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Arterial pressure compared with ambient bodily-fluid pressure. Implanted apparatus, capable of measuring blood pressure of patient, includes differential-pressure transducer connected to pressure sensor positioned in major artery. Electrical signal is function of differential pressure between blood-pressure sensor and reference-pressure sensor transmitted through skin of patient to recorder or indicator.
Device measures time-averaged component of absolute blood pressure in artery. Includes compliant cuff around artery and external monitoring unit. Ceramic construction in monitoring unit suppresses ebb and flow of pressure-transmitting fluid in sensor chamber. Transducer measures only static component of blood pressure.
The applications to medicine of various results from space exploration are examined. Improvements have been made in the management of cardiovascular disease, in particular the use of the ultrasonic scanner to image arteries in three dimensions, the use of excimer lasers to disrupt arterial plaques in coronary blood vessels, and the use of advanced electrodes for cardiac monitoring. A bone stiffness analyzer has helped to diagnose osteoporosis and aid in its treatment. An automated light microscope system is used for chromosome analysis, and an X-ray image intensifier called Lixiscope is used in emergency medical care. An advanced portable defibrillator has been developed for the heart, and an insulin delivery system has been derived from space microminiaturization techniques.
Doppler technique was used to measure the pulmonary vascular pressure gradients in dogs that received venous air emboli (VAE) at the rate of 0.35 ml/kg per min, at which the spillover of bubbles into the systemic arteries occur. It was found that, in 60 percent of dogs, venous bubbles spilled over into the arterial circulation at the pulmonary vascular pressure gradient of about 34.7 mm Hg. When the pulmonary vascular pressure gradient was raised to about 52 mm Hg, the spillover of venous bubbles occurred 100 percent of time. It is concluded that venous bubbles can cross the lungs of anesthetized dogs when the driving pressures are sufficient to overcome the normal filtering function.
An accepted method for measuring the responsiveness of the carotid-cardiac baroreflex to arterial pressure changes is to artificially stimulate the baroreceptors in the neck. This is accomplished by using a pressurized neck cuff which constricts and distends the carotid artery and subsequently stimulates the baroreceptors. Nine physiological responses to this type of stimulation are quantified and used as indicators of the baroreflex. Thirty male humans between the ages 27 and 46 underwent the carotid-cardiac baroreflex test. The data for the nine response parameters were analyzed by principle component factor analysis. The results of this analysis indicated that 93 percent of the total variance across all nine parameters could be explained in four dimensions. Examination of the factor loadings following an orthogonal rotation of the principle components indicated four well defined dimensions. The first two dimensions reflected location points for R-R interval and carotid distending pressure respectively. The third dimension was composed of measures reflecting the gain of the reflex. The fourth dimension was the ratio of the resting R-R interval to R-R interval during simulated hypertension. The data suggests that the analysis of all nine baroreflex parameters is redundant.
Resting plasma volumes, and arterial and central venous pressures (CVP) were measured in 16 men before and after exercise training to determine if training-induced hypervolemia could be explained by a change in total vascular capacitance. In addition, resting levels of plasma vasopressin (AVP), atrial natriuretic peptide (ANP), aldosterone (ALD), and norepinephrine (NE) were measured before and after training. The same measurements of vacular volume, pressures, and plasma hormones were measured in 8 subjects who did not undergo exercise and acted as controls. The exercise training program consisted of 10 weeks of controlled cycle exercise for 30 min/d, 4 d/wk at 75 to 80 percent of maximal oxygen uptake (VO2max). A training effect was verified by a 20 percent increase in VO2max, a resting bradycardia, and a 370 ml (9 percent) increase in blood volume. Mean arterial blood pressure was unaltered by exercise training, but resting CVP increased. The percent change in blood volume from before to after training was linearly related to the percent change in CVP. As a consequence of elevations in both blood volume and CVP, the volume-to-pressure ratio was essentially unchanged following exercise training. Plasma AVP, ANP, ALD, and NE were unaltered. Results indicate that elevated CVP is a consequence of training-induced hypervolemia without alteration in total effective venous capacitance. This may represent a resetting of the pressure-volume stimulus-response relation for regulation of blood volume.
