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  • 1
    Electronic Resource
    Electronic Resource
    Effects of post-treatment with low-dose propofol on inflammatory responses to lipopolysaccharide-induced shock in conscious rats (2005)
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 32 (2005), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In the present study, we used a low dose of propofol (5 mg/kg per h) to investigate its effects on the pro-inflammatory cytokines (tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-10) and changes in nitric oxide (NO) following lipopolysaccharide (LPS) for a period of 12 h in conscious rats.2. Experiments were designed to induce endotoxin shock by intravenous injection of Klebsiella pneumoniae LPS (10 mg/kg) in conscious rats. Arterial pressure (AP) and heart rate (HR) were monitored continuously for 12 h after LPS administration. Tumour necrosis factor-α, IL-1β, IL-10 and plasma nitrates/nitrites were determined before and 0.5, 1, 3, 6, 9 and 12 h after LPS administration. A low dose of intravenous propofol (5 mg/kg per h) was administered to investigate the effects on cytokine responses and changes in NO in endotoxin shock.3. Lipopolysaccharide significantly increased TNF-α, IL-1β, IL-10, nitrites/nitrates and HR, whereas mean AP was decreased. Post-treatment with propofol suppressed the release of TNF-α, IL-1β, IL-10 and NO production after endotoxin shock.4. Lipopolysaccharide also caused a decrease in the white blood cell count and haematocrit.5. Post-treatment with propofol slightly, but not significantly, affected the LPS-induced systemic hypotension, tachycardia, leukocytopenia and anaemia.6. These findings suggest that low-dose propofol may be beneficial to the inflammatory change in sepsis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.2005.04155.x
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  • 2
    Electronic Resource
    Electronic Resource
    Nitric Oxide In Mesenteric Vascular Reactivity: A Comparison Between Rats With Normotension And Hypertension (2002)
    Melbourne, Australia : Blackwell Science Asia Pty. Ltd.
    Clinical and experimental pharmacology and physiology 29 (2002), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Nitric oxide (NO) plays an important role in various physiological functions. The continuous formation of endogenous NO from endothelial cells maintains a vasodilator tone and regulates blood flow and pressure. However, the role of NO in hypertension remains controversial.2. In the present study, we used an in situ mesenteric perfusion system. The primary objectives of the study were to examine whether or not mesenteric vasoreactivity is changed by alterations in perfusion pressure and to assess the role of NO in changes of vascular reactivity in hypertension.3. Spontaneously hypertensive rats (SHR; 12–15 weeks of age) and age-matched normotensive Wistar-Kyoto (WKY) rats were used as the experimental and control groups, respectively. Endothelium-dependent and -independent vasodilation was detected by acetylcholine (ACh) or NO donors (sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP)). Dose-dependent reactivity to these agents (10–6 to 10–4 mol/L) was detected by bolus intra-arterial injections of 10 μL of the test agents at 5 min intervals. Dose-dependent responses to vasoconstrictor drugs, such as noradrenaline (NA) and phenylephrine (PE; 10–6 to 10–4 mol/L) were also observed. The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg) was given to examine the contribution of NO to the vasoreactivity of the mesenteric bed.4. Acetylcholine, SNP and SNAP produced dose-dependent vasodilation in both WKY rats and SHR. The magnitude of the vasodilation was significantly greater in SHR than in WKY rats. It was also greater at high than low flow rates in SHR. The increase in mesenteric perfusion pressure following L-NAME was significantly higher in SHR than in WKY rats. However, there were no differences in responses to L-NAME between low and high flow rates in SHR. Endothelium-independent vasoconstriction (NA and PE) was dose dependent in both SHR and WKY rats. The magnitude of the endothelium-independent vasoconstriction was greater in SHR than in WKY rats.5. The results suggest that endothelium-dependent or -independent mesenteric vasoconstriction and vasodilation is enhanced in SHR compared with WKY rats, supporting the concept of enhancement of NO function in the hypertensive state. Flow-induced shear stress is also a key factor in the regulation of peripheral resistance depending on NO formation in hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2002.03643.x
