Adverse Effects Of Nicotine Research Articles

Adverse Effects of Nicotine on Human Sperm Nuclear Proteins.

The effects of smoking on human health have long been documented. However, only a few studies have highlighted the direct effects of nicotine on sperm function. Nicotine, as a chemical compound found in tobacco, has been shown to modulate different aspects of spermatogenesis and sperm functions. Nicotine can lead to a reduction in the number of sperm, their motility and functionality. It can change the molecular expressions involved in sperm function, including genes encoding sperm nuclear proteins. The most important nuclear proteins that play a critical role in sperm function are known as H2B histone family, member W, testis-specific (H2BFWT), transition protein 1 (TNP1), transition protein 2 (TNP2), protamine-1 (PRM1), and protamine-2 (PRM2). These proteins are involved in sperm chromatin condensation, which in turn affects fertilization and embryonic development. Any alteration in the expression of these genes due to nicotine exposure/usage may lead to adverse implications in couples' fertility and the health of future generations. Since research in this area is still relatively new, it underscores the importance of understanding the potential side effects of environmental factors such as nicotine on reproductive health.

Electromembrane extraction of nicotine in inhaled aerosols from tobacco cigarettes, electronic cigarettes, and heated tobacco products

Heated tobacco products and electronic cigarettes are considered as alternatives to traditional tobacco cigarettes. However, it is crucial to monitor and compare the nicotine concentration in inhaled aerosols from these tobacco products, owing to the addictive nature and adverse effects of nicotine on human health. This study aimed to provide an electromembrane extraction (EME) combined liquid chromatography method to extract and determine nicotine in different inhaled aerosols. EME showed high extraction efficiency, selectivity, and sample clean-up capability. Under the optimal parameters, the linear range for nicotine was 0.1–200 mg L−1 (r2 > 0.9998), and the limit of detection was 0.02 mg L−1. Good precision was obtained with the intra- and inter-day relative standard deviations of 2.2 % and 2.8 %, respectively. Repeatability was satisfactory (<7.7 %), and recoveries ranged from 81.0 % to 112.8 %. Finally, this method has been successfully used for the determination and comparison of nicotine in aerosols from these three tobacco products.

Main and Interactive Effects of Nicotine Product Type on Sleep Health Among Dual Combustible and E-Cigarette Users.

E-cigarette use is associated with concurrent use of combustible cigarettes among adults and may increase the risk of future combustible cigarette use in adolescents and young adults. Detrimental effects of combustible cigarette use on sleep health are well documented, but little is known about the additive effects of concurrent e-cigarette use. The current study examined the main and interactive effects of daily nicotine product frequency on various components of sleep health. Two hundred and twenty-seven dual-product users (54.2% female, Mage = 36.89, SD = 10.17) completed questionnaires regarding demographic information, average number of cigarettes smoked per day, average number of times e-cigarettes used per day, and sleep health. Combustible cigarette frequency uniquely predicted shorter sleep duration, whereas e-cigarette frequency uniquely predicted increased daytime dysfunction due to sleepiness. Further, there was an interactive effect of combustible and electronic cigarettes on the use of sleeping medications. Findings may suggest differential adverse effects on sleep, depending on the type of nicotine product used, and highlight potential intervention targets for users. Future work should examine these associations prospectively and/or use objective measurements of sleep and nicotine use to further elucidate the nature of these relationships. This is the first study to explore the main and interactive effects of dual-product use on various dimensions of subjective sleep quality. This is important to investigate, given that dual nicotine users are at greater risk for physical health problems as well as the adverse effects of nicotine on sleep health. (Am J Addict 2020;00:00-00).

