Determining arterial wave transit time from a single aortic pressure pulse in rats: vascular impulse response analysis

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Abstract

Arterial wave transit time ( τ _w) in the lower body circulation is an effective biomarker of cardiovascular risk that substantially affects systolic workload imposed on the heart. This study evaluated a method for determining τ _w from the vascular impulse response on the basis of the measured aortic pressure and an assumed triangular flow ( Q ^tri). The base of the unknown Q ^tri was constructed with a duration set equal to ejection time. The timing of the peak triangle was derived using a fourth-order derivative of the pressure waveform. Values of τ _ws obtained using Q ^tri were compared with those obtained from the measure aortic flow wave ( Q ^m). Healthy rats ( n = 27), rats with chronic kidney disease (CKD; n = 22), and rats with type 1 ( n = 22) or type 2 ( n = 11) diabetes were analyzed. The cardiovascular conditions in the CKD rats and both diabetic groups were characterized by a decrease in τ _ws. The following significant relation was observed ( P < 0.0001): τ _w ^triQ = −1.5709 + 1.0604 × τ _w ^mQ ( r ² = 0.9641). Our finding indicates that aortic impulse response can be an effective method for the estimation of arterial τ _w by using a single pressure recording together with the assumed Q ^tri.

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Noninvasive determination of age-related changes in the human arterial pulse.

R. Kelly, C. Hayward, A. Avolio … (1989)

Arterial pressure waves were recorded noninvasively from the carotid, radial, femoral, or all three of these arteries of 1,005 normal subjects, aged 2-91 years, using a new transcutaneous tonometer containing a high fidelity Millar micromanometer. Waves were ensemble-averaged into age-decade groups. Characteristic changes were noted with increasing age. In all sites, pulse amplitude increased with advancing age (carotid, 91.3%; radial 67.5%; femoral, 50.1% from first to eighth decade), diastolic decay steepened, and diastolic waves became less prominent. In the carotid pulse, there was, in youth, a second peak on the downstroke of the waves in late systole. After the third decade, this second peak rose with age to merge with and dominate the initial rise. In the radial pulse, a late systolic wave was also apparent, but this occurred later; with age, this second peak rose but not above the initial rise in early systole, even at the eighth decade. In the femoral artery, there was a single systolic wave at all ages. Aging changes in the arterial pulse are explicable on the basis of both an increase in arterial stiffness with increased pulse-wave velocity and progressively earlier wave reflection. These two factors may be separated and effects of the latter measured from pressure wave-contour analysis using an "augmentation index," determined by a computer algorithm developed from invasive pressure and flow data. Changes in peak pressure in the central (carotid) artery show increasing cardiac afterload with increasing age in a normal population; this can account for the cardiac hypertrophy that occurs with advancing age (even as other organs atrophy) and the predisposition to cardiac failure in the elderly. Identification of mechanisms responsible offers a new approach to reduction of left ventricular afterload.

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Experimental NIDDM: development of a new model in adult rats administered streptozotocin and nicotinamide.

P. Masiello, C Broca, R. Gross … (1998)

We took advantage of the partial protection exerted by suitable dosages of nicotinamide against the beta-cytotoxic effect of streptozotocin (STZ) to create a new experimental diabetic syndrome in adult rats that appears closer to NIDDM than other available animal models with regard to insulin responsiveness to glucose and sulfonylureas. Among the various dosages of nicotinamide tested in 3-month-old Wistar rats (100-350 mg/kg body wt), the dosage of 230 mg/kg, given intraperitoneally 15 min before STZ administration (65 mg/kg i.v.) yielded a maximum of animals with moderate and stable nonfasting hyperglycemia (155 +/- 3 vs. 121 +/- 3 mg/dl in controls; P < 0.05) and 40% preservation of pancreatic insulin stores. We also evaluated beta-cell function both in vitro and in vivo 4-9 weeks after inducing diabetes. In the isolated perfused pancreas, insulin response to glucose elevation (5-11 mmol/l) was clearly present, although significantly reduced with respect to controls (P < 0.01). Moreover, the insulin response to tolbutamide (0.19 mmol/l) was similar to that observed in normal pancreases. Perfused pancreases from diabetic animals also exhibited a striking hypersensitivity to arginine infusion (7 mmol/l). In rats administered STZ plus nicotinamide, intravenous glucose tolerance tests revealed clear abnormalities in glucose tolerance and insulin responsiveness, which were interestingly reversed by tolbutamide administration (40 mg/kg i.v.). In conclusion, this novel NIDDM syndrome with reduced pancreatic insulin stores, which is similar to human NIDDM in that it has a significant response to glucose (although abnormal in kinetics) and preserved sensitivity to tolbutamide, may provide a particularly advantageous tool for pharmacological investigations of new insulinotropic agents.

