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The most consistent physiological sign is an increased pulse rate (Mendelson et al., 1972; Johnson and Domino, 1971; Renault et al., 1971; Galanter et al., 1972; Domino, 1970; Hollister et al., 1968 Manno et al., 1970; Mayor's Committee 1944; Waskow et al., 1970; Isbell and Jasinski, 1969; Meyer et al., 1971; Weil et al., 1968; Jones and Stone, 1970; Clark and Nakashima, 1968). This does not appear to be a direct drug effect on the heart (Manno et al., 1970). Instead, the drug appears to cause complex changes in the autonomic nerves regulating heart rate. Thus, Kiplinger et al. (1971) demonstrated that the increase produced by marihuana in heart rate is prevented by pretreatment with a Beta-sympathetic nervous system blocking agent, propranolol. A comparable increase rate was produced by treatment with isoprotemol, a Beta-sympathetic like drug. One subject developed an abnormal bigeminal rhythm after both marihuana and isoproternol.
Renault et al. (1971) noted a consistent effect of marihuana on the cardiac rhythm which also produced an increased heart rate. The effect was the suppression of the normal sinus arrhythmia usually produced by respiration. Respiration usually produces a slowing of heart rate mediated by the vagal parasympathetic nerve supply. This depression of normal vagal tone was further evidenced by the absence of heart rate slowing during forced expiration against a closed glotis (valsalva maneuver). This effect seemed to wax and wane over several minutes producing alternate periods of rapid and slowed heart rate.
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