Comparison of Salivary Cotinine Levels of Neonates Born to Mothers Exposed to Varying Degrees of Passive Cigarette Smoke

Introduction: Obstetrical data reveals that fetuses born to mothers who are exposed to passive smoking show adverse health outcomes. Aims &amp; Objectives: To compare the cotinine levels in neonates born to mothers exposed to varying degrees of passive cigarette smoke versus the control group i.e., mothers who are not exposed to smoking. Place and duration of study: This study was conducted in Obstetrics and Gynecology department of Shaikh Zayed Hospital, Lahore and in emergency Labor Room of Ganga Ram hospital, Lahore from December 2015 to May 2016. Material &amp; Methods: This was a cross-sectional comparative study in which neonatal salivary cotinine level were measured and its relationship with birth weight was observed in 120 subjects, divided in four groups: .i) neonates whose mothers were not-exposed to smoke, neonates whose mothers were exposed to, ii) 1-5 cigarette, iii) 6-10 cigarettes and iv) more than 10 cigarettes per day. Results: Salivary cotinine levels were raised in all four groups with maximum levels seen in group four but there was no statistical difference between groups. Changes in the birth weight were also seen with increased exposure to passive smoking. Conclusion: Salivary cotinine concentration in neonates increases due to passive exposure to cigarette smoke in mothers because of disregard of smokers to the adverse effects of nicotine inside homes and almost no governmental enforcement of laws regarding cigarette smoking in public spaces.

Possibilities of use of food protectors for prevention of adverse effects of tobacco smoke

The article presents some pathogenetic mechanisms of adverse effects of nicotine as a part of tobacco smoke such as carcinogenesis, atherogenesis, thrombogenesis, the influence on functional activity of internals and also a bone tissue and a mucous membrane of a mouth. For food correction of adverse effects the use of a number of ingredients for development of new technologies of functional products is scientifically grounded and recommended. The expected favorable biological effects at systematic consumption of these products are presented.

Androgen Receptor and Ultrastructural Features of Nigella sativa Oil and Nicotine-Treated Male Rat Reproductive Glands

Nicotine is claimed to increase free radicals, DNA damage and lipid peroxidation in male reproductive organs. Nigella sativa has been identified to ameliorate these adverse effects due to nicotine intake. This study was conducted to evaluate potential protective effects of N. sativa oil on the adverse effects of nicotine on androgen receptors (AR) and ultrastructural features of rat seminal vesicles and prostate glands. Twenty four Sprague Dawley male rats, 7-9 weeks of age and 200-250 g body weight (BW) were randomly divided into; Group 1 Saline (S), forced fed with 0.1 mL/100 g BW of 0.9% normal saline; Group 2 Nicotine (N), intramuscularly injected with 0.5 mg/100 g BW of nicotine; Group 3 N. sativa (NS), forced fed with 6.0 μL/100 g BW of N. sativa and Group 4 Nicotine-N. sativa (NNS), co-administered with 0.5 mg/100 g BW of nicotine and 6.0 μL/100 g BW of N. sativa. The seminal vesicles and prostate glands were extracted after 100 days of treatment. The seminal vesicle and prostate gland were processed for ultrastructural study and androgen receptor detection. The epithelial cells in prostate gland and seminal vesicle of the N group showed weaker brown staining intensity as compared to that of in the NS and NNS groups. This was consistent with the presence of some ultracellular changes observed in the prostate gland and seminal vesicle tissues of the N group. Findings from this study suggested that administration of N. sativa results in ameliorating effects on both the prostate gland and seminal vesicle structures and functions of the nicotine-treated rats.

Forced but not free-choice nicotine during lactation alters maternal behavior and noradrenergic system of pups: Impact on social behavior of adolescent isolated male rats

Adverse effects of nicotine during pregnancy have been greatly studied, while nowadays few works are focused on consequences of maternal tobacco smoking after birth. The present study investigated the behavioral and early neurochemical effects of nicotine treatment during first weeks of post-natal life in rats. We used “free choice” treatment (H2O+NIC dams could drink from two bottles, containing 10mg/L nicotine hydrogen tartrate salt, or water) versus “forced choice” (NIC+NIC mothers could drink from two bottles both containing nicotine hydrogen tartrate salt, range from 0.75mg/L to 4.09mg/L). We found that only “forced nicotine” had impact on maternal behavior, causing increased high-quality maternal care. This immediately impacted on neuro-chemical development, affecting NE levels (only males) in pup’s striatum and prefrontal cortex (pFC) at PND 12. After weaning, animals were reared in normal conditions (two brother rats) or in Social Isolation. After two weeks, they were tested with Social Interaction Test (isolated rats met non-isolated opponents, siblings vs. non-siblings). As expected, isolated rats displayed an aggressive form of soliciting behavior: when facing an isolated unknown partner, the non-isolated rat tried to escape. Interestingly, if their dams were exposed to forced nicotine, both rats sooner behaved very affiliative (possibly empathic) between non-sibling partners. As expected, being exposed to post-natal nicotine could alter neuro-chemical development, but with important interactions between both maternal care and adolescent social behavior.

