| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Maximal coronary conductance with adenosine in anaemic fetal sheep is twice that of non-anaemic fetuses. To investigate whether this increase in conductance persists into adulthood we studied twin sheep as fetuses and again as adults. Nine anaemic fetuses (118 days gestation) underwent isovolaemic haemorrhage for 18.0 ± 4.6 days (means ± S.D.) during which time the haematocrit was reduced from 39.9 ± 5.2 % to 16.3 ± 3.4 % and oxygen content from 8.6 ± 1.3 to 2.3 ± 0.2 ml dl-1. At 138 days the anaemic fetuses were transfused; at delivery the haematocrit was 29.3 ± 6.8 % compared to nine control fetuses in which the haematocrit was 38.5 ± 4.3 %. The weight at delivery was 3.5 ± 0.36 kg in the anaemic fetuses vs. 4.2 ± 0.83 kg in controls. Twenty-eight weeks later, we placed an occluder on the descending thoracic aorta and inferior vena cava, a flow probe around the proximal left circumflex coronary artery, and catheters in the left atrial appendage, jugular and carotid vessels. Maximal coronary conductance was determined in the adults by recording coronary blood flow as driving pressure was altered by inflating the occluders while adenosine was infused into the left atrium. Right atrial, left atrial, systolic and mean arterial pressures, systemic vascular resistance and haematocrit were not different between 'in utero anaemic' and control adults. The adults that were anaemic in utero weighed less than the controls 39.4 ± 4.6 kg vs. 45.0 ± 5.6 kg. Maximal conductance was greater in the adults that were anaemic in utero: 11.2 ± 4.0 ml min-1 (100 g)-1 mmHg-1 as compared to 6.1 ± 1.8 ml min-1 (100 g)-1 mmHg-1 in the controls. Vascular reactivity of the mesenteric arteries was not different. These data suggest that coronary conductance can be modified in utero by anaemia (high flow and hypoxaemia) and that the remodelled coronary tree persists to adulthood.
This article has been cited by other articles:
|
|
 |
|
  B. Jiang, K. M. Godfrey, C. N. Martyn, and C. R. Gale Birth Weight and Cardiac Structure in Children Pediatrics, February 1, 2006; 117(2): e257 - e261. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. A. Khan, R. Chau, C. Bertram, M. A. Hanson, and S. K. Ohri Fetal origins of coronary heart disease--implications for cardiothoracic surgery? Eur. J. Cardiothorac. Surg., June 1, 2005; 27(6): 1036 - 1042. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Davis, K. L. Thornburg, and G. D. Giraud The effects of anaemia as a programming agent in the fetal heart J. Physiol., May 15, 2005; 565(1): 35 - 41. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. C. Mcmillen and J. S. Robinson Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming Physiol Rev, April 1, 2005; 85(2): 571 - 633. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Zhang Prenatal Hypoxia and Cardiac Programming Reproductive Sciences, January 1, 2005; 12(1): 2 - 13. [Abstract] [PDF]
|
|
|
|
 |
|
 K. L. Thornburg Fetal Origins of Cardiovascular Disease NeoReviews, December 1, 2004; 5(12): e527 - e533. [Full Text] [PDF]
|
|
|
|
 |
|
 D. Brodsky and H. Christou Current Concepts in Intrauterine Growth Restriction J Intensive Care Med, November 1, 2004; 19(6): 307 - 319. [Abstract] [PDF]
|
|
|
|
 |
|
 L. Bennet and A. J. Gunn Memories of the fetal heart Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2003; 285(3): R517 - R518. [Full Text] [PDF]
|
|
|
|
|
|
C. S. Broberg, G. D. Giraud, J. M. Schultz, K. L. Thornburg, A. R. Hohimer, and L. E. Davis Fetal anemia leads to augmented contractile response to hypoxic stress in adulthood Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2003; 285(3): R649 - R655. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
