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Article ; Online: Clinical applications of remote ischemic preconditioning.

Veighey, Kristin / Macallister, Raymond J

2012 Volume 2012, Page(s) 620681

Abstract: Ischemia-reperfusion injury is a composite of damage accumulated during reduced perfusion of an organ or tissue and the additional insult sustained during reperfusion. Such injury occurs in a wide variety of clinically important syndromes, such as ... ...

Abstract	Ischemia-reperfusion injury is a composite of damage accumulated during reduced perfusion of an organ or tissue and the additional insult sustained during reperfusion. Such injury occurs in a wide variety of clinically important syndromes, such as ischemic heart disease and stroke, which are responsible for a high degree of morbidity and mortality worldwide. Basic research has identified a number of interventions that stimulate innate resistance of tissues to ischemia-reperfusion injury. Here, we summarise the experimental and clinical trial data underpinning one of these "conditioning" strategies, the phenomenon of remote ischemic preconditioning.
Language	English
Publishing date	2012-02-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2506187-2
ISSN	2090-0597 ; 2090-8016
ISSN (online)	2090-0597
ISSN	2090-8016
DOI	10.1155/2012/620681
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Article: Vasoactive peptides and the pathogenesis of pulmonary hypertension: role and potential therapeutic application.

Baliga, Reshma S / Macallister, Raymond J / Hobbs, Adrian J

Handbook of experimental pharmacology

2013 Volume 218, Page(s) 477–511

Abstract: Pulmonary hypertension (PH) is a debilitating disease with a dismal prognosis. Recent advances in therapy (e.g. prostacyclin analogues, endothelin receptor antagonists and phosphodiesterase 5 inhibitors), whilst significantly improving survival, simply ... ...

Abstract	Pulmonary hypertension (PH) is a debilitating disease with a dismal prognosis. Recent advances in therapy (e.g. prostacyclin analogues, endothelin receptor antagonists and phosphodiesterase 5 inhibitors), whilst significantly improving survival, simply delay the inexorable progression of the disease. An array of endogenous vasoconstrictors and vasodilators coordinates to maintain pulmonary vascular homeostasis and morphological integrity, and an imbalance in the expression and function of these mediators precipitates PH and related lung diseases. The vasodilator peptides, including natriuretic peptides, vasoactive intestinal peptide, calcitonin gene-related peptide and adrenomedullin, trigger the production of cyclic nucleotides (e.g. cGMP and cAMP) in many pulmonary cell types, which in tandem exert a multifaceted protection against the pathogenesis of PH, encompassing vasodilatation, inhibition of vascular smooth muscle proliferation, anti-inflammatory and anti-fibrotic effects and salutary actions on the right ventricle. This coordinated beneficial activity underpins a contemporary perception that to advance treatment of PH it is necessary to offset multiple disease mechanisms (i.e. the pulmonary vasoconstriction, pulmonary vascular remodelling, right ventricular dysfunction). Thus, there is considerable potential for harnessing the favourable activity of peptide mediators to offer a novel, efficacious therapeutic approach in PH.
MeSH term(s)	Adrenomedullin/physiology ; Animals ; Calcitonin Gene-Related Peptide/physiology ; Endothelin-1/physiology ; Humans ; Hypertension, Pulmonary/drug therapy ; Hypertension, Pulmonary/etiology ; Natriuretic Peptides/physiology ; Peptides/physiology ; Pituitary Adenylate Cyclase-Activating Polypeptide/physiology ; Vasoactive Intestinal Peptide/physiology
Chemical Substances	Endothelin-1 ; Natriuretic Peptides ; Peptides ; Pituitary Adenylate Cyclase-Activating Polypeptide ; Adrenomedullin (148498-78-6) ; Vasoactive Intestinal Peptide (37221-79-7) ; Calcitonin Gene-Related Peptide (JHB2QIZ69Z)
Language	English
Publishing date	2013-10-02
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	0171-2004
ISSN	0171-2004
DOI	10.1007/978-3-642-38664-0_19
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Article ; Online: Dietary nitrate ameliorates pulmonary hypertension: cytoprotective role for endothelial nitric oxide synthase and xanthine oxidoreductase.

