Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 14 healthy men we assessed the effects of smoking marihuana cigarettes containing 6 mg of delta-9-tetrahydrocannabinol on ultrasound measures of left ventricular function. Four of this group and four additional subjects also had measurements of plasma norepinephrine. Both heart rate and left ventricular performance (mean rate of internal diameter shortening [mean Vcf]) were significantly increased for at least 1 h after drug exposure compared with these values after placebo cigarettes. The immediate tachycardia and increase in mean Vcf were not accompanied by raised plasma norepinephrine levels. However, by 30 min after marihuana exposure, sympathetic neurotransmitter levels were significantly greater than both control values and those after placebo cigarettes, and they remained elevated for at least 2 h. Excessive sympathoadrenal discharge, as evidenced by augmented left ventricular function and prolonged catecholamine release, could adversely affect patients with heart disease.
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PMID:Effects of smoking marihuana on left ventricular performance and plasma norepinephrine: studies in normal men. 69 22

Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries. Derivatives of cannabinoids such as delta-9-tetrahydrocannabinol (THC) modulate immune functions and therefore have potential for the treatment of inflammatory diseases. We investigated the effects of THC in a murine model of established atherosclerosis. Oral administration of THC (1 mg kg(-1) per day) resulted in significant inhibition of disease progression. This effective dose is lower than the dose usually associated with psychotropic effects of THC. Furthermore, we detected the CB2 receptor (the main cannabinoid receptor expressed on immune cells) in both human and mouse atherosclerotic plaques. Lymphoid cells isolated from THC-treated mice showed diminished proliferation capacity and decreased interferon-gamma secretion. Macrophage chemotaxis, which is a crucial step for the development of atherosclerosis, was also inhibited in vitro by THC. All these effects were completely blocked by a specific CB2 receptor antagonist. Our data demonstrate that oral treatment with a low dose of THC inhibits atherosclerosis progression in the apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, THC or cannabinoids with activity at the CB2 receptor may be valuable targets for treating atherosclerosis.
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PMID:Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice. 1581 11