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  • Atenolol  (1)
  • Hindquarters bed  (1)
  • Nitric oxide synthase inhibitors  (1)
  • 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
    Effects of nitric oxide synthase inhibitors on systemic hypotension, cytokines and inducible nitric oxide synthase expression and lung injury following endotoxin administration in rats (1999)
    Springer
    Journal of biomedical science 6 (1999), S. 28-35 
    Details
    ISSN: 1423-0127
    Keywords: Lung injury ; Nitric oxide synthase inhibitors ; Nitric oxide ; IL-1β
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Endotoxin shock is characterized by systemic hypotension, hyporeactiveness to vasoconstrictors and acute lung edema. A nitric oxide synthase (NOS) inhibitor, NG-monomethyl-L-arginine (L-NMMA) has been shown to be effective in reversing acute lung injury. In the present study, we evaluated the effects of NOS blockade by different mechanisms on the endotoxin-induced changes. In anesthetized rats, lipopolysaccharide (LPS,Klebsiella pneumoniae) was administered intravenously in a dose of 10 mg/kg. LPS caused sustained systemic hypotension accompanied by an eightfold increase of exhaled NO during an observation period of 4 h. After the experiment, the lung weight was obtained and lung tissues were taken for the determination of mRNA expressions of inducible NOS (iNOS), interleukin-1β (IL-1β) and tumor necrosis factor-α-(TNF-α). Histological examination of the lungs was also performed. In the control group injected with saline solution, mRNA expressions of iNOS, IL-1β and TNF-α were absent. Four hours after LPS, the mRNA expressions of iNOS and IL-1β were still significantly enhanced, but TNF-α was not discernibly expressed. LPS also caused a twofold increase in lung weight. Pathological examination revealed endothelial damage and interstitial edema. Various NOS inhibitors were given 1 h after LPS administration. These agents included Nω-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg), a constitutive NOS and iNOS inhibitor; S,S′-1,4-phenylene-bis-(1,2-ethanedinyl) bis-isothiourea dihydrobromide (1,4-PBIT, 10 mg/kg), a relatively specific iNOS inhibitor, and dexamethasone (3 mg/kg), an inhibitor of iNOS expression. These NOS inhibitors all effectively reversed the systemic hypotension, reduced the exhaled NO concentration and prevented acute lung injury. The LPS-induced mRNA expressions of iNOS and IL-1β were also significantly depressed by these NOS inhibitors. Our results suggest that NO production through the iNOS pathway is responsible for endotoxin-induced lung injury. Certain cytokines such as IL-1β are possibly involved. These changes are minimized by NOS inhibitors through different mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02256421
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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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