Biomedical subjects

H Ikenouchi

Publications and source records attributed to H Ikenouchi.

24 records · Page 2Linked to original sources

PubMed1990

Doppler echocardiographic-determined changes in left ventricular diastolic filling flow velocity during the lower body positive and negative pressure method.

Changes in parameters of left ventricular (LV) diastolic filling flow obtained with Doppler echocardiography during the lower body positive and negative pressure method were analyzed in 15 patients (12 with coronary artery disease and 3 with dilated cardiomyopathy). Lower body pressure was altered at 5 steps (+20, +10, 0, -20 and -40 mm Hg vs atmospheric pressure). Pulmonary capillary wedge pressure measured with a balloon-tipped catheter was changed proportionally with lower body pressure during the procedures (p less than 0.01). Mean systemic arterial pressure was changed slightly during lower body positive pressure and negative pressure of -40 mm Hg. Heart rate was almost unchanged except at lower body pressure of -40 mm Hg. The peak velocity of LV early diastolic filling flow was changed with pulmonary capillary wedge pressure in an almost parallel fashion during the procedures (p less than 0.01). The peak velocity of LV late diastolic filling flow showed smaller changes than that of early diastolic filling flow. Changes in pulmonary capillary wedge pressure correlated positively with changes in the peak velocity of LV early diastolic filling flow (r = 0.759, p less than 0.01), but not with changes in the peak velocity of LV late diastolic filling flow (r = 0.039, not significant) during lower body negative pressure of -20 mm Hg. These data suggest that left atrial pressure is one of the important determinants of LV early diastolic filling flow in this acute clinical setting and that LV late diastolic filling flow is less sensitive to changes in left atrial pressure than LV early diastolic filling flow.

Adult↗

PubMed1990

Acute hemodynamic effects of nilvadipine, a new calcium channel blocker, in patients with congestive heart failure.

The acute hemodynamic effects of nilvadipine, a newly synthesized calcium channel blocker, were studied in 12 patients with congestive heart failure. Hemodynamic measurements were made before and 15, 30, and 60 min after oral administration of 6 mg nilvadipine. Substantial reductions in systemic vascular resistance (-28.8 +/- 6.3%, p less than 0.01) and forearm vascular resistance (-52.0 +/- 6.2%, p less than 0.01) after nilvadipine administration were associated with increases in cardiac index (31.1 +/- 8.3%, p less than 0.01) and forearm blood flow (105.2 +/- 27.4%, p less than 0.01). Mean arterial and pulmonary arterial pressures were decreased by 12.2 +/- 3.0% (p less than 0.01) and 14.7 +/- 5.0% (p less than 0.05), respectively, after nilvadipine administration; however, heart rate remained unchanged. Decreases in mean arterial pressure correlated with the baseline arterial pressure (y = 0.58x - 41.6, r = 0.75, p less than 0.01). Pulmonary capillary wedge pressure decreased by 33.1 +/- 9.1% (p less than 0.01) after nilvadipine administration. However, right atrial pressure and the venous stiffness constant remained unchanged, and the venous pressure-volume curve was not shifted significantly. Therefore, the decrease in pulmonary capillary wedge pressure was attributed primarily to afterload reduction. Nilvadipine holds promise as a vasodilator for the therapy of congestive heart failure.

Aged↗

PubMed1989

Wall motion asynchrony prolongs time constant of left ventricular relaxation.

To evaluate the effects of wall motion asynchrony on left ventricular (LV) relaxation, we performed atrioventricular sequential pacing with the second stimulation at six epicardial sites in open-chest anesthetized dogs. Myocardial segment lengths in the basal, mid, and apical LV free wall were measured by ultrasonic crystals. The standard deviation of interval from the onset of the QRS complex to that of elongation in each segment length was used as a quantitative index for asynchrony (asynchrony index, AI). The AI increased significantly in all sequential pacing modes compared with the control right atrial pacing. The time constant (T) of LV relaxation derived from exponential fit with zero-asymptote was prolonged significantly in all sequential pacing modes except for pacing at the LV base. In each dog there was a good correlation between changes in AI and T [r = 0.61 - 0.98 (mean = 0.84)]. Since the regional inactivation process of the myocardium is considered to be unchanged during these interventions, we concluded that asynchronous wall motion plays an important role in the impairment of LV relaxation.

