SEARCH · Search NASA
Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Research during the period 1 Oct. 1971 to 1 Oct. 1972 is reported. Studies discussed include: development of techniques for instrumentation of dogs and other animals, effects of temporary application of lower body negative pressure, and effect of infusing selected drugs on ventricular performance.
Sprague-Dawley rats were compressed to 616 kPa for 120 min then decompressed at 38 kPa/min to assess the cardiovascular and pulmonary responses to moderate decompression stress. In one series of experiments the rats were chronically instrumented with Doppler ultrasonic probes for simultaneous measurement of blood pressure, cardiac output, heart rate, left and right ventricular wall thickening fraction, and venous bubble detection. Data were collected at base-line, throughout the compression/decompression protocol, and for 120 min post decompression. In a second series of experiments the pulmonary responses to the decompression protocol were evaluated in non-instrumented rats. Analyses included blood gases, pleural and bronchoalveolar lavage (BAL) protein and hemoglobin concentration, pulmonary edema, BAL and lung tissue phospholipids, lung compliance, and cell counts. Venous bubbles were directly observed in 90% of the rats where immediate post-decompression autopsy was performed and in 37% using implanted Doppler monitors. Cardiac output, stroke volume, and right ventricular wall thickening fractions were significantly decreased post decompression, whereas systemic vascular resistance was increased suggesting a decrease in venous return. BAL Hb and total protein levels were increased 0 and 60 min post decompression, pleural and plasma levels were unchanged. BAL white blood cells and neutrophil percentages were increased 0 and 60 min post decompression and pulmonary edema was detected. Venous bubbles produced with moderate decompression profiles give detectable cardiovascular and pulmonary responses in the rat.
Various 12-lead ECG criteria have been established to detect right ventricular hypertrophy as a marker of pulmonary hypertension (PH). While some criteria offer good specificity they lack sensitivity because of a low prevalence of positive findings in the PH population. We hypothesized that three-dimensional equivalent dipole (ED) model could serve as a better detection tool of PH. We enrolled: 1) 17 patients (12 female, 5 male, mean age 57 years, range 19-79 years) with echocardiographically detected PH (systolic pulmonary arterial pressure greater than 35 mmHg) and no significant left ventricular disease; and 2) 19 healthy controls (7 female, 12 male, mean age 44, range 31-53 years) with no known heart disease. In each subject we recorded a 5-minute high-resolution 12-lead conventional ECG and constructed principal signals using singular value decomposition. Assuming a standard thorax dimension of an adult person with homogenous and isotropic distribution of thorax conductance, we determined moving equivalent dipoles (ED), characterized by the 3D location in the thorax, dipolar strength and the spatial orientation, in time intervals of 5 ms. We used the sum of all ED vectors in the second half of the QRS complex to derive the amplitude of the right-sided ED vector (RV), if the orientation of ED was to the right side of the thorax, and in the first half the QRS to derive the amplitude of the left-sided vector (LV), if the orientation was leftward. Finally, the parameter RV/LV ratio was determined over an average of 256 complexes. The groups differed in age and gender to some extent. There was a non-significant trend toward higher RV in patients with PH (438 units 284) than in controls (280 plus or minus 140) (p = 0.066) but the overlap was such that RV alone was not a good predictor of PH. On the other hand, the RV/LV ratio was a better predictor of PH, with 11/17 (64.7%) of PH patients but only in 1/19 (5.3%) control subjects having RV/LV ratio greater than or equal to 0.70 (p less than 0.001). The use of ED for evaluating PH shows good specificity at a reasonable sensitivity. The results are limited due to the small study groups and differences in age and gender, but further investigations are warranted, including of ED's diagnostic accuracy for PH versus that of other proposed ECG and VCG criteria.
By taking advantage of the capabilities of echocardiography to measure noninvasively left ventricular volume, stroke volume, and ejection fraction, and of the fact that the astronauts were routinely subjected to lower body negative pressure (whereby cardiac filling is progressively decreased), it was possible to construct classic ventricular function curves noninvasively, thereby obviating the difficulties encountered in comparing cardiac function at different end-diastolic volumes preflight and postflight. In this manner, the effect of an 84-day period of weightlessness on cardiac structure and function was evaluated in the Skylab 4 astronauts.
