ABSTRACT
Drug use among older adults is a growing concern, particularly for the burgeoning Hispanic population. Older adults seeking drug treatment will double over the next decade to almost 6 million. Cultural factors influence drug use, and more specifically, Hispanic cultural values influence heroin use. This study explored Mexican-American injection drug users' adherence to traditional Hispanic cultural values and their impact on cessation. Ethnographic interviews endorsed contextualized influences of values on heroin use. Cultural values functioned dichotomously, influencing both initiation and cessation. Understanding the impact of cultural values on substance abuse is critical given the changing demographics in American society.
Subject(s)
Culture , Heroin Dependence/ethnology , Mexican Americans/psychology , Substance Abuse, Intravenous/ethnology , Substance Withdrawal Syndrome/ethnology , Aged , Aged, 80 and over , Heroin Dependence/rehabilitation , Humans , Male , Middle Aged , Qualitative Research , Risk Factors , Substance Abuse, Intravenous/rehabilitation , Substance Withdrawal Syndrome/prevention & control , Surveys and Questionnaires , TexasABSTRACT
BACKGROUND: Cerebral blood flow (CBF) is known to be dysregulated in persons with human immunodeficiency virus 1 (HIV-1), for uncertain reasons. This is an important issue because impaired vasoreactivity has been associated with increased risk of ischemic stroke, elevated overall cardiovascular risk and cognitive impairment. METHODS: To test whether dysregulation of CBF might be due to virally-induced neuroinflammation, we used a well-defined animal model (GFAP-driven, doxycycline-inducible HIV-1 Tat transgenic (Tat-tg) mice). We then exposed the mice to a brief hypercapnic stimulus, and assessed cerebrovascular reactivity by measuring 1) changes in cerebral blood flow, using laser Doppler flowmetry and 2) changes in vascular dilation, using in vivo two-photon imaging. RESULTS: Exposure to brief hypercapnia revealed an underlying cerebrovascular pathology in Tat-tg mice. In control animals, brief hypercapnia induced a brisk increase in cortical flow (20.8% above baseline) and vascular dilation, as measured by laser Doppler flowmetry and in vivo two-photon microscopy. These responses were significantly attenuated in Tat-tg mice (11.6% above baseline), but cortical microvascular morphology and capillary density were unaltered, suggesting that the functional pathology was not secondary to vascular remodeling. To examine the mechanistic basis for the diminished cerebrovascular response to brief hypercapnia, Tat-tg mice were treated with 1) gisadenafil, a phosphodiesterase 5 (PDE5) inhibitor and 2) tetrahydrobiopterin (BH4). Gisadenafil largely restored the normal increase in cortical flow following hypercapnia in Tat-tg mice (17.5% above baseline), whereas BH4 had little effect. Gisadenafil also restored the dilation of small (<25 µm) arterioles following hypercapnia (19.1% versus 20.6% diameter increase in control and Tat-tg plus gisadenafil, respectively), although it failed to restore full dilation of larger (>25 µm) vessels. CONCLUSIONS: Taken together, these data show that HIV-associated neuroinflammation can cause cerebrovascular pathology through effects on cyclic guanosine monophosphate (cGMP) metabolism and possibly on PDE5 metabolism.