RESUMEN
Marijuana is currently the most used illicit substance in the world. With the current trend of decriminalization and legalization of marijuana in the US, physicians in the US will encounter more patients using marijuana recreationally over a diverse range of ages and health states. Therefore, it is relevant to review marijuana's effects on human cardiovascular physiology and disease. Compared with placebo, marijuana cigarettes cause increases in heart rate, supine systolic and diastolic blood pressures, and forearm blood flow via increased sympathetic nervous system activity. These actions increase myocardial oxygen demand to a degree that they can decrease the time to exercise-induced angina in patients with a history of stable angina. In addition, marijuana has been associated with triggering myocardial infarctions (MIs) in young male patients. Smoking marijuana has been shown to increase the risk of MI onset by a factor of 4.8 for the 60 minutes after marijuana consumption, and to increase the annual risk of MI in the daily cannabis user from 1.5% to 3% per year. Human and animal models suggest that this effect may be due to coronary arterial vasospasm. However, longitudinal studies have indicated that marijuana use may not have a significant effect on long-term mortality. While further research is required to definitively determine the impact of marijuana on cardiovascular disease, it is reasonable to recommend against recreational marijuana use, especially in individuals with a history of coronary artery disorders.
Asunto(s)
Cannabis/efectos adversos , Enfermedades Cardiovasculares/etiología , Animales , HumanosRESUMEN
Osteocalcin, the most abundant member of the family of extracellular mineral binding gamma-carboxyglutamic acid proteins is synthesized primarily by osteoblasts. Its affinity for calcium ions is believed to limit bone mineralization. Several of the numerous hormones that regulate synthesis of osteocalcin, including glucocorticoids and parathyroid hormone, are also affected by stressful stimuli that require energy for an appropriate response. Based on our observations of OC responding to stressful sensory stimuli, the expression of OC in mouse and rat sensory ganglia was confirmed. It was thus hypothesized that the behavioral responses of the OC knockout mouse to stressful sensory stimuli would be abnormal. To test this hypothesis, behaviors related to sensory aspects of the stress response were quantified in nine groups of mice, aged 4-14 months, comparing knockout with their wild-type counterparts in six distinctly different behavioral tests. Resulting data indicated the following statistically significant differences: open field grooming frequency following saline injection, wild-type > knockout; paw stimulation with Von Frey fibers, knockout < wild-type; balance beam, knockout mobility < WT; thermal sensitivity to heat (tail flick), knockout < wild-type; and cold, knockout < wild-type. Insignificant differences in hanging wire test indicate that these responses are unrelated to reduced muscle strength. Each of these disparate environmental stimuli provided data indicating alterations of responses in knockout mice that suggest participation of osteocalcin in transmission of information about those sensory stimuli.