Effects Of Systemic Nicotine Research Articles

Effects of Nicotine on the Central Nervous System and Sleep Quality in Relation to Other Stimulants: A Narrative Review.

Nicotine is used extensively across the globe despite the common awareness of the fact that it might stimulate the neurological system in those who indulge in its consumption. Nicotine can be consumed in a wide number of various forms and can also be delivered in a wide variety of different ways. After it has been heated, it can be smoked, consumed sublingually, or brought into touch with mucosal surfaces, with the buccal mucosa being the most popular one. These three methods of consumption account for the vast majority of its use. It has been demonstrated without a reasonable doubt that people who partake in nicotine do, in fact, experience an increase in their levels of alertness, wakefulness, attention, and focus. The half-life of the substance, in addition to its effects, is highly variable depending on the forms in which it is consumed, viz. cigarettes, tobacco, gums, lozenges, and the manner in which it is administered. This is the case regardless of whether the chemical is administered orally or intravenously. It is common for a person to require multiple "hits" of the chemical throughout the course of the day, though the frequency of these needs and the intervals between them can vary greatly. The time interval between each of these "hits" can range anywhere from a few hours to a few minutes. The user has the potential to develop a tolerance to the neurostimulatory and systemic effects of nicotine, as well as a heightened sensitivity to those effects, and even hereditary predispositions to specific adverse consequences. There is also a possibility that the user will develop an addiction to nicotine. This literature review aims to explore the relationship between nicotine consumption and its effects on the central nervous system, especially on sleep.

The Health Risks of Electronic Cigarette Use to Bystanders.

This works aimed to assess the health risks of e-cigarette use to bystanders. The exhaled breath of 17 volunteers was collected while they were vaping, and the levels of nicotine, propylene glycol, glycerol, formaldehyde, acetaldehyde, acrolein, tobacco-specific nitrosamines (TSNAs), and heavy metals were analyzed. Increased levels of nicotine, propylene glycol, TSNAs and copper were found in the exhaled breath of the volunteers. From these measurements, bystander exposure was estimated for two different scenarios: (1) A non-ventilated car with two e-cigarette users and (2) a ventilated office with one e-cigarette user. Our results show that bystanders may experience irritation of the respiratory tract as a result of exposure to propylene glycol and glycerol. Systemic effects of nicotine should also be expected if nicotine-containing e-liquid is used, including palpitations, and an increase of the systolic blood pressure. Furthermore, due to the presence of TSNAs in some e-liquids, an increased risk of tumors could not be excluded for the ‘car’ scenario. While e-cigarette use can clearly have effects on the health of bystanders, the risks depend on the rate of ventilation, dimensions of the room, and vaping behavior of the e-cigarette user. The presence of TSNAs in e-liquids can be avoided, which will prevent the most serious effect identified (increased risk of tumors).

The Effect of Systemic Nicotine on Osseointegration of Titanium Implants in the Rat Femur

The purpose of this study was to determine whether high levels of plasma nicotine, delivered via subcutaneously placed mini-osmotic pumps, had an effect on bone development and osseointegration of a titanium implant in rat femurs in both the short and long term. In this study, we hypothesized that systemic nicotine may not affect bone development, but may affect osseointegration in both the short and long term. Thirty rats were assigned to 4 groups. Group 1 (n = 10) was subdivided into 2 groups, which both received nicotine during the duration of the experiment. Half of the group (n = 5) was sacrificed at 2 weeks after implant placement, and the other half (n = 5) was sacrificed at 4 weeks after implant placement. Group 2 (n = 10) was treated identically; however, this group was given saline placebo rather than nicotine. Nicotine/saline was administered via subcutaneous mini-osmotic pumps. Serum analysis was assessed biweekly and weight was assessed weekly. Implant placement consisted of mini-implant placement in the femur of the rats under general anesthesia. After sacrifice, the femurs were harvested and analyzed. Biomechanical push-in test was used to determine the degree of osseointegration by evaluating the breakpoint load. Micro-CT was performed on the femurs of the remaining 10 rats to determine the bone density and architecture. Micro-CT showed no significant difference in bone morphometric analysis. Push-in test showed significant difference in axial load force required to dislodge the implant between the nicotine-treated and control rats both at 2 and at 4 weeks after implant placement. The evidence indicates that while there was no significant difference in bone development and remodeling with exposure to systemic nicotine, there was a significant difference in bone wound healing, specifically with the osseointegration of titanium implants at both 2 and 4 weeks after implant placement. In conclusion, systemic nicotine may have a significant impact on the osseointegration of implants in the rat femur. Additional studies need to be conducted to further understand the specific way in which nicotine adversely affects wound healing on the molecular level.