Six male subjects were exposed on two separate occasions to simulated microgravity with 28 deg head-down tilt (HD) for 1 h with baseline followed by recovery at + 17 deg head-up. Pulmonary ventilation, gas exchange, spirometry, and central and cerebral blood flow characteristics were compared while breathing ambient air and reduced F(I)O2 equivalent to 14,828 ft. With hypoxia (HY), the increased tidal volume served to attenuate the drop in arterial saturation by reducing deadspace ventilation. Arterial and mixed venous PO2, values, estimated from peripheral venous samples and cardiac output (CO), were both maintained during HD in HY. Mixed venous PO2 was elevated by an increase in CO associated with a reduction in systemic resistance. Changes in spirometric indices during HD were not accentuated by HY, making the presence of interstitial edema unlikely. Cerebral flow and resistance showed minor reductions with HD. Tissue oxygenation and cardiopulmonary function were not notably effected by HD during HY, but a combination of these two stressors may predispose subjects to subsequent orthostatic intolerance during initial recovery.
To explore the mechanism for facial puffiness, headache, and nasal congestion associated with microgravity and cephalad fluid shifts, the postural responses of the cutaneous microcirculation (CMC) in the forehead and dorsum of the foot of eight healthy men were studied by changing body position on a tilt table and measuring blood flows with a laser Doppler flowmeter. Increasing arterial pressure in the feet by moving from a -6-deg head-down tilt to a 60-deg head-up posture decreased foot CMC by 46.5 + or - 12.0 percent. Raising arterial pressure in the head increased forehead CMC by 25.5 + or - 0.7 percent (p less than 0.05). To investigate the possibility that these opposite responses could be modified by simulated microgravity, tilt test were repeated after 7 d of -6-deg head-down-tilt bed rest. The responses were not significantly different from those recorded before bed rest. Therefore, CMC in the feet is well regulated to prevent edema when shifting to an upright position, whereas there is less regulation in the head CMC.
Two critical aspects of the Applications Engineering Program were especially successful: commercializing products of Application Projects; and leveraging NASA funds for projects by developing cofunding from industry and other agencies. Results are presented in the following areas: the excimer laser was commercialized for clearing plaque in the arteries of patients with coronary artery disease; the ultrasound burn depth analysis technology is to be licensed and commercialized; a phased commercialization plan was submitted to NASA for the intracranial pressure monitor; the Flexible Agricultural Robotics Manipulator System (FARMS) is making progress in the development of sensors and a customized end effector for a roboticized greenhouse operation; a dual robot are controller was improved; a multisensor urodynamic pressure catherer was successful in clinical tests; commercial applications were examined for diamond like carbon coatings; further work was done on the multichannel flow cytometer; progress on the liquid airpack for fire fighters; a wind energy conversion device was tested in a low speed wind tunnel; and the Space Shuttle Thermal Protection System was reviewed.
The effect of a spaceflight on the vagally mediated baroreceptor-cardiac reflex responses of humans were investigated by measuring the responses (provoked by neck pressure changes) in supine position and the heart rate and blood pressure in the supine and standing positions in 16 astronauts before and after 4- to 5-day long Space Shuttle missions. The results showed that exposures to spaceflight resulted in reduced baseline levels of the vagal-cardiac outflow and the vagally mediated responses to changes of the arterial baroreceptor input and that these changes contribute to postflight reductions of astronauts' ability to maintain standing arterial pressures.
Two experiments aimed at examining the versatility of the whole body suspension (WBS) system as a ground-based model for cardiovascular effects of microgravity are described. The first experiment studied heart rate and arterial pressure responses in rats during a 7-day period of head-down tilt (HDT) or nonhead-down tilt (NHDT) and after removal from whole body suspension (WBS). Mean arterial (MAP), systolic, and diastolic pressures increased about 20 percent in HDT rats on the fist day, heart rates were elevated about 10 percent. During postsuspension most cardiovascular parameters returned to presuspension levels. The second experiment evaluated responses to rapid head-up tilt in HDT and NHDT rats. It was observed that, while pulse pressures remained unchanged, MAP, systolic and diastolic pressures, and HR were elevated in HDT and NHDT rats during head-up tilt after one day of suspension. The WBS rats are considered to be useful as a model to better understand responses of rats exposed to microgravity.
