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Noma S, Askenase AD, Weintraub WS, et al. Augmentation of contraction in remote nonischemic zone during acute ischemia. Am J Physiol. 1988;255(2):H301-10doi: 10.1152/ajpheart.1988.255.2.H301.
Noma, S., Askenase, A. D., Weintraub, W. S., Klein, L. W., Agarwal, J. B., & Helfant, R. H. (1988). Augmentation of contraction in remote nonischemic zone during acute ischemia. The American journal of physiology, 255(2), H301-10. https://doi.org/10.1152/ajpheart.1988.255.2.H301
Noma, S, et al. "Augmentation of contraction in remote nonischemic zone during acute ischemia." The American journal of physiology vol. 255,2 (1988): H301-10. doi: https://doi.org/10.1152/ajpheart.1988.255.2.H301
Noma S, Askenase AD, Weintraub WS, Klein LW, Agarwal JB, Helfant RH. Augmentation of contraction in remote nonischemic zone during acute ischemia. Am J Physiol. 1988 Aug;255(2):H301-10. doi: 10.1152/ajpheart.1988.255.2.H301. PMID: 3407791.
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Am J Physiol. 1988 Aug;255(2):H301-10. doi: 10.1152/ajpheart.1988.255.2.H301.

Augmentation of contraction in remote nonischemic zone during acute ischemia.

The American journal of physiology

S Noma, A D Askenase, W S Weintraub, L W Klein, J B Agarwal, R H Helfant

Affiliations

  1. Philadelphia Heart Institute, Presbyterian-University of Pennsylvania Medical Center.

PMID: 3407791 DOI: 10.1152/ajpheart.1988.255.2.H301

Abstract

We studied how left ventricular loading conditions and the size of the ischemic zone affect regional segmental shortening (% delta L) in ischemic (IZ) and remote nonischemic zones (NZ) after acute coronary occlusion. Distal and proximal portions of the left anterior descending artery (group I, 10 dogs) or the left circumflex artery (group II, 10 dogs) were occluded in two stages. Segment length sonomicrometers were placed in the distal and proximal IZ and in the distal and proximal NZ. % delta L was divided into isovolumic and ejection phases. Left ventricular end-diastolic pressure (LVEDP) was decreased 3 +/- 1 mmHg by blood withdrawal and then increased 6 +/- 2 mmHg by blood transfusion before and after distal and proximal coronary occlusions. LVEDP was brought back to its initial value before distal and proximal coronary occlusions. Regional blood flow and total blood flow deficit were measured with microspheres. Similar results were obtained in group I and II experiments. After coronary occlusion, the IZ showed systolic bulging occurring primarily in isovolumic systole. In the NZ, total and isovolumic % delta L increased from control, whereas ejection % delta L did not change. As LVEDP was raised, IZ isovolumic bulging decreased and ejection % delta L was unchanged, whereas NZ isovolumic % delta L decreased and ejection % delta L increased. Thus IZ bulging and NZ isovolumic % delta L changed in opposite directions when load was varied. The larger IZ after proximal coronary occlusion tended to increase the amount of NZ isovolumic % delta L. In conclusion, at low LVEDP NZ augmentation is predominantly caused by an increase in isovolumic % delta L, whereas if LVEDP is increased it is because of an increase in ejection % delta L. In addition, in open-chest animals augmented contraction in the NZ may be related to the size of the IZ.

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