Effects of Systemic Nicotine, Alcohol or Their Combination on Cholinergic Markers in the Frontal Cortex and Hippocampus of Rat

Acute alcohol (Alc) intoxication has been shown to decrease choline acetyltransferase (ChAT) in the rat brain. The present study extends that finding by examining the effects of nicotine (Nic), Alc, and their combination on ChAT and acetylcholinesterase (AChE) in the frontal cortex and hippocampus of rat. The samples were collected at 30 and 120 min after intraperitoneal administration of saline (0.9%, control), Nic (1 mg/kg), Alc (1 g/kg), and Nic + Alc and analyzed by RT-PCR, Western blot and colorimetry. Alc alone considerably reduced ChAT mRNA expression, whereas Nic alone decreased AChE mRNA expression. In contrast, Nic + Alc exposure had resulted in no significant change in the parameters. These findings are consistent with the results of the Western blot and AChE activity analysis. The results, therefore, indicate that Nic and Alc alone may interact with the central cholinergic system. This interactive effect may contribute to a frequent association of tobacco and Alc consumption.

Acute Effect of Cigarette Smoke and Nicotine on Airway Blood Flow and Airflow in Healthy Smokers

Cigarette smoke contains irritants and vasoactive substances. We wanted to determine the effect of smoking a cigarette and of nasally or orally inhaled nicotine on airway blood flow (Q(aw)) and airflow in smokers. In ten healthy current smokers, Q(aw), FEV(1), and FEF(25-75) were measured before and at 5, 30, and 180 min after smoking a cigarette. The effects of systemic nicotine using a nicotine nasal spray and local nicotine using a nicotine inhaler were also studied. Mean (+/- SE) Q(aw) increased by 81% +/- 16% (p = 0.03) 5 min after smoking a cigarette and was no longer different from baseline at 30 and 180 min. Nicotine nasal spray and nicotine oral inhaler had no effect on Q(aw.) FEV(1) and FEF(25-75) remained unchanged after smoking a cigarette and after local or systemic nicotine administration. Smoking a cigarette is followed by a transient increase in airway blood flow but no changes in airflow. Nicotine, at the rate and dose provided by the nasal spray (systemic action) and oral inhaler (local and systemic action), does not appear to be involved in the Q(aw) change, suggesting a pharmacologic or nonspecific irritant effect of other cigarette smoke constituents.

Nicotine Self-Administration in Animals: A Reevaluation

Nicotine self-administration in animals is often viewed as compelling evidence that nicotine is reinforcing to animals and as corroborating the widely accepted thesis that nicotine is a major cause of smoking. This review examines the studies of nicotine self-administration in animals in the past two decades, focusing on threats to the internal and external validity of these studies and on the extent to which they support the thesis that nicotine is reinforcing in animals. The review shows that nicotine self-administration studies are fraught with severe methodological problems. These include omission of essential controls for general activation and other systemic effects of nicotine, insufficient consideration of secondary reinforcement processes, using food-deprived or confined animals and exclusion of subjects that do not conform to the investigators' preferred behavior. As a result of these systematic flaws, the role of nicotine as a reinforcer in this paradigm has not been established.

