Are arterial blood pressure fluctuations buffered or reinforced by respiratory sinus arrhythmia (RSA)? There is still considerable argument about this simple question. recordings of each of these variables, and the phase relations between them were determined by cross-spectral analysis. MAP fluctuations increased after removing heart rate variations buy Zardaverine in both supine and tilted position, whereas SP fluctuations decreased in the supine position and increased in the head-up tilted position. RSA buffers respiration-synchronous fluctuations in MAP in both positions. However, fluctuations in SP were reinforced by RSA in the supine and buffered in the tilted position. The relationship between RSA and respiration-synchronous variance in arterial blood pressure is still under conversation. RSA is caused by changes in vagal impulse traffic at resting respiratory frequency (Saul & Cohen, 1994). Variations in arterial blood pressure may be caused by variations in total peripheral resistance (TPR) or in cardiac output (CO). At the respiratory frequency, the sympathetic nerves controlling the peripheral arteries do conduct the quick changes in arterial blood pressure, but these changes need a certain time to develop fully over the synapse and to obtain a fully contracting effect buy Zardaverine on the easy muscle tissue in the arterial wall (Toska 1994). This leaves us with fluctuations in CO to explain the respiration-synchronous blood pressure variations. Cardiac output variability is caused by variations in HR and SV: CO=HR buy Zardaverine SV. Thus, respiration-synchronous blood pressure variations could be caused by HR variations. If this is the case, they would vanish or be weakened after the administration of atropine. Blood pressure variance may also be caused by SV variations. If the respiration-synchronous blood pressure variations were reinforced by SV variations and weakened by HR variations, they would increase after atropine administration, since atropine eliminates HR variations. In a previous study from our group, this was found to happen and taken to mean that HR variations buffer blood pressure variations at respiratory frequency (Toska & Eriksen, 1993). In contrast, a recent study by Taylor & Eckberg (1996) showed a decrease in respiration-synchronous blood pressure variations after removal of heart rate variations, and concluded that respiratory HR variations contributed to blood pressure fluctuations. However, the two studies were not entirely comparable, because Toska & Eriksen (1993) recorded MAP whereas Taylor & Eckberg (1996) recorded SP and diastolic pressure (DP). In clinical practice we are used to referring to SP and DP since these are what we measure with a sphygmomanometer. With continuous measurements of arterial pressure it is possible to integrate MAP into the analysis. In order to test the influence of methodological differences we analysed respiration-synchronous variations in MAP and SP both before and after medication, in addition to the variations in HR, SV and CO both in the supine position and in a 30 deg head-up tilt position (Taylor & Eckberg, 1996; Sloan 1997). METHODS Subjects Ten healthy volunteers C five males and five females C were studied (age, 25.2 3.7 years (mean s.d.); height, 170.3 8.6 cm; excess weight, 68.2 8.4 kg). All subjects were non-smokers and none was taking any medication. Written informed consent was obtained from all participants, and the experimental protocol was approved Rabbit polyclonal to AFP (Biotin) by the Massachusetts Institute of Technology Committee on the Use of Humans as Experimental Subjects. All experiments were performed at the Clinical Research Center, Massachusetts Institute of Technology. All experiments conformed with the Declaration of Helsinki. Experimental design This investigation was a part of a more considerable study, which explains why parts of the protocol are not relevant to the present investigation. Cardiovascular recordings were obtained before, during and after medication on two different.