Classically, cold induced plasma volume reduction is explained by an increased diuresis which is generated by an inhibition of antidiuretic hormone release. However, most of the haemoconcentration appears to be reversible during rewarming. This observation weakens the former statement. The aim of this study was to clarify the mechanisms involved in the reversal of the cold induced haemoconcentration. Six young males, resting in a dorsal reclining position, were exposed successively to a thermoneutral environment (30 min), a cold environment (1 degrees C; cold) or thermoneutrality (control) for 120 min, and during a 60-min recovery period in thermoneutral conditions. During cold stress, a reduction of 15% (i.e. 510 ml) of the plasma volume was observed, and osmolality was unchanged. After the 60-min recovery under thermoneutral conditions, plasma volume variation between the Cold and the Control experiments was reduced and reached 3% (i.e. 100 ml). This volume equalled the increased amount of urine production observed during the cold stress experiment. Haemoconcentration cannot be explained by increased urinary water loss (+/- 100 ml) alone. Therefore a transient shift of plasma water from vascular to interstitial spaces, due to an increase of blood pressure, could be involved in the reduction of plasma volume.

Exposure to cold causes a vasoconstriction and a tachycardia, both resulting in a rise of blood pressure and cardiac work. This last effect may have a deleterious influence on people suffering from ischaemic heart disease (IHD). Moreover, coronary artery spasm could occur if vasoconstriction extends to the heart vessels. Epidemiologic studies have shown that mortality from IHD was correlated to the ambient temperature. There will be more deaths per day in the winter, and fewer in the summer. However, the daily number of deaths also increases during the heat waves. During a cold test, the coronary blood flow remains normal or slightly increased in normal subject. There is never a coronary artery spasm. Subjects who suffer from angina but have normal coronary arteries behave in the same way as normal subjects. Patients with IHD show a decrease in coronary blood flow. In a few cases, those patients may exhibit a coronary spasm with chest pain and even myocardial infarction. It is concluded that people with normal cardiovascular function are unaffected by cold stress whereas those with IHD may be crippled, although rarely, by exposure to cold, especially if they perform a physical work.

TcPO2 is not required in patients with Leriche stage II intermittent claudication but might be useful either in severely affected patients (Leriche stage III or IV) or in selected patients.

Five men, aged 31.2 years (SD 2.3), under semi-nude conditions and resting in a dorsal reclining position, were exposed to thermoneutral air for 30 min, followed immediately by a cold water (15 degrees C) immersion for 60 min. Cardiac output was measured using a dual-beam Doppler flow meter. During immersion in cold water, cardiac frequency (fc) showed an initial bradycardia. The lowest values were reached at about 10 min after immersion, 58.3 (SD 2.5) to 48.3 (SD 7.8) beats min-1 (P < 0.05). By the 20th min of exposure, fc had gradually risen to 70.0 beats min-1 (SD 6.6, P < 0.05). This change could be due to the inhibition of the initial vagal reflex by increased catecholamine concentration. Stroke volume (Vs) was significantly increased (P < 0.05) during the whole cold immersion period. Cardiac output, increased from 3.57 (SD 0.50) to 6.26 (SD 1.33) l min-1 (P < 0.05) and its change with time was a function of both Vs and fc. On the other hand, systolic flow acceleration was unchanged during the period of immersion. The changes in the respiratory variables (ventilation, oxygen uptake, carbon dioxide output and respiratory exchange ratio) during immersion showed an initial hyperventilation followed, as immersion proceeded, by a slower metabolic increase due to shivering.

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