Baliga, Reshma S / Milsom, Alexandra B / Ghosh, Suborno M / Trinder, Sarah L / Macallister, Raymond J / Ahluwalia, Amrita / Hobbs, Adrian J

Circulation

2012 Volume 125, Issue 23, Page(s) 2922–2932

Abstract: Background: Pulmonary hypertension (PH) is a multifactorial disease characterized by increased pulmonary vascular resistance and right ventricular failure; morbidity and mortality remain unacceptably high. Loss of nitric oxide (NO) bioactivity is ... ...

Abstract	Background: Pulmonary hypertension (PH) is a multifactorial disease characterized by increased pulmonary vascular resistance and right ventricular failure; morbidity and mortality remain unacceptably high. Loss of nitric oxide (NO) bioactivity is thought to contribute to the pathogenesis of PH, and agents that augment pulmonary NO signaling are clinically effective in the disease. Inorganic nitrate (NO(3)(-)) and nitrite (NO(2)(-)) elicit a reduction in systemic blood pressure in healthy individuals; this effect is underpinned by endogenous and sequential reduction to NO. Herein, we determined whether dietary nitrate and nitrite might be preferentially reduced to NO by the hypoxia associated with PH, and thereby offer a convenient, inexpensive method of supplementing NO functionality to reduce disease severity. Methods and results: Dietary nitrate reduced the right ventricular pressure and hypertrophy, and pulmonary vascular remodeling in wild-type mice exposed to 3 weeks of hypoxia; this beneficial activity was mirrored largely by dietary nitrite. The cytoprotective effects of dietary nitrate were associated with increased plasma and lung concentrations of nitrite and cGMP. The beneficial effects of dietary nitrate and nitrite were reduced in mice lacking endothelial NO synthase or treated with the xanthine oxidoreductase inhibitor allopurinol. Conclusions: These data demonstrate that dietary nitrate, and to a lesser extent dietary nitrite, elicit pulmonary dilatation, prevent pulmonary vascular remodeling, and reduce the right ventricular hypertrophy characteristic of PH. This favorable pharmacodynamic profile depends on endothelial NO synthase and xanthine oxidoreductase -catalyzed reduction of nitrite to NO. Exploitation of this mechanism (ie, dietary nitrate/nitrite supplementation) represents a viable, orally active therapy for PH.
MeSH term(s)	Allopurinol/pharmacology ; Animal Feed ; Animals ; Antibiotics, Antineoplastic/toxicity ; Bleomycin/toxicity ; Cyclic GMP/blood ; Disease Models, Animal ; Enzyme Inhibitors/pharmacology ; Hypertension, Pulmonary/chemically induced ; Hypertension, Pulmonary/drug therapy ; Hypertension, Pulmonary/metabolism ; Hypertrophy, Right Ventricular/drug therapy ; Hypertrophy, Right Ventricular/metabolism ; Hypoxia/metabolism ; Hypoxia/prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nitrates/blood ; Nitrates/pharmacology ; Nitrates/urine ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/metabolism ; Nitrites/blood ; Nitrites/pharmacology ; Nitrites/urine ; Pulmonary Circulation/drug effects ; Pulmonary Circulation/physiology ; Ventricular Pressure/drug effects ; Ventricular Pressure/physiology ; Xanthine Dehydrogenase/antagonists & inhibitors ; Xanthine Dehydrogenase/metabolism
Chemical Substances	Antibiotics, Antineoplastic ; Enzyme Inhibitors ; Nitrates ; Nitrites ; Bleomycin (11056-06-7) ; Allopurinol (63CZ7GJN5I) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39) ; Xanthine Dehydrogenase (EC 1.17.1.4) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2012-05-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.112.100586
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Article ; Online: Comparative efficacy and tolerability of anti-epileptic drugs for refractory focal epilepsy: systematic review and network meta-analysis reveals the need for long term comparator trials.

Bodalia, Pritesh N / Grosso, Anthony M / Sofat, Reecha / Macallister, Raymond J / Smeeth, Liam / Dhillon, Soraya / Casas, Juan-Pablo / Wonderling, David / Hingorani, Aroon D

British journal of clinical pharmacology

2013 Volume 76, Issue 5, Page(s) 649–667

Abstract: Aims: To evaluate the comparative efficacy (50% reduction in seizure frequency) and tolerability (premature withdrawal due to adverse events) of anti-epileptic drugs (AEDs) for refractory epilepsy.: Methods: We searched Cochrane Central Register of ... ...

