Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Partial coronary sinus obstruction (CSO) in the dog prevents or delays the predictable ventricular fibrillation (VF) of the early phase of acute ischemia, by normalizing regional electrophysiological disparities which presumably reflect inhomogeneous extracellular potassium ([K+]o) accumulation. To clarify whether CSO indeed affects [K+]o inhomogeneity, we determined in 12 chloralose anesthetized dogs the dynamic [K+]o changes occurring early during reversible coronary artery occlusion (CAO) involving the mid-left anterior descending branch. These changes were compared to those observed during CAO preceded by CSO sufficient to increase the coronary sinus pressure to 40 mmHg. [K+]o was determined using valinomycin coated electrodes implanted within the ischemic (IZ) and the normal (NZ) zones, as well as immediately inside (BZi) and outside (BZo) the visible border. [K+]o increased rapidly within the IZ and the BZi reaching plateau 5 min after CAO, at about three-fold control (11.89 +/- 1.12 mEq/l). Unexpectedly, [K+]o also increased initially outside the border (BZo) but declined after 3 min to a lower level (7.00 +/- 0.40 mEq/l), thus creating a steep gradient of up to 5.54 +/- 0.20 mEq/l, P < 0.001) across the visible border. In four trials, the gradient coincided with VF. With CSO preceding CAO, the development of this border zone gradient was entirely prevented. Moreover, [K+]o reached a significantly lower and similar level in the IZ, BZi and BZo (9.5 +/- 0.89 mEq/l, P < 0.001) and no VF was observed. Thus the beneficial electrophysiologic and antiarrhythmic effects of CSO in acute ischemia may be explained by [K+]o equalization.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mol Cell Cardiol 1994 Oct
PMID:Prevention of extracellular K+ inhomogeneity across the ischemic border by coronary venous obstruction in the dog: salutary antiarrhythmic effects of enhanced myocardial hydration. 786 95

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.
J Mol Cell Cardiol 1998 Feb
PMID:Coronary venous hypertension prevents the formation of the electrophysiological arrhythmogenic substrate of acute ischemia in the dog: salutary effects of preserved myocardial hydration. 951 2

In order to evaluate hemodynamics in the complex vascular system of phocid seals, intravascular pressure profiles were measured during periods of rest-associated apnea in young elephant seals (Mirounga angustirostris). There were no significant differences between apneic and eupneic mean arterial pressures. During apnea, venous pressure profiles (pulmonary artery, thoracic portion of the vena cava (thoracic vena cava), extradural vein, and hepatic sinus) demonstrated only minor, transient fluctuations. During eupnea, all venous pressure profiles were dominated by respiratory fluctuations. During inspiration, pressures in the thoracic vena cava and extradural vein decreased -9 to -21 mm Hg, and -9 to -17 mm Hg, respectively. In contrast, hepatic sinus pressure increased 2-6 mm Hg during inspiration. Nearly constant hepatic sinus and intrathoracic vascular pressure profiles during the breath-hold period are consistent with incomplete constriction of the caval sphincter during these rest-associated apneas. During eupnea, negative inspiratory intravascular pressures in the chest ("the respiratory pump") should augment venous return via both the venae cavae and the extradural vein. It is hypothesized that, in addition to the venae cavae, the prominent para-caval venous system of phocid seals (i.e., the extradural vein) is necessary to allow adequate venous return for maintenance of high cardiac outputs and blood pressure during eupnea.
Comp Biochem Physiol A Mol Integr Physiol 2006 Sep
PMID:Intravascular pressure profiles in elephant seals: hypotheses on the caval sphincter, extradural vein and venous return to the heart. 1682 Mar 12