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We have investigated the effect of severe local cooling on the vasomotor activity of the arteriovenous anastomoses (AVAs) and other finger vessels. The right third finger was subjected to local cooling (3 degrees C) for 30-45 min in 21 healthy, thermoneutral subjects. Blood velocity in the third finger arteries of both hands was simultaneously recorded using ultrasound Doppler, and skin temperature and laser-Doppler flux from the pulp of the cooled finger were also recorded. The results demonstrate that the initial cold-induced vasoconstriction during severe local cooling involves constriction of the AVAs as well as the two main arteries supplying this finger. During cold-induced vasodilatation (CIVD), the maximum velocity values were not significantly different from those before cooling. Furthermore, the velocity fluctuations in the cooled finger were in most subjects found to be synchronous with the velocity fluctuations in the control finger. This indicates that the large blood flow to the finger and the high skin temperature during CIVD are caused by relaxation of the smooth muscle cells of the AVAs.

We have examined the influence of local cooling from 35 to 19 degrees C on spontaneous arterial blood velocity fluctuations in the acral skin of thermoneutral subjects. The skin temperature of one hand was gradually lowered in a water bath in two separate experimental runs. Simultaneous continuous blood velocity was measured from the third finger artery of both hands using ultrasound-Doppler. The large blood velocity fluctuations assumed to be caused by synchronous vasomotion of the arteriovenous anastomoses were invariably seen in the control finger artery throughout the two cooling periods, indicating that the subjects were in their thermoneutral zone. The velocity fluctuations on the cooled side remained nearly unchanged and closely correlated with those in the control finger artery during local cooling from 35 to approximately 21.5 degrees C. Below this temperature (range 23-20 degrees C) the velocity fluctuations ceased abruptly, and the velocity was nonfluctuating and continuously low. These results indicate a local thermal level below which there is abrupt, sustained closure of the arteriovenous anastomoses.

In a previous study, we recorded short-term cardiovascular responses after a steep increase in arterial pressure in healthy humans [Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H199-H211, 1994]. The aim of the present study was to develop a mathematical model of the baroreflex control of arterial pressure, to use this model with the previously recorded data to estimate unknown parameters in the reflex control loop, and then to analyze the overall open- and closed-loop performance of the system by model simulations with use of individual sets of optimal parameters. The mathematical model consists of a heart, a linear elastic arterial reservoir, and two parallel resistive vascular beds. The arterial baroreflex loop is modeled by two separate time domain processing objects, each with its own gain, time constant, and delay, to simulate the action of a sympathetic signal to the peripheral vascular bed and a parasympathetic signal to the heart. In repeated model simulations, the control parameters in the model were systematically adjusted by an automated algorithm that minimized the deviations between the time courses of the cardiovascular variables simulated by the model and the previously recorded responses in each individual. In all 10 subjects, the short-term cardiovascular responses were adequately simulated by using individual sets of parameters in the model. Open-loop transfer functions for arterial pressure control were obtained by using the individual sets of optimal model parameters in new simulation runs. Open-loop gain for arterial pressure control at nearly zero frequency (steady state) was between 0.9 and 4. Model simulations also indicated an underdampened response at 0.05-0.07 Hz in the closed-loop situation in four subjects, corresponding to peaks in the mean arterial pressor power spectra obtained from separate recordings of spontaneous variations in the resting situation.

The effect of local heating on blood velocities in arteries supplying the skin of hand and fingers was studied in subjects kept in their thermoneutral zone. The temperature of one hand was steadily raised from 35 to 43 degrees C in 15 min, whereas the control hand was kept in the air or immersed in a water bath at 35 degrees C. Simultaneous blood velocity recordings from the two hands were made continuously using ultrasound Doppler. In the heated hand, a general rise in blood velocity level was seen. However, the spontaneous fluctuations in blood velocity assumed to be caused by synchronous vasomotor activity of the arteriovenous anastomoses (AVAs) remained unchanged and closely correlated with those in the control hand throughout the experiment. Thus the central nervous control of AVA vasomotion seems to be unaffected by local heating. The elevation of blood velocity in the heated hand is probably due to dilatation of other parts of the vascular bed, e.g., ordinary arterioles in the skin. Earlier investigators, using venous occlusion plethysmography, have reported vasoconstriction in the locally heated human finger. No sign of such heat-induced vasoconstriction was found in this study.

A step decrease in total peripheral conductance (TPC) was introduced in 10 healthy volunteers by rapid inflation to suprasystolic pressure of bilateral thigh cuffs. This provoked a sudden statistically significant increase in mean arterial blood pressure (MAP) of 5 mmHg during supine rest and of 8 mmHg during moderate supine exercise by the quadriceps muscles. Central venous pressure was not changed by cuff inflation. The increase in MAP was blunted by a rapid but transient decrease in both heart rate (HR) and cardiac stroke volume. At rest, a gradual increase in TPC, starting after 4 s, nearly fully restored MAP to its original value at 10 s. During exercise, MAP was halfway corrected at 10 s but then started to increase again, probably as a result of an ischaemic muscle pressor response. After cholinergic blockade by atropine, the immediate HR response was eliminated, but HR decreased gradually after a delay of 3 s. The time development of the slow increase in TPC was not changed by atropine. In conclusion, the regulatory correction of a sudden increase in arterial pressure in supine unanesthetized healthy humans is achieved through an immediate transient parasympathetic bradycardia during the first few seconds and a more gradual sympathetic peripheral vasodilation after 4 s. After cholinergic blockade, a slow presumably sympathetic HR response was observed.