Biomedical subjects

J B Hermiller

Publications and source records attributed to J B Hermiller.

47 records · Page 3Linked to original sources

PubMed1984

The electrophysiologic effects of upright posture.

In order to determine the effects of upright posture on the electrophysiologic properties of the human heart, 12 patients underwent electrophysiologic studies in the supine and upright positions. Compared to supine, the upright position significantly reduced basic cycle length from 818 +/- 111 to 680 +/- 141 msec, sinoatrial conduction time from 186 +/- 94 to 135 +/- 56 msec, corrected sinoatrial recovery time from 206 +/- 104 to 108 +/- 55 msec, interatrial conduction time from 76 +/- 17 to 70 +/- 16 msec, and the AV nodal conduction time (AH interval) from 88 +/- 19 to 78 +/- 14 msec (all p less than 0.05). Right intra-atrial and His-Purkinje (HV interval) conduction times were not altered. When the subjects assumed the upright position, the effective refractory periods of the right atrium, atrioventricular node, and right ventricle decreased significantly at basic and paced cycle lengths. For the group as a whole, the upright posture did not significantly augment repetitive responses to atrial and ventricular extrastimuli.

Adolescent↗

PubMed1984

Combined systolic time intervals and M-mode echocardiography in the evaluation of central hemodynamics in primary pulmonary hypertension.

8 patients with moderate to severe primary pulmonary hypertension underwent systolic time intervals, M-mode echocardiography, and direct hemodynamic studies in order to determine the correlation between noninvasive parameters and hemodynamic variables and to evaluate the utility of these noninvasive studies in primary pulmonary hypertension. The ratio of the pre-ejection period to left ventricular ejection time (PEP/LVET) of the systolic time intervals was abnormally increased (greater than 0.42) for each subject; the increase in the PEP/LVET was secondary to a shortening of the left ventricular ejection time in 4 patients, prolongation of the pre-ejection period in 1, or a combination of such, noted in 3. In contrast, echocardiographic parameters of left ventricular function, specifically, percent change in the minor axis of the left ventricle with systole, velocity of circumferential fiber shortening, and ejection fraction, were normal. In addition, a very good correlation was noted between PEP/LVET and total pulmonary resistance (r value = -0.89), while the echocardiographic parameters correlated well with stroke volume and cardiac indices (r values ranged from 0.68 to 0.72). These results indicate that in primary pulmonary hypertension, systolic time intervals provide an estimation of overall cardiac-cardiovascular performance, rather than left ventricular function alone, which in turn, is validly examined by M-mode echocardiography.

Adult↗

PubMed1984

The effect of age on central and regional hemodynamics.

16 normal subjects, ranging in age from 24 to 79 years, underwent simultaneous central and regional (renal, hepatic and limb) hemodynamic measurements; the purpose of this investigation was to determine the relationship between these measurements and age. Cardiac index was inversely related to age, with a correlation coefficient of -0.53 (p less than 0.05). Renal blood flow correlated inversely with age at an r value of -0.52 (p less than 0.05). Although the correlation coefficients did not achieve statistical significance, several trends were noted with increasing age: systemic vascular resistance, renal, hepatic and limb vascular resistances, and mean systemic blood pressure increase and hepatic and limb flows decrease. In normal human subjects, certain central and regional hemodynamic parameters change with age; these changes may ultimately influence function and perhaps, drug disposition (liver and kidney) as well.

Adult↗

PubMed1984

Relationship between central hemodynamics and regional blood flow in normal subjects and in patients with congestive heart failure.

Central and regional (hepatic, renal, and limb) hemodynamic data are presented for a normal population (n = 16) and for a group of patients with congestive heart failure (n = 64). The patient population represented a wide spectrum of severity of congestive heart failure. Various relationships between central and regional hemodynamics were analyzed. The results indicate that in congestive heart failure blood flow to hepatic, renal, and limb regions is significantly decreased, and that this decrease is proportional and linearly related to the reduction in cardiac output. The vascular resistances of these regions correlated directly with systemic vascular resistance. Changes in renal vascular resistance and renal blood flow became attenuated as the severity of the heart failure advanced from moderate to severe and at higher levels of systemic vascular resistance. There was little to no correlation between systemic blood pressure and liver, kidney, and limb blood flow for the range of systemic pressures studied.

