Advertisements suggest that smokers of cigarettes low in nicotine are exposed to less nicotine and tar. Nicotine yields are measured with smoking machines, but machines do not smoke cigarettes as people do. We therefore measured the actual nicotine content of commercial cigarettes with different nicotine and tar yields as determined with smoking machines, and also measured actual nicotine intake as indicated by blood concentrations of its metabolite, cotinine, in 272 subjects smoking various brands of cigarettes. We found that low-yield cigarette tobacco did not contain less nicotine; in fact, the nicotine concentration in tobacco inversely correlated (r = -0.53, P less than 0.05) with the concentration measured by smoking machines. Blood cotinine concentrations correlated with the number of cigarettes smoked per day but not with the nicotine yield measured by smoking machines. Only 3.8 to 5.0 per cent of total variance in blood cotinine was contributed by nicotine yield. We conclude that smokers of low-nicotine cigarettes do not consume less nicotine.

In urethan-anesthetized thoracotomized rats the density of myocardial capillaries that had been stained during timed infusions of a plasma label was determined. gamma-Globulin-coupled fluorochromes [lissamine-rhodamine B 200 (RB 200) and fluoresceinisothiocyanate (FITC)] were applied to the vascular system for different intervals of time. The circulation in the heart was freeze stopped, and the dye-containing capillaries were counted in histological cross sections of the organ. When the dyes had been infused into the left atrium for 1, 2, 5, or 10 s the number of stained vessels continuously increased (1,960 +/- 170, 2,780 +- 160, 3,310 +/- 130, and 3,340 +/- 140 cap/mm2 in the subepicardium and 1,990 +/- 210, 2,490 +/- 190, 3,090 +/- 160, and 3,210 +/- 160 cap/mm2 in the subendocardium, respectively). However, further prolongation of dye exposure (2, 10, or 30 min) did not increase significantly the number of marked capillaries. The induction of a general hypoxia (30-s stop of ventilation) after dye application also did not induce higher capillary counts than were found in the normoxic animals during long-time plasma labeling. Changes in red blood cell-containing capillaries were not covered by these observations. The distribution of stained capillaries in the evaluated areas was more inhomogeneous after incomplete filling with RB 200 for 1 s than after complete staining with FITC for 4 min. The results favor the view that in the rat heart at rest the blood plasma passes the microcirculation in an inhomogeneous manner; in all capillaries the slowest transit times do not exceed 5 s, however.

The effects of cocaine on a human electroencephalographic event related potential (ERP) were measured. Forty-eight subjects received one of three IV doses (0.2, 0.4, or 0.6 mg/kg) and placebo. Thirty-three subjects received one of three oral doses (2, 3, or 4 mg/kg). All IV and oral doses reduced amplitude of the auditory ERP P200 and P300 components during the oddball task. P200 latency decreased. N100 amplitude was reduced only after IV administration. The changes in ERPs occurred during the period of peak cardiovascular and subjective effects. The amplitude reduction in ERP components occurring before the P300 component is consistent with decrements in attention, specifically selective attention. The P300 amplitude reduction after cocaine suggests a disruption of stimulus evaluation resources. The findings are inconsistent with the notion that stimulants affect only response selection and execution. The degree to which stimulants alter cognitive processes prior to response selection may depend on the magnitude of the cardiovascular, subjective, and probably other noncognitive effects.

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