Inhibition of nicotine-induced hippocampal norepinephrine release in rats by alpha-conotoxins MII and AuIB microinjected into the locus coeruleus

Hippocampal norepinephrine (NE) is secreted by neurons projecting from the locus coeruleus (LC) to the hippocampus; LC nicotinic receptors (NAchRs) are involved in the effects of systemic nicotine on this pathway. To clarify the NAchR subtypes, NAchR antagonists, termed α-conotoxins, were microinjected into the LC before nicotine; MII and AulB were used to assess the potential involvement of α3 β2 and α3 β4 subunit-containing NAchRs, respectively. Nicotine dose-dependently stimulated hippocampal NE release ( P<0.01). MII (>0.25 pmol) reduced the NE response to nicotine (67% decrease; P<0.05), as did AuIB (44% reduction by 25 pmol; P<0.05). Administered together, however, MII and AuIB were no more effective than MII. Thus, MII and AuIB are capable of interacting with NAchR subtypes other than those previously defined as α3 β2 and α3 β4, respectively. NAchRs containing both β2 and β4subunits may be involved.

Specific neurophysiological effects of systemic nicotine on neurons in the nucleus accumbens

Extracellular recordings of single neurons within the nucleus accumbens (NAS) of halothane-anesthetized rats have revealed that systemic nicotine injections (0.5 and 1.0 mg/kg, s.c.) inhibit the action potentials of normally inactive NAS neurons, evoked by fimbria stimulation (fimbria-driven responses, n = 18). These nicotine inhibitions of fimbria-driven NAS action potentials appear to be centrally mediated because they were reversed by subsequent systemic injections of the centrally acting nicotinic acetylcholine (nAch) antagonist, mecamylamine (1.0 mg/kg, s.c., n = 6) but not by the peripherally acting nAch antagonist, hexamethonium (2.0 mg/kg, s.c., n = 6). Fimbria-driven NAS neurons were also tested with morphine (2.5 mg/kg, s.c.) in some experiments. Consistent with many past observations (Hakan et al., 1989), morphine did not affect these driven neurons. In other experiments, nicotine-induced inhibition of NAS fimbria-driven units was followed by haloperidol (0.5 mg/kg, s.c.), in attempts to reveal the possible role of dopamine in these effects. Haloperidol was successful at reversing nicotine inhibitions in only some cases (n = 2/6). Thus, the role of dopamine in these NAS responses to nicotine remains unclear. In contrast to the fimbria-driven NAS responses, spontaneously active NAS neurons were not affected by nicotine injections yet were subsequently inhibited with systemic morphine. These results suggest a specific neuropharmacological organization in the region of the nucleus accumbens that may relate to the qualitative and subjective differences in the experimental effects of different psychoactive drugs. Iontophoretic studies designed to localize further the site of these nicotine effects on NAS neurons are in progress.

Effects of systemic nicotine on serotonin release in rat brain

We used in vivo microdialysis to examine the acute effects of systemically administered nicotine (0.8–8.0 mg/kg, s.c.) on extracellular levels of serotonin (5-HT) in the frontal cortex of awake rats and animals anesthetized with chloralose/urethane. In anesthetized animals, 5-HT efflux was elevated during the initial 15 min after nicotine administration (2–8 mg/kg), but then returned to baseline values. All of the effective nicotine doses also lowered and then raised blood pressure in these animals. However, other drugs which raised (methoxamine, 0.07 mg/kg, i.v.) or lowered (mecamylamine, 5 mg/kg, i.p.) blood pressure without directly activating nicotinic receptors failed to alter 5-HT release. Moreover, pretreatment with a centrally active dose of mecamylamine, a known nicotinic antagonist, blocked the effects of nicotine (4 mg/kg) on 5-HT release. For studies on awake rats the perfusion fluid also contained fluoxetine, since basal 5-HT levels were barely detectable without this uptake blocker. In such animals, 1.6 mg/kg of nicotine significantly increased 5-HT release, an effect apparent in the initial 20 min after treatment and persisting for at least 2 h. These observations demonstrate that systemically administered nicotine increases frontocortical 5-HT release, that this effect is independent of the cardiovascular responses to the drug, and that it probably results from the activation of previously described nicotinic receptors on raphe neurons. The present findings are consistent with the hypothesis that the appetitive and mood disturbances associated with nicotine withdrawal may be mediated by diminished serotoninergic transmission.