Adult↗

PubMed1984

Amrinone in severe congestive heart failure: another look at an intriguing new cardioactive drug.

Seven patients with severe congestive heart failure received amrinone i.v. (continuous infusions of 10, 20 and 40 micrograms/kg/min) and orally (1.5, 3.0 and 4.5 mg/kg) in order to determine the comprehensive acute hemodynamic response of this agent. Standard hemodynamic, echocardiographic and systolic time interval measurements were made before and sequentially after amrinone administration. Intravenous amrinone significantly increased cardiac index and stroke volume index, did not alter heart rate and significantly decreased pulmonary capillary wedge pressure, mean systemic blood pressure and systemic and pulmonary vascular resistances. The determinants of left ventricular inotropy, delta P/delta t, pre-ejection period index and velocity of circumferential fiber shortening were not affected by amrinone; dobutamine (5 and 10 micrograms/kg/min), used as an internal standard for inotropy, significantly improved these determinants. Except for a significant reduction in pulmonary capillary wedge pressure, first-dose oral amrinone effected little change in central hemodynamic variables and indices of ventricular inotropy; no additional changes occurred after the fifth dose. In the setting of severe chronic congestive heart failure, short-term iv infusions and oral administration of amrinone elicit only mild to moderate hemodynamic changes. Furthermore, these changes are a result of vasodilation (preload and afterload reduction) rather than positive inotropy.

Adult↗

PubMed1983

Clonidine in congestive heart failure: a vasodilator with negative inotropic effects.

Fourteen patients with moderately severe congestive heart failure (CHF) were given clonidine orally (0.2 and 0.4 mg doses) to determine the hemodynamic effects of a typical centrally acting vasodilator. The 0.2 mg dose significantly reduced mean systemic (15%) and mean pulmonary artery (20%) pressure; the corresponding reductions in vascular resistance were not as great because of a diminished cardiac output. Pulmonary capillary wedge pressure decreased significantly (27%). Heart rate decreased 11% and stroke volume remained unchanged. At a higher dose (0.4 mg), clonidine augmented these reductions but increased stroke volume modestly (15%). Isovolumic developed pressure/duration of isovolumic contraction and the duration of the preejection period were used as indexes of inotropy. After both doses, isovolumic developed pressure/duration of isovolumic contraction decreased dramatically (greater than or equal to 33%) and the preejection period increased substantially (greater than or equal to 18%) (both p less than 0.05). Compared with currently employed vasodilating agents, the centrally acting agent clonidine appears unique in that the drug-induced systemic and pulmonary arterial vasodilation are not accompanied by a commensurate improvement in ventricular systolic function. This lack of improvement appears to be a result of negative inotropic effects.

Adult↗

PubMed1983

Amrinone therapy for congestive heart failure in outpatients with idiopathic dilated cardiomyopathy.

Amrinone, 100 mg orally every 8 hours, was administered to 13 patients with moderate-to-severe congestive heart failure (CHF) for 1 month on an outpatient basis to determine the beneficial and undesirable effects of this new cardioactive agent in this clinical setting. These subjects received conventional CHF medications during the course of study. Ten patients who received conventional CHF medications alone served as a control group. Changes in functional classification were not significantly different between the 2 treatment groups. Amrinone augmented exercise capacity 37% above baseline compared with a 12% improvement for the control group. Noninvasive indexes of resting left ventricular function (echocardiography and systolic time intervals) did not change significantly for either group, nor was there a significant change in the exercise ejection fraction. All patients treated with amrinone had greater than or equal to 1 symptom-related or laboratory-detected adverse effect. An increase in the frequency of ventricular ectopic beats was noted at rest in 4 and with exercise in 6 patients (salvos of nonsustained ventricular tachycardia in 2). Six subjects treated with amrinone had gastrointestinal symptoms and 8 developed a viral-like illness. Other adverse effects noted in the amrinone-treated group included near-syncope, headaches, marked anxiety, chest pain, palpitations, maculopapular rash, hypokalemia, and elevation of serum transaminase levels. The control patients had significantly fewer adverse effects. Although individual patients with CHF may benefit from long-term amrinone therapy, the low benefit-to-risk-adverse effect ratio does not warrant widespread application of this drug in the outpatient management of CHF and requires caution when prescribing.