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of an endogenous nitric oxide synthase inhibitor on phorbol myristate acetate-induced acute lung injury in rats (2003)
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 30 (2003), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In the present study, we determined whether the endogenous nitric oxide (NO) synthase (NOS) inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) could ameliorate the acute lung injury (ALI) induced by phorbol myristate acetate (PMA) in rat isolated lung.2. Typical ALI was induced successfully by PMA during 60 min of observation. At 2 µg/kg, PMA elicited a significant increase in microvascular permeability (measured using the capillary filtration coefficient Kfc), lung weight gain, lung weight/bodyweight ratio, pulmonary arterial pressure (PAP) and protein concentration of bronchoalveolar lavage fluid.3. Pretreatment with the NOS inhibitor l-NAME (5 mmol/L) significantly attenuated ALI. None of the parameters reflective of lung injury showed significant increase, except for PAP (P 〈 0.001). The addition of l-arginine (4 mmol/L) blocked the protective effective of l-NAME. Pretreatment with l-arginine exacerbated PMA-induced lung injury.4. These data suggest that l-NAME significantly ameliorates ALI induced by PMA in rats, indicating that endogenous NO plays a key role in the development of lung oedema in PMA-induced lung injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2003.03848.x
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  • 4
    Electronic Resource
    Electronic Resource
    EFFECTS OF INTRACRANIAL HYPERTENSION ON STEADY AND PULSATILE HAEMODYNAMICS IN DOGS (1999)
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 26 (1999), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Intracranial hypertension (ICH) tends to elicit various cardiovascular changes. Previous studies on the haemodynamic responses to ICH have been confined mainly to measurements of arterial pressure (AP), cardiac output (CO) and total peripheral resistance (TPR). In the present study, we used the technique of arterial impedance analysis for a complete assessment of steady and pulsatile haemodynamics in ICH.2. In anaesthetized dogs, aortic pressure and flow waves were obtained with high-fidelity Millar sensors. The pressure and flow waves were subjected to Fourier transformation (frequency analysis) for an analysis of impedance spectra. Intracranial pressure (ICP) was elevated by inflation of an epidural balloon. At an ICP of 50 mmHg, the changes in steady and pulsatile haemodynamics were slight.3. Haemodynamic changes became evident at an ICP of 100 mmHg. The mean AP was elevated by 31 mmHg (+32%) and heart rate (HR) was reduced by 25 b.p.m. (–18%). There was also a significant decrease in CO by 27% and large increase in TPR by 82%. With respect to pulsatile haemodynamics, an elevation of ICP to 100 mmHg caused significant increases in characteristic impedance by 45% and wave reflection by 53%. Arterial compliance was reduced by 50%. The ventricular oscillatory work was increased without a significant change in steady work.4. The results indicate that ICH causes constriction of resistance vessels to affect AP and TPR. Because the pulsatile haemodynamics reflect mainly the Windkessel functions, ICH also induces stiffness of the large vessels to affect arterial impedance, pulse wave reflection and ventricular oscillatory work.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.1999.03166.x
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  • 5
    Electronic Resource
    Electronic Resource
    NITRIC OXIDE INHIBITION ACCELERATES HYPERTENSION AND INDUCES PERIVASCULAR INFLAMMATION IN RATS (2004)
