Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02256 (Calcium chloride)
 226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hemodynamic determinants of the time-course of fall in isovolumic left ventricular pressure were assessed in isolated canine left ventricular preparations. Pressure fall was studied in isovolumic beats or during prolonged isovolumic diastole after ejection. Pressure fall was studied in isovolumic relaxation for isovolumic and ejecting beats (r less than or equal to 0.98) and was therefore characterized by a time constant, T. Higher heart rates shortened T slightly from 52.6 +/- 4.5 ms at 110/min to 48.2 +/- 6.0 ms at 160/min (P less than 0.01, n = 8). Higher ventricular volumes under isovolumic conditions resulted in higher peak left ventricular pressure but no significant change in T. T did shorten from 67.1 +/- 5.0 ms in isovolumic beats to 45.8 +/- 2.9 ms in the ejecting beats (P less than 0.001, n = 14). In the ejecting beats, peak systolic pressure was lower, and end-systolic volume smaller. To differentiate the effects of systolic shortening during ejection from those of lower systolic pressure and smaller end-systolic volume, beats with large end-diastolic volumes were compared to beats with smaller end-diastolic volumes. The beats with smaller end-diastolic volumes exhibited less shortening but similar end-systolic volumes and peak systolic pressure. T again shortened to a greater extent in the beats with greater systolic shortening. Calcium chloride and acetylstrophanthidin resulted in no significant change in T, but norepinephrine, which accelerates active relaxation, resulted in a significant shortening of T (65.6 +/- 13.4 vs. 46.3 +/- 7.0 ms, P less than 0.02). During recovery from ischemia, T increased significantly from 59.3 +/- 9.6 to 76.8 +/- 13.1 ms when compared with the preischemic control beat (P less than 0.05). Thus, the present studies show that the time-course of isovolumic pressure fall subsequent to maximum negative dP/dt is exponential, independent of systolic stress and end-systolic fiber length, and minimally dependent on heart rate. T may be an index of the activity of the active cardiac relaxing system and appears dependent on systolic fiber shortening.
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PMID:Hemodynamic determinants of the time-course of fall in canine left ventricular pressure. 95

The efficiency of transferring the total energy generated by ventricular contraction (pressure-volume area, PVA) to external work (EW) and internal work (IW) and the myocardial oxygen consumption (MVO2) at zero PVA were determined during volume loading on right heart bypass before and after a 50% augmentation (CaCl2, 0.03 mEq/kg/min, n = 7) or depression (20 minutes of 37 degrees C ischemia with 30 minutes of reperfusion, n = 7) of the contractile state. An increased EW efficiency (64% +/- 7% vs. 81% +/- 6%, p less than 0.01) with reciprocally decreased IW efficiency (36% +/- 7% vs. 19% +/- 6%, p less than 0.01) occurs with calcium chloride-augmented contractility. A reversible ischemia and reperfusion insult has the converse effect on these relative efficiencies (EW, 73% +/- 4% vs. 49% +/- 4%; IW, 27% +/- 4% vs. 51% +/- 4%; each p less than 0.01). Calcium chloride increases the oxygen requirements of both basal metabolism (28 +/- 2 vs. 67 +/- 9 ml O2/beat/100 gm LV, p less than 0.01) and fiber shortening (11 +/- 5 vs. 62 +/- 11 ml O2/beat/100 gm LV, p less than 0.01). The postischemic heart has a decreased oxygen need for shortening (20 +/- 2 vs. 3 +/- 4 ml O2/beat/100 gm LV, p less than 0.01), paralleling the depressed inotropic state. This new model of compartmentalized chemomechanical transduction may allow specific modulation of the energetic derangements attendant to the surgically treated heart.
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PMID:Compartmentalizing chemomechanical transduction in the ejecting heart. 276 28

Afterload independent, inotropic state sensitive indices of regional function were sought in 31 canine hearts instrumented with piezoelectric crystals to depict trapezoidal areas in the left anterior descending and circumflex arterial beds. Control and postinterventional end-systolic pressure versus regional length and area relationships and regional stroke work versus end-diastolic length and area relationships were inscribed during incremental volume loading on right heart bypass. Hearts were randomized to undergo afterload variation with phenylephrine infusion, contractility augmentation by calcium chloride, or 20 minutes of ischemia in the region of the left anterior descending artery with 30 minutes of reperfusion. All relationships were linear before and after each intervention (mean r = 0.726 to 0.974). The slopes of each correlation were interpreted to quantify intrinsic regional contractility, and all were afterload insensitive (unaffected by phenylephrine). Regional stroke work versus end-diastolic area and length relationships were depressed 55% and 62%, respectively, after ischemia (p less than 0.001 each), whereas neither end-systolic pressure versus regional area nor regional length was significantly altered. Calcium chloride increased regional stroke work versus area 45% in both arterial beds, but significantly increased the other indices only in the left anterior descending and not the left circumflex region. Unlike previous studies of global contractility, correlation of end-systolic events alone did not reliably discriminate perturbations in regional function. The superiority of regional stroke work versus end-diastolic area may be due to incorporating pressure-area changes during the entire cardiac cycle and obviating variability owing to crystal orientation inexactly parallel to fiber shortening.
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PMID:Assessment of the intrinsic contractile state within an area of myocardium. 281 15

Whether calcium chloride (CaCl2) should be used to reverse myocardial dysfunction during cardiac operations remains a controversial issue. Calcium chloride may reduce, rather than increase, myocardial contractility and may produce exaggerated vasoconstriction in postischemic vessels in which the endothelium has been damaged. These possibilities were investigated in an open-chest porcine model that allowed control of systemic hemodynamics. Incremental doses of CaCl2 (1, 3, and 10 mg/min) were infused directly into a coronary artery before and after 10 or 15 minutes of ischemia followed by 15 minutes of reperfusion. Calcium chloride increased regional contraction, coronary blood flow, and oxygen consumption before ischemia, whereas oxygen and lactate extraction were unchanged. After ischemia and reperfusion, contraction was impaired and lactate extraction was reduced, but a similar response to CaCl2 was observed. Contraction returned to baseline values promptly after CaCl2. Thus, CaCl2 exerts a positive inotropic effect both in normal and in postischemic myocardium. Calcium chloride does not cause direct coronary constriction nor does it worsen myocardial stunning after a short period of normothermic myocardial ischemia.
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PMID:Effects of intracoronary calcium chloride on the postischemic heart in pigs. 777 23