We examined whether acute exposure to a low dose of cigarette smoke causes an increase in airway responsiveness in guinea pigs and whether the changes in airway responsiveness are accompanied by increased vascular permeability or neutrophil influx in the trachea. Animals were divided into four groups: groups exposed to 5, 10, or 20 puffs of cigarette smoke and a control group. Airway responsiveness was assessed by measuring specific airway resistance (SRaw) as a function of increasing concentration of inhaled methacholine (Mch) aerosol immediately, 5 h, and 24 h after exposure. In parallel studies, tracheal vascular permeability was quantified by measuring the tracheal extravasation of intravenously administered Evans blue dye, and neutrophil influx into the tracheal mucosa was quantified by counting cells within whole mounts of tracheas that were stained with Giemsa. Exposure to 5 puffs of cigarette smoke caused no changes in airway responsiveness. Exposure to 10 puffs induced airway hyperresponsiveness only immediately after exposure. Exposure to 20 puffs induced airway hyperresponsiveness not only immediately but also 5 h after exposure. There was a significant correlation between the dose (puffs) of cigarette smoke and increase in airway responsiveness immediately after exposure (r = 0.77; p less than 0.001). The tracheal extravasation of intravenously administered Evans blue dye and the number of neutrophils in the tracheal mucosa did not differ significantly from the corresponding control values at any time or in any exposed group. Furthermore, none of these changes was observed in the airways distal to the trachea of any animal immediately after exposure to 20 puffs of cigarette smoke.(ABSTRACT TRUNCATED AT 250 WORDS)

As ozone (O3) is known to cause airway inflammation and hyperresponsiveness, we examined the effects of 0₃ exposure (1, 3, or 5 ppm, 2 h) on sensitization and provocation in guinea pigs sensitized with ovalbumin (OA) through the airway. In groups exposed to O₃ before sensitization, 5 ppm increased the production of IgG1 antibodies and decreased the OA sensitization threshold from 0.01 to 0.002%. In those exposed before provocation, 1, 3, or 5 ppm of O₃ decreased the OA provocation threshold from 0.5 to 0.02%, and this enhancement appeared to depend on airway hyperresponsiveness. We conclude that O₃ exposure may play an important role in causing asthmatic attacks rather than enhancing allergic sensitization.

Cough-induced rib fractures occur in every age group regardless of the presence or absence of underlying disease. Since rib fractures often occur in the lower and middle ribs, rib radiography is useful for diagnosis.

The effect of ozone dose (the product of ozone concentration and exposure time) on airway responsiveness was examined in unanesthetized, spontaneously breathing guinea pigs. Airway responsiveness was assessed by measuring specific airway resistance (sRaw) as a function of increasing concentration of inhaled methacholine (Mch) aerosol (the concentration of Mch required in order to double the baseline sRaw: PC200Mch). The airway responsiveness was measured before and at 5 min, 5 h, and 24 h after exposure. A 30-min exposure to 1 ppm ozone (dose 30 ppm.min) did not change PC200Mch at any time after exposure. Both a 90-min exposure to 1 ppm ozone and a 30-min exposure to 3 ppm ozone, which are identical in terms of ozone dose (90 ppm.min), decreased PC200Mch to a similar degree. A 120-min exposure to 3 ppm ozone (360 ppm.min) produced a much greater decrease of PC200Mch at 5 min and 5 h after exposure, compared with low-dose exposure. There was a significant correlation between ozone dose and the change in airway responsiveness. In all groups, the baseline sRaw was increased by approximately 50% at 5 min after exposure, but there was no correlation between the changes in PC200Mch and the baseline sRaw. This study suggests that ozone-induced airway hyperresponsiveness in guinea pigs is closely related to ozone dose.

Two patients developed difficulties in eyelid opening following long‐term neuroleptic treatment of more than 6–8 years. Tardive dyskinesia and dystonia apart from the face were not found in either case. The symptoms fluctuated in their severities on a daily basis and were easily aggravated by various stimuli, e.g., stress, walking, reading and watching television. Electromyographic studies of their faces clearly indicated that the symptoms resulted from spontaneous blepharospasm and were analogous to idiopathic Meige's syndrome. Therefore, the patients’ difficulties in opening their eyes were considered to be the so‐called drug‐induced Meige's syndrome and/or facial tardive dystonia. It must be stressed that this syndrome is extremely distressing to patients and is a severe complication accompanying a long‐term neuroleptic treatment.