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Arterial stiffness, systolic blood pressure, and logical treatment of arterial hypertension.

Donald M. O’Rourke (1990)

Arterial stiffening is the principal cause of increasing systolic pressure with advancing years and in patients with arterial hypertension. It is associated with progressive arterial dilation and is due to degeneration of the arterial wall, probably as a consequence of repetitive cyclic stress; it increases systolic pressure directly by increasing amplitude of the pressure wave generated by a given flow impulse from the heart and indirectly by increasing wave velocity so that wave reflection from the periphery occurs earlier, augmenting pressure in late systole. The first mechanism affects pressure in both the central and peripheral arteries, the second predominantly in the central arteries. Change in brachial systolic pressure with age underestimates the rise in systolic pressure in the aorta and left ventricle. Arterial stiffness is reduced passively with reduction in arterial pressure. Drugs have little or no direct effect on arterial stiffness but can markedly reduce wave reflection. In patients with stiffened arteries, reduction in wave reflection decreases aortic systolic pressure augmentation. The decreased systolic pressure in central arteries brought about by this mechanism is not detected when systolic pressure is measured in a peripheral (brachial or radial) artery but can be inferred from change in contour of the pressure wave recorded in peripheral arteries.

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Journal

Journal ID (nlm-ta): Sci Rep

Journal ID (iso-abbrev): Sci Rep

Title: Scientific Reports

Publisher: Nature Publishing Group

ISSN (Electronic): 2045-2322

Publication date (Electronic): 19 January 2017

Publication date Collection: 2017

Volume: 7

Electronic Location Identifier: 40998

Affiliations

[1 ]Department of Physiology, College of Medicine, National Taiwan University , Taipei, 100, Taiwan

[2 ]Department of Emergency Medicine, National Taiwan University Hospital , Chu-Tung Branch, Hsin-Chu, 310, Taiwan

[3 ]Department of Internal Medicine, National Taiwan University Hospital , Taipei, 100, Taiwan

[4 ]Institute of Biomedical Engineering, College of Medicine and Engineering, National Taiwan University , Taipei, 100, Taiwan

[5 ]Department of Surgery, National Taiwan University Hospital , Taipei, 100, Taiwan

[6 ]Department of Surgery, National Taiwan University Hospital , Hsin-Chu Branch, Hsin-Chu, 300, Taiwan

Author notes

[a ] kcchang1008@ 123456ntu.edu.tw

[*]

These authors contributed equally to this work.

Article

Publisher Item ID: srep40998

DOI: 10.1038/srep40998

PMC ID: 5244412

PubMed ID: 28102355

SO-VID: dc7264db-f5bd-4ec4-a26c-6ca29e487173

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History

Date received : 06 October 2016

Date accepted : 13 December 2016

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Determining arterial wave transit time from a single aortic pressure pulse in rats: vascular impulse response analysis

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Most cited references 16

Noninvasive determination of age-related changes in the human arterial pulse.

Experimental NIDDM: development of a new model in adult rats administered streptozotocin and nicotinamide.

Arterial stiffness, systolic blood pressure, and logical treatment of arterial hypertension.

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