Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    SYMBIOTIC RELATIONSHIP BETWEEN A RESEARCH INSTITUTE AND A PHARMACEUTICAL COMPANY: THE BAKER INSTITUTE/GLAXO AUSTRALIA STORY (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The Baker Medical Research Institute is a non-profit, charitable institution to advance knowledge and solve problems in the area of cardiovascular medicine. This allows scientists to collaborate within a critical mass and be flexible in their approach to research.2. The Institute has interactions with the pharmaceutical industry at three levels: (i) contract research on a specific molecule; (ii) clinical trials; and (iii) collaborative basic research agreements.3. The Glaxo Australia-Baker Medical Research Institute Agreement is for curiosity driven research in specified areas of vascular pharmacology of interest to Glaxo Group Research.4. The relationship between universities, research institutes and the pharmaceutical industry is discussed in terms of the starting point for drug development.5. The enormous cost (US$100 million), lead time (10 years) and uncertainty of a successful profitable drug are compelling reasons why an independent pharmaceutical company is unlikely to succeed in Australia today.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1992.tb00400.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    CONTRACTILE RESPONSES TO α1-ADRENOCEPTOR STIMULATION DURING MATURATION IN THE AORTA OF THE NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RAT: RELATION TO STRUCTURE (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 17 (1990), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The significantly greater rise in blood pressure during the first 20 weeks of life in spontaneously hypertensive rats (SHR) when compared with normotensive Wistar-Kyoto rats (WKY) may be related to increased vasoconstrictor responses caused by enhanced transmitter release or post-junctional receptor changes.2. The reactivity of rat isolated aorta to post-junctional α1-adrenoceptor stimulation by methoxamine and to transmural sympathetic nerve stimulation was studied in ring segments suspended at equivalent transmural pressures in organ baths.3. Wall stress in the SHR aorta was significantly higher at 4 weeks, but lower at 9 and 20 weeks when compared with the WKY aorta, a possible adaptation to the higher pressures seen in the SHR at the latter ages.4. The sensitivity (location of EC50) to methoxamine was similar at all ages in both strains, but the SHR aortae at 9 and 20 weeks generated higher maximal contractile force to this agent compared with the WKY aorta.5. The increase in force to methoxamine parallelled the medial hypertrophy of the SHR aorta, determined from computerized morphometric analysis.6. There was an enhanced response to transmural field stimulation in the SHR aortae at 9 weeks, that was not accounted for by medial hypertrophy or altered neuronal uptake of noradrenaline.7. These studies suggest that enhanced maximal contractile force in the SHR aorta to α1-adrenoceptor stimulation is accounted for by medial hypertrophy. However, there is an additional enhanced reactivity at 9 weeks in response to nerve stimulation in the SHR aorta that may be related to increased innervation density.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1990.tb01266.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    CARDIOVASCULAR ACTIONS OF THE VENOM FROM THE IRUKANDJI (CARUKIA BARNESI) JELLYFISH: EFFECTS IN HUMAN, RAT AND GUINEA-PIG TISSUES IN VITRO AND IN PIGS IN VITRO (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. We have investigated the cardiovascular pharmacology of the crude venom extract (CVE) from the potentially lethal, very small carybdeid jellyfish Carukia barnesi, in rat, guinea-pig and human isolated tissues and anaesthetized piglets.2. In rat and guinea-pig isolated right atria, CVE (0.1–10 µg/mL) caused tachycardia in the presence of atropine (1 µmol/L), a response almost completely abolished by pretreatment with tetrodotoxin (TTX; 0.1 µmol/L). In paced left atria from guinea-pig or rat, CVE (0.1–3 µg/mL) caused a positive inotropic response in the presence of atropine (1 µmol/L).3. In rat mesenteric small arteries, CVE (0.1–30 µg/mL) caused concentration-dependent contractions that were unaffected by 0.1 µmol/L TTX, 0.3 µmol/L prazosin or 0.1 µmol/L ω-conotoxin GVIA.4. Neither the rat right atria tachycardic response nor the contraction of rat mesenteric arteries to CVE were affected by the presence of box jellyfish (Chironex fleckeri) antivenom (92.6 units/mL).5. In human isolated driven right atrial trabeculae muscle strips, CVE (10 µg/mL) tended to cause an initial fall, followed by a more sustained increase, in contractile force. In the presence of atropine (1 µmol/L), CVE only caused a positive inotropic response. In separate experiments in the presence of propranolol (0.2 µmol/L), the negative inotropic effect of CVE was enhanced, whereas the positive inotropic response was markedly decreased.6. In anaesthetized piglets, CVE (67 µg/kg, i.v.) caused sustained tachycardia and systemic and pulmonary hypertension. Venous blood samples demonstrated a marked elevation in circulating levels of noradrenaline and adrenaline.7. We conclude that C. barnesi venom may contain a neural sodium channel activator (blocked by TTX) that, in isolated atrial tissue (and in vivo), causes the release of transmitter (and circulating) catecholamines. The venom may also contain a ‘direct’ vasoconstrictor component. These observations explain, at least in part, the clinical features of the potentially deadly Irukandji syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.2005.04258.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Cardiovascular reflex responses after intrathecal ω-conotoxins or dexmedetomidine in the rabbit (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. The effects of thoracic intrathecal doses (1 µg/kg) of the α2-adrenoceptor agonist dexmedetomidine and ω-conotoxins MVIIA and CVID on vasoconstrictor and heart rate responses to acute central hypovolaemia were studied in seven chronically instrumented rabbits.2. Gradual inflation of an inferior vena cava cuff to reduce cardiac index (CI) by 8% per minute induced progressive vasoconstriction and an increase in heart rate (phase I). At approximately 40% of resting CI, there was sudden decompensation with failure of vasoconstriction and decrease in mean arterial pressure (MAP; phase II).3. Both intrathecal MVIIA and CVID decreased resting CI (by 20% at 3 h), but only MVIIA significantly reduced resting MAP (P = 0.003). Dexmedetomidine resulted in transient bradycardia, but no other significant change in the resting circulation. With simulated haemorrhage, the relationship between CI and vascular conductance was shifted after MVIIA (1–3 h after injection) so that there was less vasoconstriction and a reduced increase in heart rate by the end of phase I compared with other treatments (P = 0.002 and P = 0.009, respectively). One hour after injection, dexmedetomidine reduced the slope of the phase I vasoconstrictor response (P = 0.03), but did not significantly alter the end-point of the response. With failure of vasoconstriction and the onset of phase II, vascular conductance was higher after MVIIA compared with controls. Both conotoxins caused progressive failure of vasoconstriction rather than recovery during phase II (P 〈 0.001).4. Intrathecal injections of these drugs to control chronic pain may compromise cardiovascular responses to changes in central blood volume. At the single doses studied, there were significant differences between the responses to simulated haemorrhage after MVIIA or dexmedetomidine compared with CVID, with the prolonged effect after MVIIA most likely to be of clinical significance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2003.03795.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    ROLE OF THE ENDOTHELIUM IN THE GENESIS OF CARDIOVASCULAR DISEASE (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 〈list xml:id="l1" style="custom"〉1Endothelial cells release nitric oxide (NO) and the putative endothelium-derived hyperpolarizing factor (EDHF) in response to an increase in shear stress and receptor stimulation.2Tests of endothelial function have principally used acetylcholine (ACh)-mediated relaxation of precontracted isolated blood vessels or increases in forearm blood flow measured by venous occlusion plethysmography. Basal NO release is tested by a rise in resistance during infusion of the NO synthase inhibitor L-NMMA. Potential traps for investigators looking to evoke endothelial dysfunction following reduced ACh responses are discussed.3Endothelial dysfunction appears to occur in large but not small arteries in human and animal hypertension. Patients with long-standing congestive heart failure have endothelial dysfunction in buttock skin resistance arteries and there is coronary artery endothelial dysfunction following coronary ischaemia.4Remodelled arteries from neointimal thickening as a result of coronary collateral development in dog heart and new angiogenic vessel growth following large artery occlusion in the rabbit hindlimb appear to have normal endothelial function in relation to NO release.5Development of specific NO synthase inhibitors, antagonists of EDHF and the constrictor peptide endothelin, will clarify the role of these endothelium-derived factors in the cause or maintenance of vascular dysfunction. Defining redundancy and hierarchy of importance of these vascular factors are areas for future resolution.