The SHARE II (Space Station Advanced Radiator Experiment II) Mid-deck Experiment was flown on board the Space Shuttle (STS-37) from April 5 to 12, 1991. The purpose of the experiment was to demonstrate the operation of several design changes proposed for the NASA/Grumman SHARE II heat pipe as a result of the lessons learned during the first SHARE flight (STS-29) in March 1989. Two test articles flew during the mission. The first, the Bubble Management Test Article, was a Plexiglas model of the monogroove heat pipe. This test article was primarily used to evaluate the performance of two 0-g bubble management devices; the redesigned evaporator screen artery and the condenser bubble trap. The second, the Blended Manifold Priming Test Article, also constructed of Plexiglas, was used to demonstrate passive self-priming of a heat pipe blended manifold connecting three evaporator legs to a single condenser leg. Both test articles used a 50/50 mixture of ethanol and water as the working fluid. Overall, the experiment was highly successful, with all the major test objectives fulfilled, including blended manifold priming, condenser bubble trap operation, screen artery bubble ingestion, and elimination of hydraulic diameter mismatch.
This study investigates cerebral blood flow (CBF) velocity in humans before, during, and after 24 h of 6 deg head-down tilt (HDT), which is a currently accepted experimental model to simulate microgravity. CBF velocity was measured by use of the transcranial Doppler technique in the right middle cerebral artery of eight healthy male subjects. Mean CBF velocity increased from the pre-HDT upright seated baseline value of 55.5 +/- 3.7 (SE) cm/s to 61.5 +/- 3.3 cm/s at 0.5 h of HDT, reached a peak value of 63.2 +/- 4.1 cm/s at 3 h of HDT, and remained significantly above the pre-HDT baseline for over 6 h of HDT. During upright seated recovery, mean CBF velocity decreased to 87 percent of the pre-HDT baseline value. Mean CBF velocity correlated well with calculated intracranial arterial pressure (IAP). As analyzed by linear regression, mean CBF velocity = 29.6 + 0.32IAP. These results suggest that HDT increases CBF velocity by increasing IAP during several hours after the onset of microgravity. Importantly, the decrease in CBF velocity after HDT may be responsible, in part, for the increased risk of syncope observed in subjects after prolonged bed rest and also in astronauts returning to Earth.
Endocrine regulation of fluids and electrolytes during seven days of 6 deg head down bed rest (HDBR) was compared in male (n = 8) and, for the first time, female (n = 8) volunteers. The subjects' responses to quiet standing for 2 hr before and after HDBR were also tested. In both sexes, diuresis and natriuresis were evident during the first 2-3 days of HDBR, resulting in a marked increase in the urinary Na/K ratio and significant Na retention on reambulation. After the first day of HDBR, plasma renin activity (PRA) was increased relative to aldosterone, plasma volume was decreased, and the renal response to aldosterone appeared to be appropriate. Circulating levels of arginine vasopressin (AVP), cortisol, and ACTH were unchanged during HDBR. Plasma testosterone decreased slightly on day 2 of HDBR in males. The ratio of AM ACTH to cortisol was lower in females than in males because ACTH was lower in females. Urinary cortisol increased and remained elevated throughout the HDBR in males only. There were no gender differences in the responses to 7 day HDBR, except those in the pituitary-adrenal system; those differences appeared unrelated to the postural change. The provocative cardiovascular test of quiet standing before and after bed rest revealed both sex differences and effects of HDBR. There were significant sex differences in cardiovascular responses to standing, before and after HDBR. Females had greater PRA and aldosterone responses to standing before bedrest and larger aldosterone responses to standing after HDBR than males. Cardiovascular responses to standing before and after bedrest differed markedly: arterial pressure and heart rates increased with standing before HDBR, by contrast, arterial pressure decreased, with greater increases in heart rates after HDBR. In both sexes, all hormonal responses to standing were greater after HDBR. The results show clearly that similar responses to standing as well as to HDBR occur in both sexes, but that females exhibit greater PRA and aldosterone responses than males.
