Disease relevance of Ventricular Pressure

• The increased ANP gene expression in cirrhosis seems to involve a novel mechanism not related to stretch because neither increased ventricular pressure nor dilation was present [1].
• In congestive heart failure (idiopathic dilated cardiomyopathy), exercise is accompanied by a smaller-than-normal decrease in end-diastolic left ventricular volume, depressed peak rates of left ventricular pressure rise and fall, and depressed heart-rate-dependent potentiation of contractility (bowditch treppe) [2].
• BACKGROUND: We have previously shown that long-term ACE inhibition with fosinopril prolongs survival and improves ventricular function despite persistent severe left ventricular pressure overload in ascending aortic-banded rats with left ventricular hypertrophy during the transition from compensation to failure [3].
• Isovolumic hearts were perfused with Tyrode's solution at 37 degrees C. Developed left ventricular pressure at 35 minutes of reperfusion was decreased significantly to 67 +/- 3% after ischemia (mean +/- SEM, n = 8) and to 79 +/- 6% after hypoxia (n = 8) relative to the control condition (n = 8), without increased cellular creatine kinase release [4].
• The mechanisms by which beta-blockade prevents dobutamine-induced ischemia appeared to be mainly through decreases in heart rate and rate of rise in left ventricular pressure, improvement of regional coronary flow per heartbeat and attenuation of regional ischemic lactate production [5].

High impact information on Ventricular Pressure

• Despite the fact that glycolytic flux had been blocked both by iodoacetate and by absence of substrate, end-diastolic left ventricular pressure (EDP) remained unchanged (P > 0.15, n = 6) [6].
• Dobutamine significantly increased the slope of the left ventricular end-systolic pressure-volume relation (Emax) and the slope of the dP/dtmax-end-diastolic volume relation (dE/dtmax), while significantly decreasing the time from end-diastole to end-systole (tmax) and the time constant (T) of the isovolumic fall in left ventricular pressure [7].
• In 9 of 11 patients there was a substantial downward displacement of the diastolic pressure-volume curve during nitroprusside infusion, with left ventricular pressure being lower for any given volume with nitroprusside [8].
• In patients with hypertrophic obstructive cardiomyopathy, synchronised and ventricular pacing at optimum AV interval for the individual reduces the intraventricular pressure gradient and improves functional tolerance [9].
• However, in MCT-treated rats, LU 135252 therapy significantly reduced right ventricular pressure (39.7 +/- 2.1 mm Hg), potentiated acetylcholine-induced vasodilatation (delta Emax, from 1.6 +/- 0.2 to 3.7 +/- 0.4 mm Hg), and improved the responses to sodium nitroprusside (delta Emax, from 2.7 +/- 0.3 to 5.6 +/- 0.6 mm Hg) [10].

Chemical compound and disease context of Ventricular Pressure

• In 14 patients with severe congestive heart failure, left ventricular pressure (measured by tip manometer) and derived variables were measured before and every 10 minutes after administration of oral milrinone (10 mg) for 50 minutes along with measurements of coronary sinus blood flow and drug plasma levels [11].
• In contrast, the patient with severe coronary artery stenosis and reproducible angina during exercise, may obtain relief because nitrates decrease venous return, left ventricular size and left ventricular pressure, thus decreasing myocardial oxygen demands [12].
• Ten weeks of banding increased in vivo peak systolic left ventricular pressure and produced medial hypertrophy, an increase in collagen deposition in the myocardial and perivascular tissues, and myocardial hypertrophy in the banded group without beta-aminopropionitrile treatment [13].
• These morphological and molecular differences between the hydralazine and ramipril groups could not be attributed to differences in left ventricular-pressures, which were markedly elevated in all aortic stenosis rats (1.9-fold, each P < 0.001 versus sham) [14].
• 6. It is concluded that propranolol treatment approximately halves the compensatory cardiac hypertrophy occurring in response to a left ventricular pressure over-load by a mechanism independent of its effect on cardiac work load [15].

Biological context of Ventricular Pressure

• Coronary blood flow, heart rate, mean arterial pressure, and the first derivation of left ventricular pressure (dP/dt) were measured at baseline, 2 minutes, and 15 minutes after cocaine administration [16].
• Sodium meglumine diatrizoate caused decreases in left ventricular peak systolic pressure (LVPSP),-12.6 +/- 3.2%, and dp/dt at a left ventricular pressure (LVP) of 40 mm Hg, -14.3 +/- 4.1% [17].
• Increasing the contraction frequency from 180 to 300 beats/min in the presence of 10(-6) M propranolol increased oxygen consumption by 45% and decreased left ventricular pressure by 29% [18].
• Infusion of hydrochloric acid caused a sustained reduction in left ventricular pressure and coronary vascular resistance [19].
• At rest, ouabain increased the maximum first derivative of the left ventricular pressure (dp/dtmax) and stroke volume by 38% and 16%, respectively [20].