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb03036.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    ω-CONOTOXIN GVIA AND PRAZOSIN, BUT NOT FELODIPINE, CAUSE POSTURAL HYPOTENSION IN RABBITS (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The aim was to compare the effect of N-type calcium channel blockade by ω-conotoxin GVIA (ω-CTX) with α1-adrenoceptor or L-type calcium channel blockade on postural adaptation in conscious rabbits.2. Orthostatic responses were assessed by rapidly tilting the rabbits through 90° for 1 min. Tilts were performed before, 30 and 60 min after i.v. bolus administration of vehicle (propylene glycol 0.17mL/kg; n = 8), prazosin (0.5mg/kg; n= 8), felodipine (30μg/kg; n= 8) or ω-CTX (3 & 7 μg/kg; n = 9).3. Prazosin, felodipine or ω-CTX caused significant falls in mean arterial pressure (MAP) with corresponding increases in heart rate (HR). Vehicle administration had no effect on MAP but caused a small fall in HR.4. Before drug or vehicle administration, a small rise in MAP and HR occurred in response to tilt in all rabbits. In the vehicle treatment group, similar responses were observed to tilt at 30 and 60 min. Postural hypotension was observed in the prazosin treatment group, but not following administration of felodipine. Tilts 30 and 60 min after ω-CTX (3μg/kg) caused an increase in HR but no change in MAP, different to the small pressor response observed following vehicle administration. However, following administration of ω-CTX 7 μg/kg (total dose, 10μg/kg), significant falls in MAP with tachycardia were observed in response to tilt.5. In conclusion, orthostatic hypotension was observed following acute αl-adrenoceptor or N-type calcium channel blockade in the conscious rabbit. These findings are compatible with the expectation that agents which are directly sympatholytic interfere with postural adaptation. In contrast, L-type calcium channel antagonism with felodipine did not elicit postural hypotension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb01924.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    SELECTIVITY OF ω-CONOTOXIN GVIA FOR N-TYPE CALCIUM CHANNELS IN RAT ISOLATED SMALL MESENTERIC ARTERIES (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 〈list xml:id="l1" style="custom"〉1The selectivity of ω-conotoxin GVIA (ω-CTX) for prejunctional N-type voltage-operated calcium channels (VOCC) was examined in rat isolated small mesenteric arteries mounted in a Mulvany-Halpern myograph. Contractile responses to perivascular nerve stimulation, noradrenaline (NA) and potassium (K+) were obtained before and after treatment with ω-CTX. The effects of ω-CTX were compared with those of felodipine, an L-type VOCC blocker.2(ω-CTX (3nmol/L-10 μmol/L) inhibited contractions to electrical field stimulation by up to 94%, compared with the corresponding time control group. Felodipine (0.1 μmol/L) had little effect on the contractions to electrical stimulation compared with the vehicle-treated vessels.3Concentration-response curves to exogenous NA (0.1–30 μmol/L) and contractions to a submaximal concentration of K+ (50 mmol/L) were unaffected by ω-CTX (3 nmol/L-10 μmol/L). In contrast, the maximum contraction to NA in vessels exposed to felodipine (0.1 μmol/L) was reduced by 37%, and the contraction to K+ (62 mmol/L) was reduced by 84% compared with vehicle-treated arteries.4The results indicate that even at concentrations up to 10 μmol/L (10000-fold higher than required to inhibit prejunctional N-type VOCC), ω-CTX inhibits only neurotransmitter release. Its effects are clearly different to felodipine as ω-CTX has no effect on post-junctional α1-adrenoceptor-mediated vasoconstriction or direct smooth muscle depolarization considered to be mediated by L-type VOCC. Therefore, at least at the vascular neuroeffector junction, ω-CTX appears to be highly selective for N-type VOCC with no effect on L-type VOCC.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb03056.