Nicotine Exposure Augments Renal Toxicity of 5-aza-cytidine Through p66shc: Prevention by Resveratrol.

We have shown that either chronic nicotine (NIC) exposure or 5-aza-cytidine (AZA) augments oxidative stress-dependent injury through stimulating p66shc in renal cells. Hence, NIC could exacerbate adverse effects of AZA while antioxidants such as resveratrol (RES) could prevent it. Renal proximal tubule cells (NRK52E) were treated with 20 μM RES prior to 200 μM NIC plus 100 nM AZA and cell injury (LDH release) was determined. Reporter luciferase assays determined p66shc activation and RES-induced antioxidant responses. Genetic manipulations identified the mechanism of RES action. NIC exacerbated AZA-dependent injury via augmenting p66shc transcription. While RES suppressed NIC+AZA-mediated injury, -surprisingly-it further enhanced activity of the p66shc promoter. RES protected cells via the cytoplasmic p66shc/Nrf2/heme oxygenase-1 (HO-1) axis. RES can protect the kidney from adverse effects of NIC in patients undergoing anticancer therapy.

The Effect of TENS on Random Pattern Flap Survival in Nicotinized Rats

The adverse effects of cigarettes, due to their nicotine content, may cause important ischemic complications in flaps. Electrical stimulation increases blood flow in ischemic tissues, the level of vascular endothelial growth factor, capillary density, and angiogenesis while decreasing oxygen tension in tissues. Electrical stimulation is also known to increase survival rate in flaps. In this study, which tests the hypothesis that TENS (a type of electrical stimulation) contributes to enhancement of flap viability by eliminating the adverse effects of nicotine, 40 rats were divided into 4 groups of 10 rats. Nicotinization was achieved by subcutaneous administration of 2 mg/kg per day to the rats, other than those in the Control group, for 4 weeks. The rats in one of the nicotinized groups received 20 mA, 80 Hz TENS (TENS1 group) for 1 hour daily throughout the last week before McFarlane flaps of random pattern were made in the backs of all the rats. Another nicotinized group was subjected to TENS in a similar dose after flap elevation (TENS2 group). Flap blood flow was measured before and 48 hours after their construction, and their fluorescein perfusion was measured immediately after the flap elevation. The comparison of the survival rates of the flaps revealed that, although the blood flow in the Nicotine group was significantly lower than in the Control group, it was significantly higher in the TENS1 group than in both the Control and Nicotine groups. The proportion of the area stained with fluorescein, immediately after the elevation of flaps, was significantly reduced in the Nicotine group compared to the Control group. In the TENS1 group, however, it was greater than in the nicotine and TENS2 groups. Flap viability rates decreased significantly in the Nicotine group compared with the Control group. In the TENS2 group, however, an increase was observed compared with the Nicotine group.These findings suggest that although TENS performed before flap elevation does not contribute to flap survival, despite causing a rise in blood flow, it enhances flap survival when applied postoperatively. Given the practicality and low cost of TENS, it can be concluded that it may be possible to use it in the management of ischemic complications in flap operations in smokers.