Anatomical context of Ventricular Pressure

• This study validates in humans an equation relating tau to left ventricular pressure at peak -dP/dt (P0), pressure at mitral valve opening (PMV), and isovolumic relaxation time (IVRTinv) [21].
• Diastolic active left ventricular pressure decay, extrapolated from the exponential fit, was subtracted from the measured left ventricular pressure (which is equal in magnitude but opposite in sign to the radial stress at the endocardium) to calculate residual left ventricular pressure (PR) and hence residual stress (sigma R = -PR) [22].
• We examined the late coronary vascular response to carotid chemoreceptor reflex activation in normal, conscious dogs instrumented for the measurement of right main and left circumflex coronary artery blood flows, arterial and right ventricular pressures, and arterial and coronary sinus blood gases and O2 contents [23].
• To compare the effects of isolated right ventricular pressure and volume overload on left ventricular diastolic geometry and filling, 11 patients with primary pulmonary hypertension, 11 patients with severe tricuspid regurgitation due to tricuspid valve resection and 11 normal subjects were studied with use of Doppler echocardiographic techniques [24].
• Triamcinolone treatment (12 mg/kg intraperitoneally, once daily for 3 days) reduced mean right ventricular pressure (11 +/- 1 versus 14 +/- 1 mm Hg) and protein content of pulmonary arteries (1.8 +/- 0.1 versus 2.7 +/- 0.1 mg/vessel) (both p < 0.05) [25].

Associations of Ventricular Pressure with chemical compounds

• During isoproterenol compared with pacing, peak left ventricular pressure was higher (205 +/- 33 vs. 142 +/- 21 mm Hg, p less than 0.001), ejection fraction was higher (77 +/- 10% vs. 71 +/- 12%, p less than 0.02), and regional systolic nonuniformity was diminished [26].
• The significant upward shift and attenuation by propranolol were also observed even when the left ventricular pressure was corrected by the subtraction of right atrial pressure [27].
• Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished [28].
• We investigated the effects of nifedipine on left ventricular diastolic function in 17 asymptomatic or minimally symptomatic patients with hypertrophic cardiomyopathy by simultaneously measuring left ventricular pressure and volume with a catheter-tipped manometer and biplane cineangiography [29].
• In 13 patients left ventricular pressure measurements were made with a micromanometer to permit assessment of peak negative dP/dt and the time constant of left ventricular isovolumic relaxation, T, before and after milrinone [30].

Gene context of Ventricular Pressure

• The increase of isovolumic peak first derivative of left ventricular pressure (ET-1: -2%; molsidomine+ET-1: +16%; BQ 610+ET-1: +19%) after pretreatment with molsidomine or BQ 610 indicates that these drugs unmask the positive inotropy of ET-1 [31].
• The first derivatives of intraventricular pressure (+/- dP/dt) were also significantly elevated, and this was associated with an increase in the affinity of the SR Ca(2+)-ATPase for Ca2+ in the phospholamban-deficient hearts [32].
• 3.In the unstimulated perfused heart, the left ventricular pressure (LVP) and maximal rate of left ventricular force development (dP/dtmax) of eNOS-/- hearts were not significantly different from those of WT hearts (LVP: 97 +/- 11 mmHg WT vs. 111 +/- 11 mmHg eNOS-/-; dP/dtmax: 3700 +/- 712 mmHg s(-1) WT vs. 4493 +/- 320 mmHg s)-1) eNOS-/-) [33].
• In HCM patients, the plasma BNP concentration may reflect the intraventricular pressure gradient and left ventricular diastolic dysfunction whereas the plasma ANP concentration reflects only the left ventricular diastolic dysfunction [34].
• Balloon inflation to raise ventricular pressure in hearts perfused with cardioplegic solution also activated FAK and ERK1/2 [35].

Analytical, diagnostic and therapeutic context of Ventricular Pressure

• After nidefipine (10 mg sublingually), the prolonged left ventricular isovolumic relaxation time assessed by echocardiography decreased from 112 +/- 26 to 83 +/- 23 msec (p less than 0.0001), and the left ventricular pressure decay as measured by time constant T improved from 63 +/- 20 to 49 +/- 11 msec (p less than 0.05) [36].
• Perfusion of hearts with 0.1 microM isoproterenol increased myocardial cAMP content 2.8-fold, activation of cAMP-dependent protein kinase 4.4-fold, phosphorylase a formation 3.4-fold, left ventricular pressure 1.8-fold, rate of ventricular pressure development 2.1-fold, and rate of ventricular relaxation 2.2-fold within 1 minute [37].
• BACKGROUND: Myocardial glucose utilization is increased in animal models with ventricular pressure overload [38].
• METHODS AND RESULTS: Left ventricular pressures and dimensions were measured simultaneously during supine bicycle exercise in 23 patients with nonobstructive hypertrophic cardiomyopathy, before and after intravenous injection of either nicorandil (0.1 mg/kg) or propranolol (0.15 mg/kg) [39].
• Thus the isovolumetric left ventricular pressure measured after 15 min ischaemia, which represents 59(SEM 6)% of the preischaemic value in the control group, was increased to 82(9) and 94(8)% in presence of glibenclamide (1 and 10 microM, p < 0.05 respectively) [40].

References