It has been reported that hypokinesia and bed rest induce cardiovascular changes similar to those observed in space flights. Using an animal model that was developed in our laboratory and that was extensively studied and characterized in our laboratory and other laboratories in this country and abroad, we have studied circulatory mechanisms that occur during exposure to hypokinesia (with or without negative tilt) as well as during readaptation to control conditions (free activity). We believe that this study contributes to better understanding of mammalian circulatory mechanisms that operate under 1-g force and will serve to provide control data to be compared with cardiovascular data obtained in conditions of a Space lab. Because survey and anesthesia drastically decrease cardiac output and other circulatory parameters in rats, only unanesthetized rats were used in experiments. Aorta and right atrium of the animals were permanently cannulated fifteen to twenty days before experiments. Arterial and right ventricular blood pressures, cardiac output, cerebral and other regional blood flow, ECG, other cardiovascular parameters, and oxygen consumption were measured with techniques routinely used in our laboratory. Specifically, we undertook the following investigations during the period of three years: (1) A study of circulatory changes (right ventricular pressure, arterial blood pressure, heart rate, cardiac output) during exposure of rats to hypokinetic conditions. Used the head down tilted Holton-Musacchia system in order to compare the results with the results already obtained on unrestrained rats, (2) Humoral changes were investigated in animals exposed to hypokinesia; also, lymphocyte and neutrophil levels in hypokinetic animals (with or without tilt) were determined to ascertain the level of induced stress and possible changes observed in weightless animals, and (3) circulating blood volume was determined during and after hypokinesia.
Changes in autonomic outflow to peripheral organs during the development of bedrest induced orthostatic intolerance have not been determined. Recent studies have indicated that spectral analysis provides an indirect assessment of these changes. Eight male subjects were studied before and after 22 hours of 6 degree head down bedrest plus Lasix (40 mg. P.P.). Cardiovascular spectra (using an autoregressive technique) were determined for heart rate (HR, ECG), arterial pressure (AP, Finapres), radial artery flow (RF, Hokansen) and respiration rate (RR, BoMed). Spectra were obtained from 2.5 minute segments during control, lower body negative pressure (minus 10, 20, 30, 40, 50 mmHg) and recovery. Bedrest increased HR spectra power in the low frequency (.001 to .041 Hz) range, increased RF power in the low and mid (.04 to .18 Hz) range and increased AP power in the high (.18 to .50 Hz) frequency range. Increasing levels of lower body negative pressure decreased HR power and increased RF power in the high frequency range and decreased AP power in the low frequency range. Since spectral power of HR in the high frequency range has been shown to indicate parasympathetically mediated regulation and power in the low and mid frequency ranges indicates a sympathetic / parasympathetic mixture, then both bedrest and lower body negative pressure appeared to shift sympathetic / parasympathetic balance toward sympathetic regulation of HR. The interpretation of the spectral content of AP and RF with respect to their autonomic origins remains unclear.
To determine the effects of simulated microgravity on aortic baroreflex control of heart rate, we exposed seven male subjects to 15 days of bed rest in the 6 deg head-down position. The sensitivity of the aortic-cardiac baroreflex was determined during a steady-state phenylephrine-induced increase in mean arterial pressure combined with lower body negative pressure to counteract central venous pressure increases and neck pressure to offset the increased carotid sinus transmural pressure. The aortic-cardiac baroreflex gain was assessed by determining the ratio of the change in heart rate to the change in mean arterial pressure between baseline conditions and aortic baroreceptor-isolated conditions (i.e., phenylephrine + lower body negative pressure + neck pressure stage). Fifteen days of head-down tilt increased the gain of the aortic-cardiac baroreflex. Reductions in blood volume and/or maximal aerobic capacity may represent the underlying mechanism(s) responsible for increased aortic baroreflex responsiveness after exposure to a ground-based analogue of microgravity.
To determine whether extended exposure to a simulation of microgravity alters thermoregulatory reflex control of skin blood flow, six adult males were exposed to 15 days of 6 deg head-down tilt (HDT). On an ambulatory control day before HDT exposure and on HDT day 15 the core temperature of each subject was increased by 0.5 - 1.0 C by whole body heating with a water-perfused suit. Mean skin temperature, oral temperature (T (sub or)), mean arterial pressure, and forearm blood flow were measured throughout the protocol. Forearm vascular conductance (FVC) was calculated from the ratio of forearm blood flow to mean arterial pressure. After HDT exposure, the T(sub or) threshold at which reflex thermally induced increases in FVC began was elevated, whereas the slope of the T(sub or)-FVC relationship after this threshold was reduced. Moreover, normothermic FVC and FVC at the highest common T(sub or) between pre- and post-HDT trials were reduced after HDT. These data suggest that HDT exposure reduces thermoregulatory responses to heat stress. The mechanisms resulting in such an impaired thermoregulatory response are unknown but are likely related to the relative dehydration that accompanies this exposure.