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  • Arterial impedance  (2)
  • Mesenteric bed  (1)
  • Pulmonary hypertension  (1)
  • Pulsatile haemodynamics  (1)
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Material
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Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Beta-adrenergic mechanisms in arterial hemodynamics: A comparison between normotensive and hypertensive rats (1996)
    Springer
    Journal of biomedical science 3 (1996), S. 286-292 
    Details
    ISSN: 1423-0127
    Keywords: β-Adrenergic blockade ; Propranolol ; Atenolol ; Hemodynamics ; Arterial impedance ; Hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The purpose of this study was to determine whether β-adrenergically mediated cardiovascular functions such as arterial pressure (AP), heart rate (HR), stroke volume (SV), cardiac output (CO), peripheral resistance (Rp), arterial impedance (Zc), mean arterial compliance (Cm) and pulse wave reflection (Pb) were altered in the spontaneously hypertensive rat (SHR) compared to the normotensive Wistar Kyoto rat (WKY). In pentobarbital-anesthetized and artificially ventilated rats, the aortic pressure wave was recorded with a high-fidelity Millar sensor, and aortic flow wave with an electromagnetic flow probe. The pressure and flow waves were subjected to Fourier transform so as to analyze impedance spectra. Acute β-adrenergic blockade was produced by an intravenous injection of propranolol (nonselective) and atenolol (selective β1-blocker) at doses of 2 and 5 mg/kg, respectively. Steady-state parameters were obtained 15–20 min after intravenous administration. The SHR had higher AP, HR, Rp and Zc than the WKY. SV and CO remained unaltered while Cm was lower. In response to propranolol, the mean AP was increased by 7 mm Hg in the WKY, but did not change in the SHR. Moreover, significant decreases occurred in HR, CO and Cm in addition to increases in Rp, Zc and Pb. These changes between the SHR and WKY were only slight. Atenolol caused decreases in AP, HR and CO in both SHR and WKY, but did not significantly alter the Rp, Zc, Cm and Pb. Again, the atenolol-induced changes in AP, HR and CO did not appear to be significantly different between SHR and WKY. The results indicate that β-adrenergic effects on the heart, Windkessel and resistance vessels are neither greatly enhanced nor impaired during the development of hypertension. In the hypertensive state, significant β-adrenergic mechanisms still exert tonic vasodilatory effects on the large and small arterial system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253709
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Nitric oxide in systemic and pulmonary hypertension (1997)
    Springer
    Journal of biomedical science 4 (1997), S. 244-248 
    Details
    ISSN: 1423-0127
    Keywords: Nitric oxide ; NO synthase inhibitor ; Hypertension ; Arterial hemodynamics ; Vasodilatation ; Hypoxia ; Pulmonary hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Endothelium-derived nitric oxide (NO) is an important gas molecule in the regulation of vascular tone and arterial pressure. It has been considered that endothelial dysfunction with impairment of NO production contributes to a hypertensive state. Alternatively, long-term hypertension may affect the endothelial function, depress NO production, and thereby reduce the dilator action on vasculatures. There were many studies to support that endothelium-dependent vasodilatation was impaired in animals and humans with long-term hypertension. However, results of some reports were not always consistent with this consensus. Recent experiments in our laboratory revealed that an NO synthase inhibitor, NG-nitro-L-arginine monomethyl ester (L-NAME) caused elevation of arterial pressure (AP) in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). The magnitude of AP increase following NO blockade with L-NAME was much higher in SHR than WKY. In other experiments with the use of arterial impedance analysis, we found that L-NAME slightly or little affected the pulsatile hemodynamics including characteristic impedance, wave reflection and ventricular work. Furthermore, these changes were not different between SHR and WKY. The increase in AP and total peripheral resistance (TPR) following NO blockade in SHR were significantly greater than those in WKY, despite higher resting values of AP and TPR in SHR. In connection with the results of other studies, we propose that heterogeneity with respect to the involvement of NO (impairment, no change or enhancement) in the development of hypertension may exist among animal species, hypertensive models and different organ vessels. Our study in SHR provide evidence to indicate that the effects of basal release of NO on the arterial pressure and peripheral resistance are not impaired, but enhanced in the hypertensive state. The increase in NO production may provide a compensatory mechanism to keep the blood pressure and peripheral resistance at lower levels. The phenomenon of enhanced NO release also occurs in certain type of pulmonary hypertension. We first hypothesized that a decrease in NO formation might be responsible for the pulmonary vasoconstriction during hypoxia. With the measurement of NO release in the pulmonary vein, we found that ventilatory hypoxia produced pulmonary hypertension accompanying an increase in NO production. Addition of NO inhibitor (L-NAME), blood or RBC into the perfusate attenuated or abolished the NO release, while potentiating pulmonary vasoconstriction. During hypoxia, the increased NO formation in the pulmonary circulation similarly exerts a compensatory mechanism to offset the degree of pulmonary vasoconstriction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253424
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Acute adaptation and resetting of the baroreflex control of vascular resistance in the canine hindquarters and mesentery (1993)
