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Professor Dino A Giussani

Professor Dino A Giussani

Professor of Developmental Cardiovascular Physiology and Medicine

Director of Perinatal Physiology Research Group


Office Phone: 01223 333894

Research Interests

Developmental Origins of Heart Disease

We work with small and large animal models to investigate the effects of adverse pregnancy on the development of the heart and circulation and in programming cardiovascular disease in the adult offspring.  In particular, we are able to study the cardiovascular system using an integrative approach at the in vivo, isolated organ, cellular and molecular levels. 

We have expertise with in vivo Transonic flowmetry and measurement of arterial blood pressure, even in the fetal offspring.  This is coupled with experience with isolated Langendorff and Working Heart preparations as well establishing changes in the reactivity of isolated vessels via in vitro wire myography.

Our programmes of work have identified a role of the carotid chemoreflex in mediating the fetal brain sparing response to hypoxia, the first description of an operational vascular oxidant tone during the fetal period and an important role of prenatal hypoxia and oxidative stress in programming heart disease in later life, giving insight to mechanism and potential intervention.  

Keywords

development ; endothelial function ; molecular biology ; oxidative stress ; cardiovascular therapy ; pulmonary hypertension ; echocardiography ; hypoxia ; epigenetics ; hypertension ; arterial stiffness ; myocardial ischaemia ; cardiovascular physiology ; heart development ; cardiometabolic disease ; haemodynamic monitoring

Collaborators

Key Publications

Most recent publications are available through PubMed.

Antioxidant treatment improves neonatal survival and prevents impaired cardiac function at adulthood following neonatal glucocorticoid therapy. Niu Y, Herrera EA, Evans RD, Giussani DA. J Physiol. 2013 Oct 15;591(20):5083-93.

A role for xanthine oxidase in the control of fetal cardiovascular function in late gestation sheep. Herrera EA, Kane AD, Hansell JA, Thakor AS, Allison BJ, Niu Y, Giussani DA. J Physiol. 2012 Apr 15;590(8):1825-37. Editorial Focus by Peebles, D.M. (2012).  “Radical change for the fetus.” Journal of Physiology 590.8, 1773.

Developmental programming of cardiovascular dysfunction by prenatal hypoxia and oxidative stress. Giussani DA, Camm EJ, Niu Y, Richter HG, Blanco CE, Gottschalk R, Blake EZ, Horder KA, Thakor AS, Hansell JA, Kane AD, Wooding FB, Cross CM, Herrera EA. PLoS One. 2012;7(2):e31017. News piece written in Science Magazine about this work entitled: Embryos Starved of Oxygen May Be 'Programmed' for Heart Disease by Jean Friedman-Rudovsky on 13 February 2012.

Statin treatment depresses the fetal defence to acute hypoxia via increasing nitric oxide bioavailability. Kane AD, Herrera EA, Hansell JA, Giussani DA. J Physiol. 2012 Jan 15;590(2):323-34.

The vulnerable developing brain. Giussani DA. Proc Natl Acad Sci U S A. 2011 Feb 15;108(7):2641-2.

Prenatal hypoxia independent of undernutrition promotes molecular markers of insulin resistance in adult offspring. Camm EJ, Martin-Gronert MS, Wright NL, Hansell JA, Ozanne SE, Giussani DA. FASEB J. 2011 Jan;25(1):420-7.

Enhanced umbilical blood flow during acute hypoxemia after chronic umbilical cord compression: a role for nitric oxide. Gardner DS, Giussani DA. Circulation. 2003 Jul 22;108(3):331-5.

Adverse intrauterine conditions diminish the fetal defense against acute hypoxia by increasing nitric oxide activity. Gardner DS, Fowden AL, Giussani DA. Circulation. 2002 Oct 22;106(17):2278-83.

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