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    EVIDENCE FOR IMPAIRED ENDOTHELIUM DEPENDENT VASODILATION IN EXPERIMENTAL LEFT VENTRICULAR DYSFUNCTION (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The full range of vascular reactivity was investigated in the hindlimb circulation of conscious, autonomically blocked rabbits with experimental (adriamycin-induced) cardiomyopathy.2. Adriamycin treatment caused a significant reduction in left ventricular systolic function, as assessed by echocardiography (left ventricular fractional shortening, controls vs adriamycin treatment; 36.7 ± 1.7%vs 27.3 ± 2.6%, P〈0.05).3. Under pharmacological autonomic effector block, the range of the vasodilator response (resistance range, from resting to full vasodilatation) to acetylcholine was reduced by 41% (P〈0.05) and by 37% for adenosine (P〈0.05). Despite these changes the sensitivity (ED50) of the responses were unaltered.4. The ED50 of constrictor responses to noradrenaline and angiotensin II were similarly unaltered, in conjunction with a non-significant attenuation of the constrictor-response range.5. These results suggest that in this model of experimental left ventricular dysfunction, the capacity of the hindlimb circulation to respond to regionally infused endothelium dependent vasodilators is attenuated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02574.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    THE EFFECTS OF CENTRAL ADMINISTRATION OF ω-CONOTOXIN GVIA ON CARDIOVASCULAR PARAMETERS AND AUTONOMIC REFLEXES IN CONSCIOUS RABBITS (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of central administration of ω-conotoxin GVIA (ω-CTX), an N-type calcium channel blocker, were examined in conscious rabbits implanted with lateral intracerebroventricular (i.c.v.) cannulae.2. Experiments were performed over 4 consecutive days. On day 1, the baroreceptor heart rate (induced by glyceryl trinitrate and phenylephrine) and Bezold-Jarisch like (elicited by serotonin) reflexes were measured before (0 h) and 2 h after central administration of ω-CTX (3 or 30 pmol/ kg, i.c.v.) or vehicle. On days 2–4, resting parameters and reflexes were again monitored but no further ω-CTX was administered.3. No change in heart rate (HR) was observed in any rabbit treatment group during the experimental period. In the vehicle (n= 6) and ω-CTX 3 pmol/kg (n = 6) groups, small falls in mean arterial pressure (MAP) of 6 ± 2 and 10 ± 3 mmHg, respectively, occurred between 0 and 24 h; MAP then remained stable. Baroreceptor-heart rate reflex curve parameters did not change in either of these groups during the 4 day period.4. Following administration of w-CTX 30 pmol/kg (n = 7), MAP decreased progressively and by 48 h had fallen by 19 ± 4 mmHg. Also at 48 h, a 20% decrease in HR range of the baroreceptor-heart rate reflex curve was seen without any change in the lower HR plateau from the 0 h control. This indicates that there was an attenuation of the sympathetically mediated upper component of the curve while the vagally mediated component was unaffected.5. The Bezold-Jarisch like reflex-induced bradycardia, mediated by the efferent vagus nerve, was unaffected by i.c.v. administration of vehicle or either dose of ω-CTX.6. Therefore, central administration of ω-CTX resulted in a slowly developing hypotensive response consistent with a sympatholytic action while vagally mediated reflexes were unaffected.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02457.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    THE ACETYLCHOLINE PARADOX: A CONSTRICTOR OF HUMAN SMALL CORONARY ARTERIES EVEN IN THE PRESENCE OF ENDOTHELIUM (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In animal experiments, acetylcholine is generally a vasodilator acting indirectly by releasing endothelium-derived relaxing factor (EDRF); for example, in dog and rabbit small coronaries mounted in a myograph, acetylcholine caused concentration-dependent relaxation.2. In human small coronary arteries taken from the atrial appendage, however, acetylcholine caused concentration-dependent contraction with a funcionally intact endothelium as shown by the relaxation in response to substance P, another stimulant of EDRF release.3. We propose that coronary microvessels from various species have variable populations of acetylcholine receptors on the medial smooth muscle that cause contraction and on the endothelium that cause the release of EDRF. In humans, the medial smooth muscle receptors appear to predominate, and may thus play a role in coronary vasoconstriction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1991.tb01373.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...