    Springer
    Pflügers Archiv 424 (1993), S. 276-284 
    Details
    ISSN: 1432-2013
    Keywords: Carotid sinus ; Baroreflex adaptation ; Resetting ; Vascular resistance ; Hindquarters bed ; Mesenteric bed
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To determine whether acute adaptation and resetting occur in the baroreflex control of regional vascular resistance, experiments were conducted in anesthetized and vagotomized dogs. The carotid sinuses were vascularly isolated to regulate the carotid sinus pressure (CSP) in an open-loop fashion. The hindquarters (n= 12) and mesenteric (n=10) beds were perfused with constant flow and arterial perfusion pressures (HPP and MPP) were used to reflect changes in hindquarters and mesenteric resistance respectively. We first observed alterations in HPP and MPP during the course of CSP holding (conditioning pressure) at various levels for 15 min. Thereafter, the CSP was lowered to 50 mm Hg and increased stepwise to obtain the CSP-HPP and CSP-MPP baroreflex function curves. In experiments in the hindquarters bed, HPP stabilized at an average of 104.7 mm Hg during the initial conditioning pressure at 100 mm Hg. When conditioning pressure decreased to 50 mm Hg, the HPP increased to 125.5 mm Hg and then gradually declined to a steady level (115.6 mm Hg) in 5 min. An increase in conditioning pressure from 100 to 150 mm Hg caused HPP to decrease to 54.8 mm Hg followed by an upward adaptation to a steady level (80.2 mm Hg) in 5 min. The CSP/HPP curves constructed from the CSP step protocol were also affected by conditioning pressure. There were significant increases in the threshold and saturation pressures as conditioning pressure was elevated. However, the resetting was characterized by a parallel shift of the CSP/HPP curves without significant changes in baroreflex gain or sensitivity. Although the changes in mesenteric resistance in response to CSP changes were relatively weaker (lower gain), the phenomena of acute adaptation (MPP changes during 15-min conditioning pressure) and resetting (curve shift following different conditioning pressures) were still observed. In addition to the demonstration of adaptation and resetting of baroreflex control on the resistance in these two vascular beds, a graphical analysis is used to indicate that acute adaptation of the baroreflex responses is part of the resetting process. It is not necessarily associated with a decrease in sensitivity. Adaptation occurs as the baroreceptors “recognize” a new pressure in minutes and results from a shift of the HPP or MPP to a new level along the newly reset function curve.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00384353
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    The correlation of cardiac mass with arterial haemodynamics of resistive and capacitive load in rats with normotension and established hypertension (1994)
    Springer
    Pflügers Archiv 428 (1994), S. 533-541 
    Details
    ISSN: 1432-2013
    Keywords: Hypertension ; Ventricular afterload ; Cardiac hypertrophy ; Arterial impedance ; Pulsatile haemodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In hypertensive animals and humans, cardiac hypertrophy may occur as a consequence of an external load on the heart. Several studies have suggested that the non-pulsatile components of arterial haemodynamics, such as arterial pressure and vascular resistance, do not adequately represent the ventricular afterload and are not well correlated with the degree of cardiac hypertrophy (CH). The present study was undertaken to analyse the correlation between the degree of CH and various haemodynamic parameters in the spontaneously hypertensive rat (SHR) with established hypertension. A total of 36 SHRs (6–8 months) with a tail-cuff pressure above 190 mm Hg were used. Control data were obtained from 32 age-matched normotensive Wistar Kyoto rats (WKY). Animals were anaesthetized with pentobarbitone sodium (40 mg/kg i.p.) and artificially ventilated with a respirator. A Millar catheter with a high-fidelity pressure sensor was used to record the aortic pressure and an electromagnetic flow transducer to monitor the aortic flow. The pressure and flow signals were subjected to Fourier transformation for the analysis of the arterial impedance spectrum. The left ventricular weight-to-body weight ratio (LVW/BW) was taken as a measure of the degree of CH. The measured haemodynamic parameters in these anaesthetized, open-chest SHRs were systolic pressure (SP) (mean ± SE) 172±4 mm Hg, diastolic pressure (DP), 120±3 mm Hg, pulse pressure (PP) 52±2 mm Hg, peripheral resistance (R p) 344,032±8,012 dyne · s · cm−5, characteristic impedance (Zc) 6,442±313 dyne · s · cm−5, the impedance modulus at the first harmonic (Z1) 26,611±1,061 dyne · s · cm−5, mean arterial compliance (C m) 0.87 ±0.04 μl/mm Hg and LVW/BW 3.092±0.026 mg/g. These parameters were significantly greater than the corresponding values in WKY, except that C m was much decreased. In SHR, the LVW/BW was not significantly correlated with the SP, DP, R p and steady external power. In contrast, the degree of CH was positively correlated with Zc (r=0.66, P〈0.001), Z1 (r=0.62, P〈0.001) and pulsatile external work (r=0.41, P〈0.05). It was also positively correlated with the backward pressure wave (r=0.42, P〈0.05) and negatively correlated with C m (r=-0.72, P〈0.01). Such correlations of LVW/BW with pulsatile haemodynamics were not found in the normotensive WKY. The results indicate that the degree of cardiac hypertrophy in hypertensive rats, with a high blood pressure and increased stiffness of the arterial tree, is more closely related to pulsatile arterial haemodynamics than to the nonpulsatile components.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374575
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    Paper (German National Licenses)
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