Animals↗

PubMed1989

Pathophysiology and evaluation of severity of congestive heart failure on the basis of venous characteristics.

To elucidate the possibility of grading the severity of congestive heart failure by using venous characteristics, we constructed venous pressure-volume curves (PVR) and calculated venous stiffness constants (K). In addition, effects of vasoactive drugs on venous distensibility were studied. A venous pressure-volume curve could be fit well by an exponential curve (r = 0.98 +/- 0.01). The PVR was shifted to the left with an increase in the clinical severity of congestive heart failure. The exponent of these curves, K, increased as the PVR was shifted to the left. K correlated with heart rate (r = 0.52, p less than 0.01), right atrial pressure (r = 0.54, p less than 0.02) and mean pulmonary arterial pressure (r = 0.47, p less than 0.04). Nitroglycerin and amrinone dilated veins and decreased K by 19.6 +/- 6.9% (p less than 0.03) and 14.0 +/- 4.3% (p less than 0.02), respectively. Changes in K (delta K) during the nitroglycerin and amrinone infusions correlated closely with the baseline K (delta K = -0.41 K + 0.22, r = 0.92, p less than 0.01). Therefore, the venodilating effects of these drugs were greater in patients with more severe congestive heart failure. The venous stiffness constant could be useful to grade the severity of congestive heart failure.

Adult↗

PubMed1989

Lack of venodilative activity of alpha human atrial natriuretic polypeptide in patients with congestive heart failure.

We studied the effect of alpha human atrial natriuretic polypeptide (hANP) on venous vessels by occlusion plethysmography in 7 patients with congestive heart failure. In another 8 patients the effect of nitroglycerin was studied to validate the methodology. Forearm venous pressure (VP) and volume change (delta V) were measured simultaneously. The relationship between venous pressure and volume change was described by the equation VP = C x e(K x delta V) (r = 0.98 +/- 0.01) and the venous stiffness constant (K) was calculated. Alpha human atrial natriuretic polypeptide (0.1 microM/kg/min) was infused intravenously at a dose sufficient to cause arteriodilation. The pressure-volume curve of the peripheral veins was shifted rightward on the volume axis and the stiffness constant (K) was decreased (-28.1%, p less than 0.03) significantly by nitroglycerin. Alpha human atrial natriuretic polypeptide significantly decreased systemic vascular resistance but did not shift the pressure-volume curve of the vein nor did it decrease the stiffness constant (K). We conclude that hANP has far less venodilating effect than arteriodilating effect in congestive heart failure patients.

Atrial Natriuretic Factor↗

PubMed1988

Combined factor VII and protein C deficiency found in a patient with peripheral pulmonary artery stenosis accompanied by progressive pulmonary hypertension and hemoptysis.

A congenital deficiency of factor VII and protein C was found in a 21-year-old female suffering from recurrent and progressive attacks of dyspnea and hemoptysis over the last four years. She has been followed in our Department since the age of 17 under a diagnosis of peripheral pulmonary artery stenosis and pulmonary hypertension as confirmed by cardiac catheterization and angiography. Prolonged prothrombin time repeatedly examined during this time period prompted us to perform detailed coagulation studies. We found that factor VII and protein C were both half normal in activity as well as in antigen. Three other members of her immediate family were also found to be affected with this combined deficiency. Since the genes encoding factor VII and protein C are located in different chromosomes, the 13th and the second chromosomes, respectively, expression of the combined hereditary deficiency is a random and very rare association on the basis of frequencies of 1:50,000 for factor VII and 1:16,000 for protein C deficiencies.

Adult↗