Abstract	Aims: To evaluate the comparative efficacy (50% reduction in seizure frequency) and tolerability (premature withdrawal due to adverse events) of anti-epileptic drugs (AEDs) for refractory epilepsy. Methods: We searched Cochrane Central Register of Controlled Trials (Cochrane Library 2009, issue 2) including Epilepsy Group's specialized register, MEDLINE (1950 to March 2009), EMBASE (1980 to March 2009), and Current Contents Connect (1998 to March 2009) to conduct a systematic review of published studies, developed a treatment network and undertook a network meta-analysis. Results: Forty-three eligible trials with 6346 patients and 12 interventions, including placebo, contributed to the analysis. Only three direct drug comparator trials were identified, the remaining 40 trials being placebo-controlled. Conventional random-effects meta-analysis indicated all drugs were superior in efficacy to placebo (overall odds ratio (OR] 3.78, 95% CI 3.14, 4.55) but did not permit firm distinction between drugs on the basis of the efficacy or tolerability. A Bayesian network meta-analysis prioritized oxcarbazepine, topiramate and pregabalin on the basis of short term efficacy. However, sodium valproate, levetiracetam, gabapentin and vigabatrin were prioritized on the basis of short-term efficacy and tolerability, with the caveat that vigabatrin is recognized as being associated with serious visual disturbance with chronic use. Conclusion: Of the wide range of AEDs licensed for the treatment of refractory epilepsy, sodium valproate, levetiracetam and gabapentin demonstrated the best balance of efficacy and tolerability. Until regulators mandate greater use of active comparator trials with longer term follow-up, network meta-analysis provides the only available means to quantify these clinically important parameters.
MeSH term(s)	Anticonvulsants/administration & dosage ; Anticonvulsants/adverse effects ; Anticonvulsants/therapeutic use ; Bayes Theorem ; Clinical Trials as Topic/methods ; Epilepsies, Partial/drug therapy ; Epilepsies, Partial/physiopathology ; Humans ; Research Design ; Time Factors
Chemical Substances	Anticonvulsants
Language	English
Publishing date	2013-01-25
Publishing country	England
Document type	Comparative Study ; Journal Article ; Multicenter Study ; Review ; Systematic Review
ZDB-ID	188974-6
ISSN	1365-2125 ; 0306-5251 ; 0264-3774
ISSN (online)	1365-2125
ISSN	0306-5251 ; 0264-3774
DOI	10.1111/bcp.12083
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Article ; Online: Remote ischemic preconditioning protects the brain against injury after hypothermic circulatory arrest.

Jensen, Hanna A / Loukogeorgakis, Stavros / Yannopoulos, Fredrik / Rimpiläinen, Eija / Petzold, Axel / Tuominen, Hannu / Lepola, Pasi / Macallister, Raymond J / Deanfield, John E / Mäkelä, Tuomas / Alestalo, Kirsi / Kiviluoma, Kai / Anttila, Vesa / Tsang, Victor / Juvonen, Tatu

Circulation

2011 Volume 123, Issue 7, Page(s) 714–721

Abstract: Background: Ischemic preconditioning (IPC) is a mechanism protecting tissues from injury during ischemia and reperfusion. Remote IPC (RIPC) can be elicited by applying brief periods of ischemia to tissues with ischemic tolerance, thus protecting vital ... ...

