Israel Medical Association Journal

Objectives: To study the effects of purified allicin on the cardiovascular system.

Methods: Spontaneously hypertensive rats treated for 6 weeks with a daily dose of 80 mg/kg/day of purified allicin added to their chow were compared to control rats that were fed regular chow. Weight, systolic blood pressure (SBP), triglycerides, cholesterol, insulin and adiponectin were measured at baseline and at the end of the study.

Results: Allicin had no effect on body weight whereas it reduced SBP significantly from 190 ± 7.5 mmHg to 168 ± 5.7 (P < 0.0001) and triglyceride levels from 96 ± 25 mg/dl to 71 ± 19 (P =0.009). Allicin had no effect on plasma cholesterol, insulin and adiponectin levels.

Conclusions: Allicin lowers blood pressure and triglyceride levels in spontaneously hypertensive rats. This effect is not mediated through weight loss.

Background: Splanchnic nerve stimulation evokes adrenomedullary catecholamine secretion via acetylcholine release and occupation of nicotinic cholinergic receptors on chromaffin cells.

Objectives: To assess whether among cultured adrenomedullary cells there exists a population that tonically secretes acetylcholine. If so, then blockade of enzymatic breakdown of acetylcholine by addition of a cholinesterase inhibitor to the medium would increase occupation of nicotinic receptors by endogenous acetylcholine and thereby induce catecholamine release.

Methods: Primary cultures of bovine adrenomedullary cells in 24-well plates (1 million cells per well) were incubated after 48–72 hours with fresh incubation medium (control), medium with added secretagogues (nicotine, angiotensin II, or K+) or the acetylcholinesterase inhibitor, edrophonium (10-7 to 10-³ M), for 1–20 minutes. Fractional release rates of epinephrine, norepinephrine and dopamine were compared to a control. We also examined whether co-incubation with edrophonium enhanced the effects of the secretagogues. All experiments were performed in quadruplicate and repeated three times.

Results: Nicotine, angiotensin II, and K+ each elicited time-related release of epinephrine, norepinephrine and dopamine by up to fourfold compared to the control. At all tested concentrations, edrophonium had no such effect. Co-incubation with edrophonium also failed to augment the secretory responses to nicotine, angiotensin II, or K+.

Conclusion: Bovine adrenomedullary cells in primary culture do not include a population of tonically active cholinergic cells.

Background: Some studies have indicated a possible link between cigarette smoking and hearing loss.

Objectives: To analyze the association between smoking and hearing loss, other than that induced by noise, and to characterize the type of HL impairment found in smokers.

Methods: We conducted a retrospective cross-sectional study in 13,308 men aged 20±68 (median 34.6 years) who underwent a hearing test as part of a routine periodic examination. For each subject, age, smoking status (current, past or non-smokers) and number of cigarettes per day were noted and a hearing test was performed. The test was performed in a sealed, soundproof room by an experienced audiologist and included pure tone audiometry of 250±8,000 Hz. The audiograms were analyzed and subjects were accordingly divided into two groups: those with HL and at least one of the following impairments in at least one ear: sensorineural, conductive or mixed; and those with no hearing loss (control). Audiograms showing HL typical to noise exposure were excluded.

Results: The prevalence of any type of HL among subjects <35 years was 4.5%, compared to 10.5% among those >35 years (P < 0.0001). A significantly higher incidence of any type of HL was found in current (11.8%) and past smokers (11.7%) than in non-smokers (8.1%) (P < 0.0001). The risk increment of the smoking status for developing HL among subjects under age 35 was 43%, and 17% among those above 35 years. Both mild, flat, sensorineural impairment and conductive impairment were found to be associated particularly with smoking (odds ratio 2.2 and 1.9, respectively).

Conclusions: The incidence of HL unrelated to noise exposure is higher in smokers than in non-smokers, and in young adults the effect is greater.