Considering the age and longer service time of firefighters who have a substantial amount of field activities, they are exposed to chemical and biological risk factors, physical and mental stress, diverse and complex work environments, and repetitive motions, which may increase the rates of gastrointestinal disorders, musculoskeletal diseases, cancers, and cardiovascular diseases. Therefore, based on the regular specific health examination results for 215 firefighters who were working in the N fire department located in B metropolitan city, an analysis of occupational diseases was performed, which showed that the most common chronic disease was diabetes mellitus (28.8%), followed by hyperlipidemia (27.9%) and thoracic diseases (19.5%). This trend appears to be consistent with the incidence rates reported in a representative study of adult diseases in Korea. In addition, it was found that 82 officers maintained healthy states, while those who needed further medical inspection and those with clinical symptoms were more frequently exposed to disease when they were older and had longer service time; moreover, the fire captain and lieutenant had higher rates of disease.

In this study, we explore the inhibitory effects of protriptyline, a tricyclic antidepressant drug, on voltage-dependent K+ (Kv) channels of rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Protriptyline inhibited the vascular Kv current in a concentration-dependent manner, with an IC50 value of 5.05 ± 0.97 μM and a Hill coefficient of 0.73 ± 0.04. Protriptyline did not affect the steady-state activation kinetics. However, the drug shifted the steady-state inactivation curve to the left, suggesting that protriptyline inhibited the Kv channels by changing their voltage sensitivity. Application of 20 repetitive train pulses (1 or 2 Hz) progressively increased the protriptyline-induced inhibition of the Kv current, suggesting that protriptyline inhibited Kv channels in a use (state)-dependent manner. The extent of Kv current inhibition by protriptyline was similar during the first, second, and third step pulses. These results suggest that protriptyline-induced inhibition of the Kv current mainly occurs principally in the closed state. The increase in the inactivation recovery time constant in the presence of protriptyline also supported use (state)-dependent inhibition of Kv channels by the drug. In the presence of the Kv1.5 inhibitor, protriptyline did not induce further inhibition of the Kv channels. However, pretreatment with a Kv2.1 or Kv7 inhibitor induced further inhibition of Kv current to a similar extent to that observed with protriptyline alone. Thus, we conclude that protriptyline inhibits the vascular Kv channels in a concentration- and use-dependent manner by changing their gating properties. Furthermore, protriptyline-induced inhibition of Kv channels mainly involves the Kv1.5.

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