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Professor Dino A Giussani

My research group is interested in how adverse conditions during pregnancy can programme heart disease in the adult offspring.
Professor Dino A Giussani

Professor of Developmental Cardiovascular Physiology and Medicine

Director of Studies in Medicine, Gonville & Caius College

Dino Giussani is accepting applications for PhD students.

Office Phone: +44 (0) 1223 333894, Fax: +44 (0) 1223 333840

Research Interests

My research is in Fetal and Neonatal Physiology and in Developmental Programming, broad fields of Reproduction. There are three main strands to my research programmes, each of which uses an integrative approach at the whole animal, isolated organ, cellular and molecular levels to ask focused questions on the roles of fetal oxygenation in cardiovascular development.

Fetal brain sparing during hypoxia

A serious problem in pregnancy is reduced oxygen delivery to the unborn child (fetal hypoxia).  Understanding the mechanisms which underpin the fetal defence to hypoxia is therefore fundamental to developing prevention and treatment of adverse outcomes.  In response to hypoxia, the fetus redistributes its cardiac output away from peripheral circulations and towards the brain - the so called brain sparing effect.  We made the discovery that fetal brain-sparing is triggered exclusively by a carotid chemoreflex. While the field understood that the mechanisms driving this cardiovascular defence to hypoxia included neural and endocrine components, my research group also discovered that nitric oxide (NO) and reactive oxygen species (ROS) are involved.  The net fetal brain-sparing response to hypoxia thus represents the balance between neural, endocrine and local redox mechanisms.

Perinatal glucocorticoid therapy and fetal cardiovascular function

The second strand of my research investigates how the fetal defence to hypoxia may be modified by the intrauterine environment, triggering beneficial as well as detrimental consequences. We have shown that the fetal cardiovascular defence to hypoxia matures with advancing gestation together with the prepartum surge in fetal cortisol.  This maturational effect can be mimicked by treating the preterm fetus with exogenous glucocorticoids in human clinical doses.  The law in the UK, Canada, USA and Australia states that women at risk of preterm labour should be treated with exogenous glucocorticoids to accelerate fetal lung maturation.  Obstetric practice worldwide now appreciates that this treatment also accelerates maturation of the fetal cardiovascular system in addition to the fetal lung.

Prenatal hypoxia and developmental programming of cardiovascular disease

Intrauterine growth restriction (IUGR) is one of the greatest killers in obstetrics today.  It is also associated with the developmental programming of heart disease in adulthood. The third strand of my research has pioneered the contribution of chronic fetal hypoxia and oxidative stress to IUGR and the developmental programming of heart disease in complicated pregnancy, giving the UK an international lead in the subject.  We isolated the role of chronic fetal hypoxia in promoting IUGR and a prenatal origin of cardiometabolic disease in animals and in humans.  For instance, in human populations in Bolivia, we have shown that despite greater poverty, Andean ancestry confers graded protection against fetal growth restriction in pregnancy at high altitude.  Most recently, we have made the exciting discovery that the mechanism promoting adverse outcomes in the offspring of hypoxic pregnancy is oxidative stress in the fetal heart and circulation, thereby identifying potential targets for intervention.

Combined, therefore, our research programmes have components of basic, clinical, anthropological and translational science with direct relevance to cardiovascular and perinatal medicine.


Professor Sue Ozanne
Professor Abigail Fowden
Professor Anne Ferguson Smith
Professor Anibal Llanos
Dr Mike Murphy
Dr Emilio Herrera


Dr Youguo Niu
Dr Kim Botting
Dr Ana-Mishel Spiroski
Dr Emily Camm


MVST 1A Homeostasis, NST1A Physiology of Organisms, Part II NST Module P3: Fetal and Placental Physiology.

Director of Studies in Medicine, Gonville & Caius College

Above: Isolated fetal sheep heart studied in a Langendorff/Working Heart preparation

Above: Tabulae XII from William Hunter’s Anatomia uteri humani gravidi tabulis Illustrata. The Anatomy of the Human Gravid Uterus Explained by Figures, Birmingham, John Baskerville, 1774. Regarding Plate XII, the opened abdomen exposes the fetus of a woman near term, with the placenta previa from which the woman had bled to death.  In one of the most significant obstetric atlases ever published with life sized figures, “anatomically exact and artistically perfect”, this work, illustrates the gravid uteri of three women who died during the last third of gestation, and several others that succumbed earlier in pregnancy.  Hunter (1718-1783), a Scotsman who worked in London, commenced working on the atlas in 1751 and it required nearly twenty-three years to complete.  Hunter spared no expense in having one of the leading anatomical artists of the time, Jan van Rymsdyk (fl. 1750-1788) draw the plates, which then were engraved by over a dozen engravers.  The work was printed by John Baskerville (1706-1775) the finest printer of that age.  The 34 life-size line engravings, achieve effects of depth and contrast without losing sharpness of detail, and present a wide range of normal and pathologic conditions of the womb and fetus.  Each page of text is printed in two columns, one in Latin and the other in English.

Above: Programmed pulmonary hypertension by chronic fetal hypoxia. Histochemical staining of pulmonary arterioles in adult sheep showing pronounced vessel muscularisation in those born from pregnancies complicated by chronic hypoxia. Double staining with antibodies against vWF (Endothel) + α-smooth muscle actin (α-sma). 

Above: Programmed dilated cardiomyopathy by chronic fetal hypoxia. Fixed mid cardiac sections of adult chickens showing pronounced bi-ventricular dilatation in those incubated under chronic hypoxic conditions.