Over the past decade, Doppler echocardiography has become a well-established tool for the diagnosis of left ventricular diastolic dysfunction. Unfortunately, in many clinical situations traditional Doppler indices of transmittal and pulmonary venous flow are inconclusive, primarily due to their dependence on left atrial pressure. Recently, new Doppler indices that are much less dependent on preload have been developed, based on intraventricular flow propagation and intrinsic myocardial velocity. These methodologies provide direct assessment of ventricular relaxation and the small intraventricular pressure gradients essential to efficient filling of the ventricle. We review in this article the theoretical and experiment background of these new echo techniques as well as how they can be implemented in routine clinical practice.
The effects of lower body negative pressure (LBNP) on the cardiovascular response of 20 women between 23-43 years are evaluated. Calf circumference and cardiovascular data were recorded for women in the follicular and luteal phases of the menstrual cycle at -30, -40, and -50 mm Hg LBNP. The data reveal that the two menstrual phases did not cause differences in the way women respond to LBNP. It is observed that during LBNP calf circumference is enlarged; transthoracic impedance, and heart rate are increased; stroke volume, left ventricular ejection time, the Heather Index of contractility and systolic pressure, and cardiac output are reduced; and total peripheral resistance is elevated. The experimental data are compared to Montgomery et al. (1979). It is noted that the response of women to -50 mm Hg LBNP is similar to that of men; however, women adapt to stresses on the cardiovascular system with greater heart rate adjustments.
Several tables are presented giving left ventricular (LV) data for normal patients and patients with heart disease of varied etiologies, pointing out the salient features. Graphs showing LV pressure-volume relationships (compliance) are presented and discussed. The method developed by Rackley et al. (1964) for determining left ventricular mass in man is described, and limitations to the method are discussed. Some clinical methods for determining LV oxygen consumption are briefly described, and the relation of various abnormalities of ventricular performance to coronary artery disease and ischemic heart disease is characterized.
A cerebrospinal fluid shunt in the form of a ventricular catheter for controlling the condition of hydrocephalus by relieving the excessive cerebrospinal fluid pressure is described. A method for fabrication of the catheter and shunting the cerebral fluid from the cerebral ventricles to other areas of the body is also considered. Shunt flow failure occurs if the ventricle collapse due to improper valve function causing overdrainage. The ventricular catheter comprises a multiplicity of inlet microtubules. Each microtubule has both a large openings at its inlet end and a multiplicity of microscopic openings along its lateral surfaces.
The cardiovascular system's adaptive changes during and after spaceflight are discussed. Cephalic fluid shifts are demonstrated by photographs along with calf girth and leg volume changes. Inflight measurements show an increase in average resting heart rate and systolic blood pressure, and a sympathetic-parasympathetic neural imbalance. Postflight findings include a small but reversible decrease in the left ventricular muscle mass. Since 1980, NASA's research has emphasized cardiovascular deconditioning and countermeasures: hemodynamic changes, endocrine and neurohumoral aspects, etiologic factors, and lower body negative pressure devices. Though human beings acclimate to the space environment, questions concerning the immediate and long-term aspects of spaceflight need to be answered for adequate planning of extended space missions.
The data collected from a Space Shuttle crew to investigate cardiovascular changes due to microgravity are presented. The experimental procedures which involved preflight, immediate postflight, and one week following postflight echocardiograms of 13 individuals are described. The immediate postflight results reveal a 20 percent decrease in stroke volume, a 16 percent decrease in left ventricular diastolic volume index (LVDVI), no change in systolic volume, blood pressure, or cardiac index, and a 24 percent increase in heart rate. One week later a 17 percent stroke volume increase, a 29 percent increase in cardiac index, and normal blood pressure, and LVDVI were observed. It is concluded that upon reexposure to gravity a readaptation process for the cardiovascular system occurs.
A major change for crewmembers during weightlessness in microgravity is the redistribution of body fluids from the legs into the abdomen, thorax, and head. The fluids continue to be sequestered in these areas throughout the flight. Upon reentry into gravity on landing, these same body fluids are displaced again to their normal locations, however, not without hazardous incidence to the crewmembers. The problem remains that upon landing, crewmembers are subject to orthostasis, that is, the blood flowing into the legs reduces the blood supply to the brain and may result in the crewmember fainting. The purpose of this study was to develop a model of testing orthostatic responses of blood pressure regulating mechanisms of the cardiovascular system, when challenged, to maintain blood pressure to the brain. To accomplish this, subjects' responses were assessed as they proceeded from the supine position of progressive head-up tilt positions of 30 deg, 60 deg, and 90 deg angles. A convenience sample consisted of 21 subjects, females (N=11) and males (N=10), selected from a list of potential subjects available through the NASA subject screening office. The methodology included all non-invasive measurements of blood pressure, heart rate, echocardiograms, cardiac output, cardiac stroke volume, fluid shifts in the thorax, ventricular ejection and velocity times, and skin blood perfusion. The Fischer statistical analysis was done of all data with the significance level at .05. Significant differences were demonstrated in many instances of changes of posture for all variables. Based on the significance of the findings of this study, this model for assessing orthostatic responses does provide an adequate challenge to the blood pressure regulatory systems. While individuals may use different adaptations to incremental changes in gravity, the subjects, in aggregate, demonstrated significant adaptive cardiovascular changes to orthostatic challenges which were presented to them.
