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Biomedical subjects

K Toska

Publications and source records attributed to K Toska.

9 recordsLinked to original sources
PubMed1996

Short-term control of cardiovascular function: estimation of control parameters in healthy humans.

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.

Baroreflex↗
PubMed1994

Short-term cardiovascular responses to a step decrease in peripheral conductance in humans.

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.

Adult↗
PubMed1994

Peripheral vasoconstriction shortly after onset of moderate exercise in humans.

The immediate cardiovascular responses at the onset of supine dynamic leg exercise were studied by noninvasive methods in healthy humans. Total peripheral conductance (TPC), heart rate, and cardiac output increased very rapidly at the onset of exercise. Mean arterial pressure (MAP) showed a moderate anticipatory increase during a 10-s countdown to exercise and then decreased (but not below resting level) during the first 10 s of exercise. The TPC response was biphasic, and TPC started to fall from its peak value approximately 12 s after onset of exercise. This peripheral vasoconstriction increased MAP. After 25 s, the cardiovascular variables were stable for the rest of the 2-min exercise period. In the same subjects, cholinergic blockade was induced by atropine sulfate (0.035 mg/kg) and resting cardiac output, MAP, and TPC increased considerably. The exercise protocol was repeated after atropine, and the increase in heart rate at onset of exercise was slower and smaller. MAP decreased and remained depressed throughout the exercise period. A monophasic increase in TPC was seen. We suggest that, in the normal situation, the biphasic response in TPC reflects a baroreflex sympathetic vasoconstriction very shortly after onset of exercise and that this response is due to a rapid increase in set point for arterial pressure control at the onset of exercise. After cholinergic blockade, MAP was probably continuously well above the set point for arterial pressure control both before and during exercise and no reflex vasoconstriction was observed in this situation.

Adult↗
PubMed1993

Respiration-synchronous fluctuations in stroke volume, heart rate and arterial pressure in humans.

1. Simultaneous recordings of beat-to-beat left cardiac stroke volume (SV, pulsed ultrasound Doppler), mean arterial pressure (MAP) and heart rate (HR) were obtained in ten healthy young adults during spontaneous respiration at supine rest, before and after cholinergic blockade by atropine (0.035 mg kg-1). 2. Respiration-synchronous fluctuations in SV, HR, cardiac output (CO) and MAP were quantified by spectral analysis of the recordings of each of these variables. 3. Before atropine administration, respiration-synchronous fluctuations in HR and SV were prominent. The changes in HR and SV were inversely related and variation in SV was the main source of respiratory variability in CO. Respiration-synchronous fluctuations in MAP were mainly caused by variations in CO. 4. After cholinergic blockade, respiratory HR variations were eliminated, whereas the respiratory fluctuations in SV persisted. The fluctuations in CO and MAP increased. In this situation, mechanically induced variations in SV were not counteracted by inverse HR fluctuations and the influence on CO thus increased. 5. The main source of respiratory fluctuations in MAP in supine humans is thus variation in SV, while inverse, vagally mediated HR variations tend to reduce the fluctuations in CO and MAP.

Adult↗
PubMed1991

The effect of meal size on postprandial increase in cardiac output.

Heart rate, stroke volume, cardiac output and mean arterial blood pressure were followed from the resting pre-meal situation and for 2 hours after intake of standardized meals in four healthy individuals. Continuous records of stroke volume and cardiac output were achieved with an improved method of Doppler ultrasonography. A smallish meal and one 2 1/2 times larger were both given twice and in random order to each of the four test persons. The consumption of a meal invariably resulted in a cardiac output increase, which developed gradually to reach a maximum level 30 to 60 min after end of the meal. The postprandial cardiac output increase resulted from significant increases in both heart rate and stroke volume. There were distinct and significant differences between the circulatory responses to small and large meals. The increase in cardiac output after a large meal was considerably larger and lasted for longer than the increase after a small meal. Two hours after a small meal cardiac output was nearly or fully back to pre-meal values, while cardiac output was still markedly elevated 2 hours after a large meal. Consequently, the total 'extra' amount of blood delivered by the heart over 2 post-meal hours was significantly--about 100%--larger after the large meal than after the small one. Mean arterial blood pressure either fell or remained almost unchanged in the hour after a meal, so that total peripheral resistance was consistently and significantly reduced in the postprandial period--and considerably more so after a large meal than after a small one.

Adult↗