ABSTRACT
Background: Although use of Cannabis sativa is not associated with serious adverse effects, recreational use of aminoalkylindole (AAI) cannabinoid receptor agonists found in K2/Spice herbal blends has been reported to cause adverse cardiovascular events, including angina, arrhythmia, changes in blood pressure, ischemic stroke, and myocardial infarction. Δ9-Tetrahydrocannabinol (Δ9-THC) is the primary CB1 agonist found in cannabis and JWH-073 is one of the AAI CB1 agonists found in K2/Spice brands sold to the public. Methods: This study used in vitro, in vivo, and ex vivo approaches to investigate potential differences on cardiac tissue and vascular effects betweenJWH-073 and Δ9-THC. Male C57BL/6 mice were treated with JWH-073 or Δ9-THC and cardiac injury was assessed by histology. Effects of JWH-073 and Δ9-THC on H9C2 cell viability and ex vivo mesenteric vascular reactivity were also determined. Results: JWH-073 or Δ9-THC induced typical cannabinoid effects of antinociception and hypothermia but did not promote death of cardiac myocytes. No differences in cell viability were observed in cultured H9C2 cardiac myocytes after 24 h of treatment. In isolated mesenteric arteries from drug-naive animals, JWH-073 produced significantly greater maximal relaxation (96%±2% vs. 73%±5%, p<0.05) and significantly greater inhibition of phenylephrine-mediated maximal contraction (Control 174%±11%KMAX) compared with Δ9-THC (50%±17% vs. 119%±16%KMAX, p<0.05). Discussion: These findings suggest that neither cannabinoid at the concentrations/dose studied caused cardiac cell death, but JWH-073 has the potential for greater vascular adverse events than Δ9-THC through an increased vasodilatory effect.
ABSTRACT
Several human pathogens are transmitted by the blacklegged tick, Ixodes scapularis. These include the spirochetes that cause Lyme disease (Borrelia burgdorferi) which is endemic to the Lehigh Valley region of eastern Pennsylvania. Emerging and currently rare tick-borne diseases have been of increasing concern in this region, including tick-borne relapsing fever (caused by Borrelia miyamotoi), human granulocytic anaplasmosis (caused by Anaplasma phagocytophilum), and human babesiosis (caused by Babesia microti). Real-time PCR assays and in some instances, conventional PCR followed by DNA sequencing, were used to screen 423 DNA samples that were prepared from questing adult and nymph stage I. scapularis ticks for infection with four tick-borne human pathogens. B. burgdorferi was detected in 23.2% of the sampled ticks, while B. miyamotoi, B. microti and a human variant of A. phagocytophilum were detected in less than 0.5% of the ticks. Our results are consistent with those expected in a region where Lyme disease is prevalent and human cases of tick-borne relapsing fever, babesiosis and human granulocytic anaplasmosis are not currently widespread. It is expected that this study will serve as a baseline for future studies of tick-borne pathogens in an area that is in close proximity to regions of high endemicity for Lyme disease, human granulocytic anaplasmosis and human babesiosis.