We have shown that the cellular contractile dysfunction characteristic of pressure-overload cardiac hypertrophy results not from an abnormality intrinsic to the myofilament portion of the cardiocyte cytoskeleton but rather from an increased density of the microtubule component of the extramyofilament portion of the cardiocyte cytoskeleton. To determine how, in physical terms, this increased microtubule density mechanically overloads the contractile apparatus at the cellular level, we measured cytoskeletal stiffness and apparent viscosity in isolated cardiocytes via magnetic twisting cytometry, a technique by which magnetically induced force is applied directly to the cytoskeleton through integrin-coupled ferromagnetic beads coated with Arg-Gly-Asp (RGD) peptide. Measurements were made in two groups of cardiocytes from cats with right ventricular (RV) hypertrophy induced by pulmonary artery banding: (1) those from the pressure-overloaded RV and (2) those from the normally loaded same-animal control left ventricle (LV). Cytoskeletal stiffness increased almost twofold, from 8.53 +/- 0.77 dyne/cm2 in the normally loaded LV cardiocytes to 16.46 +/- 1.32 dyne/cm2 in the hypertrophied RV cardiocytes. Cytoskeletal apparent viscosity increased almost fourfold, from 20.97 +/- 1.92 poise in the normally loaded LV cardiocytes to 87.85 +/- 6.95 poise in the hypertrophied RV cardiocytes. In addition to these baseline data showing differing stiffness and, especially, apparent viscosity in the two groups of cardiocytes, microtubule depolymerization by colchicine was found to return both the stiffness and the apparent viscosity of the pressure overload-hypertrophied RV cells fully to normal. Conversely, microtubule hyperpolymerization by taxol increased the stiffness and apparent viscosity values of normally loaded LV cardiocytes to the abnormal values given above for pressure-hypertrophied RV cardiocytes. Thus, increased microtubule density constitutes primarily a viscous load on the cardiocyte contractile apparatus in pressure-overload cardiac hypertrophy.
BACKGROUND. Although postprandial hypotension is a common cause of falls and syncope in elderly persons and in patients with autonomic insufficiency, the pathophysiology of this disorder remains unknown. METHODS AND RESULTS. We examined the hemodynamic, splanchnic blood pool, plasma norepinephrine (NE), and heart rate (HR) power spectra responses to a standardized 400-kcal mixed meal in 11 healthy young (age, 26 +/- 5 years) and nine healthy elderly (age, 80 +/- 5 years) subjects and 10 dysautonomic patients with symptomatic postprandial hypotension (age, 65 +/- 16 years). Cardiac and splanchnic blood pools were determined noninvasively by radionuclide scans, and forearm vascular resistance was determined using venous occlusion plethysmography. In healthy young and old subjects, splanchnic blood volume increased, but supine blood pressure remained unchanged after the meal. In both groups, HR increased and systemic vascular resistance remained stable. Forearm vascular resistance and cardiac index increased after the meal in elderly subjects, whereas these responses were highly variable and of smaller magnitude in the young. Young subjects demonstrated postprandial increases in low-frequency HR spectral power, representing cardiac sympatho-excitation, but plasma NE remained unchanged. In elderly subjects, plasma NE increased after the meal but without changes in the HR power spectrum. Patients with dysautonomia had a large postprandial decline in blood pressure associated with no change in forearm vascular resistance, a fall in systemic vascular resistance, and reduction in left ventricular end diastolic volume index. HR increased in these patients but without changes in plasma NE or the HR power spectrum. CONCLUSIONS. 1) In healthy elderly subjects, the maintenance of blood pressure homeostasis after food ingestion is associated with an increase in HR, forearm vascular resistance, cardiac index, and plasma NE. In both young and old, systemic vascular resistance is maintained. 2) Dysautonomic patients with postprandial hypotension fail to maintain systemic vascular resistance after a meal. This impairment in vascular response to meal ingestion may underlie the development of postprandial hypotension. 3) The measurement of mean HR or plasma NE does not adequately characterize autonomic cardiac control. Power spectral analysis suggests an impairment in the postprandial autonomic modulation of HR in healthy elderly and dysautonomic subjects, possibly predisposing to hypotension when vascular compensation is inadequate.