Abstract	Background: Ischemic preconditioning (IPC) is a mechanism protecting tissues from injury during ischemia and reperfusion. Remote IPC (RIPC) can be elicited by applying brief periods of ischemia to tissues with ischemic tolerance, thus protecting vital organs more susceptible to ischemic damage. Using a porcine model, we determined whether RIPC of the limb is protective against brain injury caused by hypothermic circulatory arrest (HCA). Methods and results: Twelve piglets were randomized to control and RIPC groups. RIPC was induced in advance of cardiopulmonary bypass by 4 cycles of 5 minutes of ischemia of the hind limb. All animals underwent cardiopulmonary bypass followed by 60 minutes of HCA at 18°C. Brain metabolism and electroencephalographic activity were monitored for 8 hours after HCA. Assessment of neurological status was performed for a week postoperatively. Finally, brain tissue was harvested for histopathological analysis. Study groups were balanced for baseline and intraoperative parameters. Brain lactate concentration was significantly lower (P<0.0001, ANOVA) and recovery of electroencephalographic activity faster (P<0.05, ANOVA) in the RIPC group. RIPC had a beneficial effect on neurological function during the 7-day follow-up (behavioral score; P<0.0001 versus control, ANOVA). Histopathological analysis demonstrated a significant reduction in cerebral injury in RIPC animals (injury score; mean [interquartile range]: control 5.8 [3.8 to 7.5] versus RIPC 1.5 [0.5 to 2.5], P<0.001, t test). Conclusions: These data demonstrate that RIPC protects the brain against HCA-induced injury, resulting in accelerated recovery of neurological function. RIPC might be neuroprotective in patients undergoing surgery with HCA and improve long-term outcomes. Clinical trials to test this hypothesis are warranted.
MeSH term(s)	Animals ; Brain Ischemia/etiology ; Brain Ischemia/therapy ; Cardiac Surgical Procedures ; Cardiopulmonary Bypass/methods ; Circulatory Arrest, Deep Hypothermia Induced/adverse effects ; Circulatory Arrest, Deep Hypothermia Induced/methods ; Creatine Kinase, MB Form/blood ; Disease Models, Animal ; Electroencephalography ; Heart Function Tests ; Humans ; Ischemic Preconditioning/methods ; Recovery of Function ; Reperfusion Injury/etiology ; Reperfusion Injury/therapy ; Sus scrofa ; Troponin I/blood
Chemical Substances	Troponin I ; Creatine Kinase, MB Form (EC 2.7.3.2)
Language	English
Publishing date	2011-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.110.986497
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Article: Vitamin C improves resistance but not conduit artery endothelial function in patients with chronic renal failure.

Cross, Jenny M / Donald, Ann E / Nuttall, Sarah L / Deanfield, John E / Woolfson, Robin G / Macallister, Raymond J

Kidney international

2003 Volume 63, Issue 4, Page(s) 1433–1442

Abstract: Background: Chronic renal failure is associated with impaired endothelium-dependent vasodilation and accelerated atherogenesis. To examine whether endogenous reactive oxygen species (ROS) modify endothelial function in renal failure, we evaluated the ... ...

Abstract	Background: Chronic renal failure is associated with impaired endothelium-dependent vasodilation and accelerated atherogenesis. To examine whether endogenous reactive oxygen species (ROS) modify endothelial function in renal failure, we evaluated the effect of the antioxidant vitamin C on endothelium-dependent responses in both the conduit and resistance vasculature of subjects with severe renal impairment. Methods: Endothelial function of the forearm resistance vasculature was assessed using plethysmography to measure the dilator response to intra-arterial acetylcholine (Ach) (25 to 100 nmol/min). Endothelial function of radial and brachial arteries was assessed using vascular ultrasound to measure the dilator response to flow during reactive hyperemia [flow-mediated dilatation (FMD)]. Studies were performed before and after administration of vitamin C by intra-arterial infusion (25 mg/min) in 33 predialysis patients or by intravenous infusion (3 g) in 17 hemodialysis patients. Results: Parenteral administration of vitamin C resulted in a 100-fold increase (intra-arterial studies) and a 4.5-fold increase (intravenous studies) in serum antioxidant activity. Vitamin C administration increased the dilator response to ACh in resistance vessels (P = 0.01), but did not alter the dilator response to flow in conduit vessels of either dialysis (P = 0.3) or predialysis subjects (P = 0.8). In the presence of the nitric oxide (NO) synthase inhibitor NGmonomethyl-L-arginine (L-NMMA), there was no effect of vitamin C on resistance vessel endothelial function. In all cases the dilator response to the endothelium-independent dilators was unaffected by vitamin C. Conclusion: Acute administration of vitamin C reduces oxidant stress in renal failure and improves NO-mediated resistance vessel dilatation.
MeSH term(s)	Adult ; Antioxidants/administration & dosage ; Ascorbic Acid/administration & dosage ; Biomarkers ; Brachial Artery/physiology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/physiology ; Female ; Humans ; Kidney Failure, Chronic/drug therapy ; Kidney Failure, Chronic/physiopathology ; Male ; Middle Aged ; Nitric Oxide/metabolism ; Oxidative Stress/drug effects ; Radial Artery/physiology ; Renal Dialysis ; Vascular Resistance/drug effects ; Vasodilation/drug effects
Chemical Substances	Antioxidants ; Biomarkers ; Nitric Oxide (31C4KY9ESH) ; Ascorbic Acid (PQ6CK8PD0R)
Language	English
Publishing date	2003-04
Publishing country	United States
Document type	Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1046/j.1523-1755.2003.00852.x
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Article: Tetrahydrobiopterin corrects Escherichia coli endotoxin-induced endothelial dysfunction.