Aminopyridines↗

PubMed1983

Captopril in primary pulmonary hypertension.

Seven women with primary pulmonary hypertension underwent hemodynamic evaluation, at rest and during exercise, before and after the oral administration of captopril. Dose-response curves were generated for the 25-, 50- and 100-mg doses. Captopril significantly reduced systemic blood pressure and systemic vascular resistance; these effects persisted at submaximal levels of exercise. Captopril did not alter pulmonary artery pressure or resistance, cardiac output or stroke volume at rest or during exercise. Exercise tolerance did not improve. Four of the patients also received captopril chronically for 12 weeks at doses of 75 and 100 mg every 8 hours. Resting and exercise hemodynamic evaluation was repeated at the end of the 12-week period. Except for a persistent reduction in mean systemic blood pressure at rest, chronic captopril administration did not elicit hemodynamic changes. Measured exercise duration did not change during continuous captopril treatment, although one patient reported mild subjective improvement in activity tolerance. In primary pulmonary hypertension, captopril exerts its major effect on systemic vasculature, with little or no effect on the pulmonary circuit. While an occasional patient may experience some clinical improvement with captopril therapy, the majority of adult patients with severe primary pulmonary hypertension will not benefit from its chronic administration.

Adult↗

PubMed1982

Vasodilators and prostaglandin inhibitors in primary pulmonary hypertension.

Ten women with primary pulmonary hypertension had resting hemodynamic measurements taken before and after the nonparenteral administration of various vasodilators and prostaglandin inhibitors. Only sublingual isoproterenol, alone or combined with sublingual isosorbide dinitrate, effected a substantial (greater than 20%) drop in pulmonary vascular resistance; this decrease was accompanied by little change in pulmonary artery pressure. Isosorbide dinitrate was the only drug that elicited any reduction in pulmonary artery pressure; pulmonary vascular resistance decreased modestly. The oral administration of diazoxide, hydralazine, phentolamine, and tolazoline elicited little change in pulmonary artery pressure or resistance. Except for tolazoline, all these agents significantly decreased systemic blood pressure and resistance. Prostaglandin inhibition by indomethacin (acute and chronic dosing) increased pulmonary and systemic vascular resistances and reduced cardiac output. Aspirin combined with dipyridamole elicited no changes. The vasodilators and prostaglandin inhibitors studied evoked little improvement in resting pulmonary hemodynamic abnormalities in primary pulmonary hypertension.

Adolescent↗

PubMed1981

Carrier-mediated transport of D-ribose by Rhodotorula glutinis.

The kinetics of D-ribose transport by Rhodotorula glutinis were investigated over a 1 000-fold range of sugar concentrations. Analysis of the saturation isotherm revealed the presence of two carrier systems for D-ribose in the Rhodotorula plasma membrane. These two carriers exhibited Km values of 1.3 and 30 mM. At saturating concentrations of D-ribose, the low Km carrier contributes less than 10% to the total rate of transport. Although D-ribose is metabolized rapidly by Rhodotorula, intracellular free sugar concentrations exceed those in the medium. In addition, the transport of this pentose is inhibited by the proton-conductors, 2,4-dinitrophenol and carbonylcyanide m-chlorophenylhydrazone. These data suggest that Rhodotorula cells are capable of an energy-dependent, concentrative transport of D-ribose.

2,4-Dinitrophenol↗

PubMedDate not supplied

Regional hemodynamic effects of clonidine in congestive heart failure.

Regional and central hemodynamic variables were ascertained in 10 patients with congestive heart failure before and after the oral administration of clonidine. Following the 0.2 mg dose, renal, hepatic, and limb blood flow remained unaltered, whereas a reduction was noted in heart rate (10%), mean systemic (14%), and pulmonary capillary wedge pressures (27%). Cardiac index and systemic vascular resistance fell slightly, however the changes were not statistically significant. Higher dose clonidine (0.4 mg) elicited similar regional hemodynamic effects whereas systemic vascular resistance significantly diminished (21%) and cardiac index remained unchanged. In congestive heart failure, the central antihypertensive agent, clonidine, effects a significant reduction in preload (left ventricular filling pressure) and afterload (systemic blood pressure) without markedly altering other central and regional hemodynamic variables.

Adult↗