Sleep Deprivation: A Forgotten Risk Factor for Renal Dysfunction in Healthy Individuals

Sleep Deprivation: A Forgotten Risk Factor for Renal Dysfunction in Healthy Individuals Typically, internal circadian clock of humans entrains to the 24-hour light-dark pattern internal where they sleep at night and are awake during the day. This pattern is maintained primarily by light exposure, which affects melatonin secretion. Dim light Melatonin onset (DLMO) is considered to be the best marker of circadian phase. Melatonin secretion normally increases at bedtime and remains high until early morning. In patients with sleep disruption, the circadian release of melatonin is impaired [1]. Experimental evidence suggest that via glutathione production, melatonin serves as an antioxidant in various tissues including the kidney [2,3]. In the same manner, melatonin protects blood vessels from adverse effects of nicotine [4], and against atherogenesis [5,6]. Melatonin also reduces interstitial renal inflammation and improves blood pressure in spontaneously hypertensive rats [7]. A recent study has also shown that melatonin stimulates renoprotective effects of endothelial progenitor cells in acute ischemic kidney injury [8]. Thus, as a first mechanism, we hypothesize that during sleep disruption protective effects of melatonin may diminish, which may in turn result in renal dysfunction.

Maternal smoking during pregnancy and child emotional problems: The relevance of maternal and child 5‐HTTLPR genotype

Serotonin is involved in the development of neural circuits modulating emotional behavior. The short allele (s) of a polymorphism (5-HTTLPR) of the serotonin transporter gene is a risk factor for psychopathology in the presence of environmental stressors. Maternal smoking is associated with growth restriction of the human fetal brain and adverse effects of nicotine on the developing serotonin system have been documented. We hypothesized that maternal smoking interacts with both child and mother 5-HTTLPR genotype as a risk factor for later child emotional problems. In a sample of n = 1,529 mother-child dyads, smoking habits were assessed by questionnaires during pregnancy. Child emotional problems were measured by the Child Behavior Checklist at the child's age of 3 years. Maternal smoking during pregnancy significantly increased the risk for emotional problems in children carrying the s-allele; β = 0.24, P = 0.03 (mother-report), and β = 0.46, P = 0.001 (father-report). In children heterozygous at 5-HTTLPR and exposed to maternal prenatal smoking (n = 79) risk of emotional problems increased with each additional s-allele the mother carried. The associations between 5-HTTLPR and child emotional problems were not moderated by paternal prenatal smoking. These findings imply that the vulnerability for emotional problems in s-allele carriers may already originate in fetal life.

Adverse Effects of Nicotine and Immunosuppression on Proximal Tubular Epithelial Cell Viability, Tissue Repair and Oxidative Stress Gene Expression

Renal dysfunction in non-renal transplantation is a major arbiter of poor late allograft outcomes. Tobacco recidivism is an important modifiable risk marker for cardiac allograft loss, but its effects on renal dysfunction remain poorly studied. In a 96-well plate, 10(-5) proximal tubular epithelial (PTE) cells (HK-2, American Type Culture Collection) were cultured overnight and treated with sirolimus (SRL; 100 nmol/liter), nicotine (N; 10(-7) mol/liter) and mycophenolate mofetil (MMF; 10 micromol/liter), alone or in combination for 24 hours. Cell viability was quantified by treatment with tetrazolium salt WST-1 and calculated as the difference in percent inhibition with respect to the optical densitometry (OD) of treated and untreated cells. Gene and protein expression was analyzed using real-time polymerase chain reaction and Western blot techniques. OD decreased with SRL (-52.7 +/- 2.85%), N (-47.3 +/- 3.84%) and MMF (-53.3 +/- 2.4%) in isolation. Further reduction in OD occurred when N was combined with SRL (-63 +/- 2.3%, p < 0.04), MMF (-64.3 +/- 1.45%, p < 0.02) or the combination of SRL and MMF (-78.2%, p < 0.007). Compared with control, treatment of PTE cells with N increased mRNA expression of transforming growth factor-beta (TGF-beta; 10-fold), connective tissue growth factor (CTGF; 25-fold), osteopontin (OPN; 10-fold) and NADPH oxidase components (p22(phox), NOX-1 and Rac-1 at 18-, 16- and 12-fold, respectively). The pre-treatment of cells with inhibitor of superoxide generator diphenylene iodonium (DPI) reversed these effects. Nicotine adversely amplified the effects of SRL and MMF on tissue repair and oxidative stress markers, subsequently modulating PTE viability. However, caution is advised in extrapolating these in vitro findings to the human model.

