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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.

  1. Itani, N., Skeffington, K.L., Beck, C. & Giussani, D.A. (2017). Sildenafil therapy for fetal cardiovascular dysfunction during hypoxic development:  Studies in the chick embryo.  The Journal of Physiology 595(5), 1563-1573.
  2. Allison, B.J., Kaandorp, J.J., Kane, A.D., Camm, E.J., Lusbu, C., Cross, C.M., Nevin-Dolan, R., Thakor, A.S., Derks, J.B., Tarry-Adkins, J.L., Ozanne, S.E. & Giussani, D.A. (2016).  Divergence of mechanistic pathways mediating cardiovascular aging and developmental programming of cardiovascular disease.  FASEB J. 30(5), 1968-75.
  3. Allison, B.J., Brain, K.L., Niu, Y., Kane, A.D., Herrera, E.A., Thakor, A.S., Botting, K.L., Itani, N., Cross, C.M., Skeffington, K.L., Beck, C. & Giussani, D.A. (2016).  Fetal in vivo continuous cardiovascular function during chronic hypoxia. The Journal of Physiology 594(5), 1247-64.
  4. Giussani, D.A. (2016). The Fetal Brain Sparing Response to Hypoxia: Physiological Mechanisms.  The Journal of Physiology 594(5), 1215-30.
  5. Thakor, A.S., Allison, B.J., Niu, Y., Botting, K.J., Serón-Ferré, M., Herrera, E.A. & Giussani D.A. (2015). Melatonin modulates the fetal defense to acute hypoxia.  Journal of Pineal Research 59, 80-90.
  6. Giussani, D.A. & Davidge, S.T. (2013).  Developmental programming of cardiovascular disease by prenatal hypoxia. J DoHAD 4(5), 328–337.
  7. Giussani, D.A., Camm, E.J., Niu, Y., Richter, H.G., Blanco, C.E., Gottschalk, R., Blake, E.Z., Horder, K.A., Thakor, A.S., Hansell, J.A., Kane, A.D., Wooding, F.B.P., Cross C.M. & Herrera. E.A. (2012).  Developmental programming of cardiovascular dysfunction by prenatal hypoxia and oxidative stress.  PLoS ONE 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.

http://news.sciencemag.org/sciencenow/2012/02/embryos-starved-of-oxygen-may-be.html

      This article is among the top 10% most cited PLOS ONE articles since    the creation of the Journal.

      8. Giussani, D.A. (2011).  The vulnerable developing brain. Proc Natl Acad   Sci USA. 108(7), 2641-2. (Featured in the March 2011 issue of the North American Vascular Biology Organization (NAVBO) Vascular Biology Publications Alert).

      9. Thakor, A.S. & Giussani, D.A. (2005).  The role of nitric oxide in mediating in vivo vascular responses to calcitonin gene related peptide in essential and peripheral circulations in the fetus. Circulation 112(16):2510-6.

      10.Gardner, D.S., Fowden, A.L. & Giussani, D.A. (2002). Adverse  intrauterine conditions diminish the fetal defense to acute hypoxia by  increasing nitric oxide activity. Circulation 106: 2278-2283

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