Abstract
Local peripheral cooling (immerson of legs up to the knees into 12degreesC water) increased heart rate and blood pressure by 10-20 % within the first 3-10 min of cooling. During further cooling heart rate remained elevated, while systolic and diastolic blood pressures decreased to the control value.
Data on heart rate indicate a permanent activation of the sympathetic nervous system during local cooling. Skin temperatures (measured topically by thermosensors) decreased on some non-cooled areas of the body (fingers, palms and thighs) immediately after the start of local cooling.
On the other hand, skin temperatures on chest and forehead were not influenced. During cooling skin temperatures on thighs remained low, but skin temperatures on fingers tended to increase.
Changes in skin temperatures on non-cooled areas of the body indicate that a permanent and generalized activation of the sympathetic nervous system occurs during local cooling. Cold induced cycles of vasodilation (CIVD) were observed on fingers, palms and forearms during local cooling.
Minute cycles in skin temperatures were observed on forehead, thighs and chest. Minute cycles coincided with those in the heart rate, indicating a permanent, generalized but discontinuous control of vasomotion by the sympathetic nervous system during local cooling.
Infrared thermographic recordings from different body areas indicated that local peripheral cooling lowered skin temperatures in all areas of the body within 5 min. Distant areas of the body (extremities) and pectoral muscles showed greater hypothermia than abdominal areas and head.
After 10 min of cooling average skin temperatures in all areas of the body returned to the original level and further fluctuated at approximately 10-15 min intervals. Data indicate that during local cooling skin blood flow in all areas-of the body surface permanently fluctuates forming a mosaic of dynamic changes in skin temperatures.
Since tympanic temperature increases, while skin temperature decreases immediately after the start of the local cooling, it appears that the initial vasoconstrictor response is being controlled independently of the central temperature input.