PMID- 9515002
OWN - NLM
STAT- MEDLINE
DCOM- 19980528
LR  - 20131121
IS  - 0022-2828 (Print)
IS  - 0022-2828 (Linking)
VI  - 30
IP  - 2
DP  - 1998 Feb
TI  - Coronary venous hypertension prevents the formation of the electrophysiological 
      arrhythmogenic substrate of acute ischemia in the dog: salutary effects of 
      preserved myocardial hydration.
PG  - 255-68
AB  - Coronary venous hypertension induced by partial coronary sinus obstruction (CSO) 
      in the dog, prevents or delays the predictable ventricular fibrillation (VF) of 
      the early phase of acute ischemia. Also, CSO acting presumably through enhanced 
      myocardial hydration, normalizes the inhomogenous extracellular potassium ([K+]o) 
      accumulation, a major factor in producing the electrophysiological disparities, 
      characteristic of arrhythmogenic substrate. To further clarify the mechanism of 
      early ischemic VF prevention in dogs, radioactive microspheres were used to 
      evaluate regional perfusion changes, resulting from CSO sufficient to raise the 
      coronary sinus pressure to 40 mmHg, before and during ischemia induced by double 
      coronary artery occlusion (CAO) (n=5). Also, global or regional unipolar 
      electrogram mapping was used to assess changes of epicardial ventricular 
      activation times (AT) and sequence and activation recovery intervals (ARI) during 
      CSO, CAO and combined CSO and CAO, induced in random order (n=8). CSO did not 
      affect regional perfusion nor improved collateral blood flow during ischemia. 
      With CSO, AT shortened modestly over time (0.41+/-1.1 ms/min, r=0.85, P<0. 05) 
      and ARI transiently decreased by up to 5.5%. With CAO, AT became variably delayed 
      and isochrone map distortions were indicative of localized conduction delays or 
      blocks, consistent with elevated [K+]o. In contrast, when CAO was preceded by 
      CSO, AT delays were homogenous and normal activation sequence was preserved. 
      Also, whereas with CAO, ARI shortened unequally over the ischemic region by as 
      much as 43% at individual sites (average of 38.3+/-6.8 ms, P<0. 001), with 
      combined CSO and CAO, ARI shortening was less pronounced and more homogenous 
      (26.1+/-5.6 ms, P<0.05), not exceeding 29% at any site. Thus, in accordance with 
      previous findings of enhanced [K+]o homogeneity, coronary venous hypertension 
      reduces the disparities of activation and refractoriness of ischemia 
      attributable, at least in part, to disparate [K+]o accumulation. Since no 
      collateral blood flow improvement could be identified, the salutary 
      electrophysiological effects of CSO may reflect a more homogenous extracellular 
      environment, due to preservation of normal microvascular pressure (Pmv) and 
      sustained filtration and lymph flow.
CI  - Copyright 1998 Academic Press Limited.
FAU - Kralios, A C
AU  - Kralios AC
AD  - Department of Veterans Affairs Medical Center, Cardiology Section, University of 
      Utah, Salt Lake City 84148, USA.
FAU - Kralios, F A
AU  - Kralios FA
FAU - Anderson, F L
AU  - Anderson FL
FAU - Leonard, M
AU  - Leonard M
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - England
TA  - J Mol Cell Cardiol
JT  - Journal of molecular and cellular cardiology
JID - 0262322
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Body Water/metabolism
MH  - Constriction
MH  - Coronary Vessels/*physiopathology
MH  - Dogs
MH  - Electrophysiology
MH  - Extracellular Space/metabolism
MH  - Hypertension/*physiopathology
MH  - Myocardial Ischemia/*complications/*physiopathology
MH  - Potassium/metabolism
MH  - Ventricular Fibrillation/etiology/physiopathology/*prevention & control
EDAT- 1998/05/30 00:00
MHDA- 1998/05/30 00:01
CRDT- 1998/05/30 00:00
PHST- 1998/05/30 00:00 [pubmed]
PHST- 1998/05/30 00:01 [medline]
PHST- 1998/05/30 00:00 [entrez]
AID - S0022-2828(97)90589-7 [pii]
AID - 10.1006/jmcc.1997.0589 [doi]
PST - ppublish
SO  - J Mol Cell Cardiol. 1998 Feb;30(2):255-68. doi: 10.1006/jmcc.1997.0589.