Mittermayer, Friedrich / Pleiner, Johannes / Schaller, Georg / Zorn, Stefan / Namiranian, Khodadad / Kapiotis, Stylianos / Bartel, Gregor / Wolfrum, Mathias / Brügel, Mathias / Thiery, Joachim / Macallister, Raymond J / Wolzt, Michael

American journal of physiology. Heart and circulatory physiology

2005 Volume 289, Issue 4, Page(s) H1752–7

Abstract: Acute inflammation causes endothelial dysfunction, which is partly mediated by oxidant stress and inactivation of nitric oxide. The contribution of depletion of tetrahydrobiopterin (BH(4)), the cofactor required for nitric oxide generation, is unclear. ... ...

Abstract	Acute inflammation causes endothelial dysfunction, which is partly mediated by oxidant stress and inactivation of nitric oxide. The contribution of depletion of tetrahydrobiopterin (BH(4)), the cofactor required for nitric oxide generation, is unclear. In this randomized, double-blind, three-way crossover study, forearm blood flow (FBF) responses to ACh and glyceryltrinitrate (GTN) were measured before and 3.5 h after infusion of Escherichia coli endotoxin (LPS, 20 IU/kg iv) in eight healthy men. The effect of intra-arterial BH(4) (500 microg/min), placebo, or vitamin C (24 mg/min) was studied on separate days 3.5 h after LPS infusion. In addition, human umbilical vein endothelial cells were incubated for 24 h with vitamin C and LPS. ACh and GTN caused dose-dependent forearm vasodilation. The FBF response to ACh, which was decreased by 23 +/- 17% (P < 0.05) by LPS infusion, was restored to baseline reactivity by BH(4) and vitamin C. FBF responses to GTN were not affected by BH(4) or vitamin C. LPS increased leukocyte count, high-sensitivity C-reactive protein, IL-6, IL-1beta, IFN-gamma, monocyte chemoattractant protein-1, pulse rate, and body temperature and decreased platelet count and vitamin C concentration. Vitamin C increased forearm plasma concentration of BH(4) by 32% (P < 0.02). Incubation with LPS and vitamin C, but not LPS alone, increased intracellular BH(4) concentration in human umbilical vein endothelial cells. Impaired endothelial function during acute inflammation can be restored by BH(4) or vitamin C. Vitamin C may exert some of its salutary effects by increasing BH(4) concentration.
MeSH term(s)	Acetylcholine/administration & dosage ; Adult ; Antioxidants/administration & dosage ; Ascorbic Acid/administration & dosage ; Biopterins/administration & dosage ; Biopterins/analogs & derivatives ; Biopterins/metabolism ; Cells, Cultured ; Cross-Over Studies ; Cytokines/blood ; Endothelium, Vascular/cytology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Endotoxemia/chemically induced ; Endotoxemia/drug therapy ; Endotoxins/adverse effects ; Forearm/blood supply ; Humans ; Male ; Nitric Oxide/metabolism ; Regional Blood Flow/drug effects ; Umbilical Veins/cytology ; Vasodilation/drug effects
Chemical Substances	Antioxidants ; Cytokines ; Endotoxins ; Biopterins ; Nitric Oxide (31C4KY9ESH) ; endotoxin, Escherichia coli (67924-63-4) ; sapropterin (EGX657432I) ; Acetylcholine (N9YNS0M02X) ; Ascorbic Acid (PQ6CK8PD0R)
Language	English
Publishing date	2005-06-17
Publishing country	United States
Document type	Clinical Trial ; Journal Article ; Randomized Controlled Trial
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00057.2005
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Article ; Online: Clinical applications of remote ischemic preconditioning.

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Article: Vasoactive peptides and the pathogenesis of pulmonary hypertension: role and potential therapeutic application.

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Article ; Online: Dietary nitrate ameliorates pulmonary hypertension: cytoprotective role for endothelial nitric oxide synthase and xanthine oxidoreductase.

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Article ; Online: Comparative efficacy and tolerability of anti-epileptic drugs for refractory focal epilepsy: systematic review and network meta-analysis reveals the need for long term comparator trials.

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Article ; Online: Remote ischemic preconditioning protects the brain against injury after hypothermic circulatory arrest.

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Article: Vitamin C improves resistance but not conduit artery endothelial function in patients with chronic renal failure.

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Article: Tetrahydrobiopterin corrects Escherichia coli endotoxin-induced endothelial dysfunction.

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