Neurohumoral control systems operation in adjustment of ventricular performance - effects of carotid sinus hypotension on cardiac function and aortic pressure in awake, intact dogs
The multipurpose ventricular actuating system is a pneumatic signal generating device that provides controlled driving pressures for actuating pulsatile blood pumps. Overall system capabilities, the timing circuitry, and calibration instruction are included.
Mouse myocyte contractility and the changes induced by pressure overload are not fully understood. We studied contractile reserve in isolated left ventricular myocytes from mice with ascending aortic stenosis (AS) during compensatory hypertrophy (4-week AS) and the later stage of early failure (7-week AS) and from control mice. Myocyte contraction and [Ca(2+)](i) transients with fluo-3 were measured simultaneously. At baseline (0.5 Hz, 1.5 mmol/L [Ca(2+)](o), 25 degrees C), the amplitude of myocyte shortening and peak-systolic [Ca(2+)](i) in 7-week AS were not different from those of controls, whereas contraction, relaxation, and the decline of [Ca(2+)](i) transients were slower. In response to the challenge of high [Ca(2+)](o), fractional cell shortening was severely depressed with reduced peak-systolic [Ca(2+)](i) in 7-week AS compared with controls. In response to rapid pacing stimulation, cell shortening and peak-systolic [Ca(2+)](i) increased in controls, but this response was depressed in 7-week AS. In contrast, the responses to both challenge with high [Ca(2+)](o) and rapid pacing in 4-week AS were similar to those of controls. Although protein levels of Na(+)-Ca(2+) exchanger were increased in both 4-week and 7-week AS, the ratio of SR Ca(2+)-ATPase to phospholamban protein levels was depressed in 7-week AS compared with controls but not in 4-week AS. This was associated with an impaired capacity to increase sarcoplasmic reticulum Ca(2+) load during high work states in 7-week AS myocytes. In hypertrophied failing mouse myocytes, depressed contractile reserve is related to an impaired augmentation of systolic [Ca(2+)](i) and SR Ca(2+) load and simulates findings in human failing myocytes.
Before and after the 59 day Skylab 3 flight, the astronauts were stressed with lower body negative pressure (LBNP), and their vectorcardiograms, pneumograms, phonocardiograms, and carotid pulse tracings were monitored together with the intervals of systole. In the immediate postflight period elevations in heart rate and blood pressure were observed in response to -50 mm Hg of LBNP. Postflight abnormalities in the systolic time intervals (STI) at rest and during stress were due to an increase in afterload and a decrease in preload. As blood volume was restored and blood pressure reduced, STI abnormalities persisted as long as one month, suggesting a possible reduction in ventricular contractility and/or a functional impairment to venous return.
BACKGROUND: Hypertension is a major independent risk factor for cardiac deaths, and diastolic dysfunction is a usual finding during the course of this disease. HYPOTHESIS: This study was designed to investigate the effects of chronic therapy with perindopril on left ventricular (LV) mass, left atrial size, diastolic function, and plasma level of atrial natriuretic peptide (ANP) in patients with hypertension. METHODS: Twenty four patients who had not been previously taking any antihypertensive medication and without prior history of angina pectoris, myocardial infarction, congestive heart failure, dysrhythmias, valvular heart disease, or systemic illnesses received 4-8 mg/day of perindopril orally. Echocardiographic studies were acquired at baseline and 6 months after the initiation of therapy. RESULTS: Systolic and diastolic blood pressure decreased from 174 +/- 19.7 and 107.5 +/- 7.8 mmHg to 134 +/- 10.6 and 82 +/- 6.7 mmHg, respectively (p < 0.001). Left ventricular mass decreased from 252.4 +/- 8.3 to 205.7 +/- 7.08 g and left atrial volume from 20.4 +/- 5.1 to 17.6 +/- 5.2 ml, respectively (p < 0.001). Transmitral Doppler early and atrial filling velocity ratio (E/A) increased from 0.69 +/- 0.06 to 0.92 +/- 0.05 m/s and plasma ANP level decreased from 71.9 +/- 11.7 to 35.3 +/- 7.8 pg/ml (p < 0.001). Reduction of LV mass correlated positively with a reduction in ANP levels (r = 0.66, p < 0.0005). CONCLUSIONS: Perindopril caused a significant reduction of LV mass, left atrial volume, and plasma ANP levels, as well as improvement in Doppler parameters of LV filling in this group of patients with hypertension.