Serotonin, gasping, autoresuscitation, and SIDS—a contrarian view

in their study in the Journal of Applied Physiology , Erikson and Sposato ([4][1]) induced anoxic apnea in neonatal Pet -1 knockout (KO) and wild-type mice at postnatal day (P) 4.5 and P9 and examined the subsequent quality of gasping and autoresuscitation while the animals breathed room air. Pet-1

Maternal tobacco smoking, nicotine replacement and neurobehavioural development

Abstract The adverse effects of prenatal cigarette smoke exposure on human reproductive outcomes are a major scientific and public health concern. In the United States, approximately 25% of women of childbearing age currently smoke cigarettes, and only a small percentage of these individuals quit after learning of their pregnancy. Women interested in smoking cessation during pregnancy have a number of options, including behavioural and pharmacological aids, but nicotine replacement therapy (NRT) is by far the most common approach. While NRT avoids exposure to the myriad compounds present in tobacco smoke, nicotine itself causes damage to the developing nervous system. The purpose of this article is to review the detrimental effects of developmental tobacco smoke exposure on short- and long-term outcomes with particular emphasis on neurobehavioural consequences. In conclusion based on the clear, adverse effects of nicotine on brain development observed in human and animal studies, we suggest that safer alternatives for smoking cessation in pregnancy are badly needed.

Nicotine impairs cancer vaccines

Smokers constitute a majority of patients with cancer and hence, are frequently subjected to vaccination. Vaccines, designed to enhance host immunity against infectious agents and neoplastic cells, depend on functional dendritic cells (DCs), the body's key immune cells that are pivotal in the initiation immune responses. Our recent studies indicate that the presence of nicotine in the microenvironment severely affects the properties of DCs and impairs their ability to induce the development of effective immune responses. These observations raised some doubts on the ability of cancer vaccines to generate sufficient immune responses in smokers in order to mediate tumor regression or prevent tumor occurrence. Thus, in this study, we investigated whether the adverse effects of nicotine on DC system decrease the effectiveness of cancer vaccines in tumor‐bearing mice exposed to nicotine. We found that the vaccine effectively controls the tumor growth in control mice. However, the same vaccine provides little tumor regression in nicotine‐exposed mice as evidenced by a larger tumor mass. We also found that compared to control mice, lymphoid cells isolated from nicotine‐exposed mice produce up to 50% less IFN‐γ after re‐exposure to tumor antigen and exhibit markedly reduced CTL killing activity against inoculated tumor cells. Collectively, our data suggests that vaccines provide only partial protection in nicotine‐exposed individuals. Philip Morris USA Inc., and Philip Morris International.

ACUTE NICOTINE TREATMENT ACCELERATES PHOTOCHEMICALLY INDUCED PLATELET AGGREGATION IN CEREBRAL ARTERIOLES OF MICE: AN IN VIVO STUDY

When tobacco is smoked, chewed or snuffed, nicotine is absorbed by the lungs or mucous membrane and quickly moved into the bloodstream, where it is circulated throughout the brain. In fact nicotine is highly dangerous to be consumed in any form. The present study was conducted to know the adverse effects of nicotine on the platelet aggregation in cerebral microvessels of mice. Male mice of average weight 33 g were injected with Saline (control) or Nicotine (1 mg/kg, 0.1 ml/10 g) one hour before the experiment. Animals were anaesthetized and trachea was intubated. Craniotomy was performed and a window was opened on the skull. Layer of dura was removed. Brain surface microvessels were exposed and animal was placed on the microscope stage. Microscope was connected to a monitor and VCR to record all events. Exposed brain surface was continuously irrigated with ACSF solution. After the body temp was maintained at 37? C, Sodium fluorescein (2%, 0.1 ml/10 g) was injected i.v. through tail injection. High intensity mercury light was switched on to induce photochemically induced platelet aggregation. Appearance of the 1st platelet aggregation and total blood flow stop were timed in seconds. Our results showed that in the animals treated with nicotine, venule did not show any alteration in the platelet aggregation timings in comparison to the controls. But in arterioles platelet aggregation timings were significantly accelerated (P

9:43 Spinal fusion and smoking: is pseudarthrosis the cause for poorer clinical outcome?

