and AVR changes.


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