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Coronary reserves in myocardial hypertrophy

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Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 70))

Abstract

The purpose of the present investigation was to determine the effects of thyroxine (T4) induced myocardial hypertrophy on coronary flow reserve, O2 extraction reserve and the reserve of unperfused capillaries. Studies were conducted in anesthetized open chest New Zealand white rabbits. One group had blood flow determined with radioactive microspheres and O2 extraction determined microspectrophotometrically. Reserves were tested with hypoxia. In the other group, FITC-dextran was injected to label the perfused microvessels. An alkaline phosphatase stain was employed to locate the total microvascular bed. O2 consumption increased 280% in the 16-day T4 group and this was accompanied by significant increases in coronary flow and O2 extraction. Blood flow further increased 101% for the hypoxic 16-day T4 group. Venous O2 saturation also decreased significantly in hypoxia. There were 2544 ± 210 capillaries/mm2 and 5 ± 1 arterioles/mm2 in control subendocardium. These decreased significantly to 1457 ± 65/mm2 and 1 ± 1/mm2 respectively after 16 days of T4. In controls, 59 ± 2% of the capillaries and 56 ± 9% of the arterioles were perfused in the subendocardium. This increased significantly to 88 ± 3% and 79 ± 8% respectively by 16 days of T4 treatment. Thus, the physiological response to the increased work and decreased capillary density is to increase the proportion of the capillary bed perfused to at least maintain physiological diffusion distances. The T4 hypertrophied hearts were also able to increase their blood flow and decrease their venous O2 saturation in response to further stress.

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© 1987 Martinus Nijhoff Publishers, Dordrecht

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Weiss, H.R., Grover, G.J. (1987). Coronary reserves in myocardial hypertrophy. In: Sideman, S., Beyar, R. (eds) Activation, Metabolism and Perfusion of the Heart. Developments in Cardiovascular Medicine, vol 70. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-3313-2_36

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  • DOI: https://doi.org/10.1007/978-94-009-3313-2_36

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-7987-7

  • Online ISBN: 978-94-009-3313-2

  • eBook Packages: Springer Book Archive

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