Purpose of study: Nicotine consumption by spinal fusion patients is associated with increased pseudarthrosis risk and poorer clinical outcome. This study examines the relationship between smoking and clinical outcome independent of fusion success.Methods used: Patients with symptomatic lumbar disc disease were enrolled in prospective studies to examine the efficacy of recombinant human bone morphogenic protein (rhBMP)-2 on an absorbable collagen sponge (InFuse; Medtronic, Minneapolis, MN) as a bone graft substitute for anterior lumbar interbody fusion (ALIF). All patients underwent single level ALIF with an LT-cage (Medtronic) containing either iliac crest autograft (control) or InFuse. Clinical outcome data were collected preoperatively, and at 1.5, 3, 6, 12 and 24 months after surgery. This included the Oswestry Disability Questionnaire Short Form (SF)-36 back profile and back pain questionnaires. Radiographic outcomes were assessed at 6, 12 and 24 months after surgery. Successful fusion required evidence of bridging trabecular bone on computed tomography scans and radiographs, and the presence of less than 50 of angular motion and less than 3 mm translation on flexion-extension radiographs, and no radiolucent lines covering more than 50% of the implant surface. Patients who had consumed nicotine by smoking within 6 months of surgery were identified as smokers. In order to exclude the effect of pseudarthrosis, we compared the outcome data between smokers and nonsmokers in the subgroup of patients who had achieved successful fusion.of findings: At 24 months after surgery, a total of 303 patients had achieved successful fusion: 211 nonsmokers (93.3% fusion rate) and 92 smokers (88.3% fusion rate). The following graphs depict the clinical outcome in these patients (Figs. 1, 2, 3, and 4) .Relationship between findings and existing knowledge: There is a significant relationship between smoking and clinical outcome independent of fusion success for ALIF procedure.Overall significance of findings: Independent of fusion outcome, there were differences in clinical outcome between smokers and nonsmokers. Nonsmoking patients with successful fusion had superior Oswestry scores (significant 6 and 12 months postoperative), superior SF-36 physical scores (significant 12 and 24 months postoperative), superior SF-36 mental scores (significant 6 and 12 months postoperative) and less back pain (significant 6 months postoperative) compared with smoking patients with successful fusion. The adverse effects of nicotine on osteogenesis and spinal fusion may not fully explain the poorer clinical outcome in patients who smoke.Disclosures: Device or drug: rhBMP-2 / absorbable collagen, investigational device. Status: investigational.Conflict of interest: Harvinder Sandhu, grant research support; Harvinder Sandhu, consultant for Medtronic Sofamor Danek.

Adverse Effects of Nicotine and Interleukin-1β on Autoresuscitation After Apnea in Piglets: Implications for Sudden Infant Death Syndrome