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 31 (2004), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Inflammatory changes in peripheral arteries have been reported in animal models of hypertension. Whether they occur in cerebral arteries (CA) with hypertension induced by deprivation of endogenous nitric oxide (NO) remains unknown.2. In the present study, we compared the arteriolar injury score (AIS) and perivascular inflammation in CA between hypertensive and normotensive rats following NO deprivation with the NO synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME). Five-week-old male spontaneously hypertensive rats (SHR) and Wistar -Kyoto (WKY) rats were fed with l-NAME (1 mg/mL) for 4 weeks.3. Nitric oxide deprivation resulted in time-dependent elevations in tail-cuff pressure (representing systolic blood pressure (SBP)) in both SHR and WKY rats. The magnitude of increase in SBP was larger in SHR (+81.0 ± 3.2 vs+25.0 ± 2.2 mmHg; P 〈 0.01). Arteriolar hyalinosis and AIS in various segments of the CA were assessed with periodic acid-Schiff staining and inflammatory cells were immunostained with the antibody against macrophage/monocyte marker (ED1). The ED1+ cells appeared in the middle CA of l-NAME-treated SHR as early as 2 weeks after treatment. These cells were not observed in l-NAME-treated WKY rats and untreated SHR. More ED1+ cells were found in l-NAME-treated SHR than l-NAME-treated WKY rats after 4 weeks treatment.4. The AIS and number of ED1+ cells around the perivascular area of the internal carotid artery were significantly higher in l-NAME-treated compared with untreated rats (AIS: 137 ± 28 vs 46 ± 10 for WKY rats, respectively; 169 ± 18 vs 53 ± 6 for SHR, respectively (P 〈 0.01); ED1+ cells: 7.9 ± 0.6 vs 1.3 ± 0.9 for WKY rats, respectively; 13.6 ± 2.7 vs 2.1 ± 0.9 for SHR, respectively (P 〈 0.01)), although SBP was higher in untreated SHR than in l-NAME-treated WKY rats (170 ± 4 vs 137 ± 4 mmHg, respectively; P 〈 0.05).5. These findings suggest that ED1+ cells appeared in the middle CA of l-NAME-SHR as early as 2 weeks after treatment. Chronic inhibition of NO accelerates hypertension and induces perivascular inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.2004.03977.x
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  • 6
    Electronic Resource
    Electronic Resource
    The Lung Is The Major Site That Produces Nitric Oxide To Induce Acute Pulmonary Oedema In Endotoxin Shock (2001)
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 28 (2001), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The present study was undertaken to determine the locus of nitric oxide (NO) production that is toxic to the lung and produces acute pulmonary oedema in endotoxin shock, to examine and compare the effects of changes in lung perfusate on endotoxin-induced pulmonary oedema (EPE) and to evaluate the involvement of constitutive and inducible NO synthase (cNOS and iNOS, respectively).2. Experiments were designed to induce septic shock in anaesthetized rats with the administration of Escherichia coli lipopolysaccharide (LPS). Exhaled NO, lung weight (LW)/bodyweight (BW) ratio, LW gain (LWG) and lung histology were measured and observed to determine the degree of EPE 4 h following LPS. The EPE was compared between groups in which LPS had been injected either into the systemic circulation or into the isolated perfused lung. The lung perfusate was altered from whole blood to physiological saline solution (PSS) with 6% albumin to test whether different lung perfusions affected EPE. Pretreatment with various NOS inhibitors was undertaken 10 min before LPS to investigate the contribution of cNOS and iNOS to the observed effects.3. Endotoxin caused profound systemic hypotension, but little change in pulmonary arterial pressure. The extent of EPE was not different between that induced by systemic injection and that following administration to isolated lungs preparations. Replacement of whole blood with PSS greatly attenuated (P 〈 0.05) EPE. In blood-perfused lungs, pretreatment with NOS inhibitors, such as Nω-nitro-L-arginine methyl ester, aminoguanidine and dexamethasone, significantly prevented EPE (P 〈 0.05).4. The major site of NO production through the whole blood is in the lung. The NO production mediated by the iNOS system is toxic to the endothelium in the pulmonary microvasculature. Inhalation of NO for patients with sepsis may be used with clinical caution. Therapeutic consideration of lung extracorporeal perfusion with PSS and pharmacological pretreatment with iNOS inhibitors may be warranted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2001.03446.x
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  • 7
    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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  • 8
    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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  • 9
    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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  • 10
    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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