Spt 301

A vascular tonometer (SPT301, Millar Inc., Houston, TX, USA) was used to obtain the radial artery pulse wave. The original pulse wave signal and electrocardiogram were integrated and sent to a physiological signal monitoring system (MP36, Biopac Systems, Inc., Goleta, CA, USA) for later analyses. A customized Matlab program was used to convert the radial artery waveform into a carotid artery waveform to obtain central systolic blood pressure (cSBP), diastolic pressure (cDBP), pulse pressure (cPP), augmented pressure, and augmentation index (AI%). By using the triangulation method, the carotid artery waveform was separated into the incident and reflected waves [28 (link),29 (link)], to determine the forward (Pf) and backward (Pb) pressure waves, aortic characteristic impedance (Zc), systolic time (ST; an index of cardiac sympathetic activity) [30 (link)], and the subendocardial viability ratio (SEVR) [28 (link)]. SEVR, also known as the Buckberg index, has been used as a surrogate measure of myocardial perfusion that correlates with the ratio of subendocardial to subepicardial blood flow, which is indicative of poorer perfusion if the SEVR value is lower than 1.0 [31 (link)].

Each participant rested in the supine position at least for 10 min before this measurement. Arterial stiffness was assessed by carotid-femoral pulse wave velocity (cfPWV) that calculated from the traveling distance and foot-to-foot wave transit time between two arterial recording sites (Huang et al., 2015 (link), 2016 (link)). Non-invasive pulse tonometer (SPT-301, Millar Inc., Houston, TX, USA) that was connected to a physiological signaling processing system (MP36, Biopac, Goleta, CA, USA) was used to detect pulse waves on the carotid and femoral arteries, and cfPWV (cm/s) was calculated by the distance (cm) and pulse waves (s) between carotid and femoral arteries (Huang et al., 2015 (link), 2016 (link)).

Measures of arterial stiffness were determined at baseline and in response to AngII infusion, as outlined above. Peripheral arterial pressure waveforms were recording by application tonometry using Sphygmocor system. Pulse‐wave velocity (PWV) was determined by sequential acquisition of pressure waveform from two sites sequentially (carotid and femoral arteries). The timing of the waveforms was compared with that of the R‐wave on a simultaneously recorded ECG. The distance travelled was calculated by subtracting the distance from carotid pulsation to femoral pulsation, following the anatomic line to avoid the influence of breast and abdomen on the distance measurement. The aortic augmentation index (AIx) was determined by applanation tonometry of the right radial artery using a Millar piezoresistive pressure transducer (Millar SPT 301; Millar Instruments, Houston, TX) coupled to a Sphygmocor device (PWV Medical).

Measures of arterial stiffness were determined at baseline and in response to Ang‐II infusion, as outlined above. The aortic augmentation index (AIx) was determined by applanation tonometry of the right radial artery using a Millar piezoresistive pressure transducer (Millar SPT 301; Millar Instruments, Houston, TX) coupled to a Sphygmocor device (PWV Medical).
Pulse‐wave velocity (PWV) was determined by sequential acquisition of pressure waveforms from the carotid to the radial arteries or from the carotid to the femoral arteries by the use of same tonometer. The timing of these waveforms was compared with that of the R‐wave on a simultaneously recorded ECG. PWV_{carotid‐radial} was measured in the first 33 subjects before a protocol change resulting in measurement of PWV_{carotid‐femoral} in the subsequent 19 subjects. No individuals had both their PWV_{carotid‐femoral} and PWV_{carotid‐radial} measured. However, a sensitivity analysis using only carotid‐femoral/carotid‐radial PWV revealed similar results.

We recorded the arterial pulse waveform from the right common carotid artery with the patient in a supine position, using a high-fidelity external applanation tonometric device (Millar SPT-301, Millar Instruments Inc., Houston, USA). Recordings were obtained semi-simultaneously with echocardiographic doppler recordings (Vivid 7 ultrasound scanner, GE Vingmed ultrasound, Norway) of blood flow from the left ventricular outflow tract and the parasternal short axis midventricular cineloops. The tonometric signal was amplified and transferred to a personal computer for processing in Matlab 7 application [11 (link)]. We selected at least three cardiac cycles for analysis. The carotid pulse trace peak and nadir were then calibrated with the systolic and diastolic brachial arterial pressures, respectively.

cfPWV was determined in anaesthetised mice under 1.5–2.5% (v/v) isoflurane (Forene; Abbvie, Wavre, Belgium), as previously described by our research group [58 (link)]. In brief, two pulse tonometers (SPT-301, Millar Instruments, Wokingham, United Kingdom) were applied on the skin using a micromanipulator. Carotid–femoral transit time (Δt) was determined using the time difference between the foot of carotid and femoral artery pulses (foot-to-foot method). The foot of the pressure wave was defined as the second derivative maximum. Twenty consecutive pulses with sufficient amplitude and a reproducible waveform were analysed; pulses that interfered with respiratory movement peaks were excluded.