Maternal cigarette smoking is established as a major dose-dependent risk factor for sudden infant death syndrome (SIDS). Both prenatal and postnatal exposures to constituents of tobacco smoke are associated with SIDS, but no mechanism of death attributable to nicotine has been found. Breastfeeding gives a substantial increase in absorbed nicotine compared with only environmental tobacco smoke when the mother smokes, because the milk:plasma concentration ratio of nicotine is 2.9 in smoking mothers. Furthermore, many SIDS victims have a slight infection and a triggered immune system before their death, thus experiencing a release of cytokines like interleukin-1beta (IL-1beta) that may depress respiration. Because apneas in infancy are associated with SIDS, we have tested the hypothesis that postnatal exposure to tobacco constituents and infections might adversely affect an infant's ability to cope with an apneic episode. This is performed by investigating the acute effects of nicotine and IL-1beta on apnea by laryngeal reflex stimulation and on the subsequent autoresuscitation. Thirty 1-week-old piglets (+/-1 day) were sedated with azaperone. A tracheal and an arterial catheter were inserted during a short halothane anesthesia. The piglets were allowed a 30-minute stabilization period before baseline values were recorded and they were randomized to 4 pretreatment groups (avoiding siblings in the same group): 1) immediate infusion of 10 pmol IL-1beta intravenously/kg (IL-1beta group; n = 8); 2) slow infusion of 5 microg nicotine intravenously/kg 5 minutes later (NIC group; n = 8); 3) both IL-1beta and NIC combined (NIC + IL-1beta group; n = 6); or 4) placebo by infusion of 1 ml .9% NaCl (CTR group; n = 8). Fifteen minutes later, apnea was induced by insufflation of .1 ml of acidified saline (pH = 2) in the subglottic space 5 times with 5-minute intervals, and variables of respiration, heart rate, blood pressure, and blood gases were recorded. Stimulation of the laryngeal chemoreflex by insufflation of acidified saline in the subglottic space produced apneas, primarily of central origin. This was followed by a decrease in heart rate, a fall in blood pressure, swallowing, occasional coughs, and finally autoresuscitation with gasping followed by rapid increase in heart rate, rise in blood pressure, and (in the CTR group) an increase of respiratory rate. Piglets pretreated with nicotine had more spontaneous apneas, and repeated spontaneous apneas caused an inability to perform a compensatory increase of the respiratory rate after induced apnea. This resulted in a lower SaO(2) than did CTR at 2 minutes after apnea (data shown as median [interquartile range]: 91% [91-94] vs 97% [94-98]). The pretreatment with IL-1beta caused prolonged apneas in piglets and an inability to hyperventilate causing a postapneic respiratory rate similar to the NIC. When nicotine and IL-1beta were combined, additive adverse effects on respiratory control and autoresuscitation compared with CTR were observed: NIC + IL-1beta had significantly more spontaneous apneas the last 5 minutes before induction of apnea (2 [.3-3] vs 0 [0-0]). Apneas were prolonged (46 seconds [39-51] vs 26 seconds [22-31]) and followed by far more spontaneous apneas the following 5 minutes (6.6 [4.0-7.9] vs.5 [.2- .9]). Instead of normal hyperventilation after apnea, a dramatic decrease in respiratory rate was seen (at 20 seconds: -45% [-28 to -53] vs +29% [+24-+50], and at 60 seconds: -27% [-23 to -32] vs +3% [-2-+6), leading to SaO(2) below 90% 3 minutes after end of apnea: 89% (87-93) versus 97% (95-98). These prolonged adverse effects on ventilation were reflected in lowered PaO(2), elevated PaCO(2) and lowered pH 2 minutes, and even 5 minutes, after induction of apnea. Nicotine interferes with normal autoresuscitation after apnea when given in doses within the range of what the child of a smoking mother could receive through environmental t

Chronic nitric oxide treatment reverses the adverse effects of nicotine on ethanol-induced gastric mucosal injury

Chronic nitric oxide treatment reverses the adverse effects of nicotine on ethanol-induced gastric mucosal injury

Pharmacologic effects of nicotine upon the fetus and mother in the rhesus monkey

The short-term pharmacologic effects of nicotine upon the cardiovascular performance, acid-base status, and oxygenation of the mother and fetus were investigated in 43 rhesus monkeys in the second half of gestation. Nicotine given intravenously to the mother in either a single dose of 1.0 mg. per kilogram or a constant infusion at a rate of 100 μg per kilogram per minute elicited bradycardia and hypertension which was followed by persistent hypotension. The fetus responded with hypotension and bradycardia (single injection) or tachycardia (constant infusion). Direct intravenous injection of nicotine into the fetus in a single dose of 0.9 to 2.5 mg. per kilogram produced changes similar to those seen in the mother but quite different from those which occurred in the fetus when nicotine was given to the mother. The cardiovascular responses were more pronounced in the mature fetuses than in the less mature ónes, indicating that sensitivity to nicotine is related to the development of the autonomic nervous system. Hypoxia and acidosis of the metabolic and respiratory type developed in the more mature fetus following administration of nicotine to the mother while the less mature fetus showed no significant changes in its acid-base status. The adverse effects of nicotine on the fetus following its administration to the mother seem to be due to the combined effects of impaired placental perfusion and a direct action of the transmitted nicotine upon the cardiovascular system of the fetus.