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  • 1
    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
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  • 2
    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
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  • 3
    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
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  • 4
    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
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  • 5
    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
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  • 6
    Electronic Resource
    Electronic Resource
    Acute Effects Of L- And T-Type Calcium Channel Antagonists On Cardiovascular Reflexes In Conscious Rabbits (2002)
    Melbourne, Australia : Blackwell Science Pty
    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. The effects of the relatively selective T-type voltage- operated calcium channel (VOCC) antagonist mibefradil were compared with verapamil, an L-type VOCC antagonist, on a range of autonomic reflexes in conscious rabbits.2. Mean arterial pressure (MAP), heart rate (HR), the baroreceptor–HR reflex, postural adaptation reflex (90° head-up tilt), Bezold–Jarisch-like reflex and the vasoconstrictor component of the nasopharyngeal reflex were assessed before and during i.v. infusion of vehicle (saline), mibefradil or verapamil. Doses of mibefradil that gave low (M1; 0.45 ± 0.02 μg/mL) and high (M2; 0.93 ± 0.05 μg/mL) plasma concentrations, or verapamil (0.059 ± 0.004 μg/mL; n = 6 each) were chosen to mimic clinically observed therapeutic levels.3. At steady state infusion over 30–90 min, MAP was significantly lower in M2 (– 7 mmHg) and verapamil (– 6 mmHg) treatments, but only verapamil caused a significant tachycardia (+ 31 b.p.m.) compared with vehicle. Mibefradil (M2) and verapamil decreased the HR range of the baroreflex by 27 and 29%, respectively, but neither treatment affected the vagal or sympathetic constrictor components of the Bezold–Jarisch-like and nasopharyngeal reflexes, respectively.4. In response to 90° tilt, vehicle- and verapamil-treated rabbits responded with small rises in MAP of 4 ± 2 and 8 ± 2 mmHg, respectively, 5 s into the upright posture, while M1 and M2 caused falls in MAP of 6 ± 4 and 9 ± 3 mmHg, respectively, at 5 s.5. Thus, both L- and T-type VOCC antagonists, at plasma concentrations in the clinical range, lowered MAP in the conscious rabbit, but only mibefradil caused postural hypotension. We conclude that T-type VOCC may play an important role in the venoconstrictor reflex in response to tilt in the rabbit.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2002.03670.x
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of vascular endothelial growth factor (VEGF)A and VEGFB gene transfer on vascular reserve in a conscious rabbit hindlimb ischaemia model (2002)
    Oxford, UK : Blackwell Science Pty
    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. As a result of the ageing population, there are increasing numbers of patients with severe peripheral vascular occlusive disease associated with intermittent claudication (pain on walking) and decreased exercise tolerance. There is a great clinical need for pharmacological treatments that may stimulate collateral blood vessel growth, increase vascularity and improve skeletal muscle function.2. Therapeutic angiogenesis using growth factors such as vascular endothelial growth factor (VEGF) has been used to improve collateral artery development in myocardial or skeletal muscle ischaemia. The broad aims of the work briefly summarized here were to compare the effects of VEGFA165 and VEGFB167 (500 µg, i.m., gene transfer) on calf blood pressure ratio and reactive hyperaemia in a chronic rabbit preparation with unilateral limb ischaemia.3. Unilateral femoral artery ligation caused an immediate deficit (compared with the contralateral limb) of 72% in calf systolic blood pressure. There were improvements 14 days after ligation with VEGFA and VEGFB treatments compared with the vehicle control plasmid treatment, but a deficit remained of some 32%.4. Reactive hyperaemic responses were significantly attenuated 7 days after ligation in the vehicle and VEGFA treatment groups. On day 14, this loss of vascular reserve was restored in the VEGFA group, but remained in the vehicle group (−30%). In VEGFB-treated animals, there was no deficit in reserve 7–14 days post-ligation.5. In conclusion, there is considerable value in the serial measurements of calf blood pressure ratio and reactive hyperaemia in the rabbit unilateral hindlimb ischaemia model. Gene transfer of either VEGFA or VEGFB allowed significant improvements in these indices compared with vehicle but, at 14 days post-ligation, large deficits still remained. Studies extending this experimental period are in progress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2002.03773.x
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  • 8
    Electronic Resource
    Electronic Resource
    PI 3-kinase p110β: a new target for antithrombotic therapy (2005)
    [s.l.] : Nature Publishing Group
    Nature medicine 11 (2005), S. 507-514 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Platelet activation at sites of vascular injury is essential for the arrest of bleeding; however, excessive platelet accumulation at regions of atherosclerotic plaque rupture can result in the development of arterial thrombi, precipitating diseases such as acute myocardial infarction and ischemic ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nm1232
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  • 9
    Electronic Resource
    Electronic Resource
    The influence of age on the spatial and temporal contrast sensitivity function (1985)
    Springer
    Documenta ophthalmologica 59 (1985), S. 385-395 
    Details
    ISSN: 1573-2622
    Keywords: contrast sensitivity function ; spatial vision ; temporal vision ; de Lange curve ; ageing
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A clinical technique for sampling the spatial and temporal CSF at low, intermediate and high frequencies is described. Reductions in contrast sensitivity with age were shown with the highest spatial and temporal frequency stimuli. The reductions can be almost completely accounted for by the reduction of pupil area with age, causing a reduction in retinal illuminance. The results show a significant deterioration in vision with age that is not revealed by standard visual acuity testing.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00159172
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