Left and right ventricular pressures in mice
Transthoracic measurements of left and right ventricular systolic pressures in anesthetized mice, using fiber optics and strain gage manometer techniques
Abelmann, W. H.↗
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Cytoskeletal role in the transition from compensated to decompensated hypertrophy during adult canine left ventricular pressure overloading
Increased microtubule density causes cardiocyte contractile dysfunction in right ventricular (RV) pressure-overload hypertrophy, and these linked phenotypic and contractile abnormalities persist and progress during the transition to failure. Although more severe in cells from failing than hypertrophied RVs, the mechanical defects are normalized in each case by microtubule depolymerization. To define the role of increased microtubule density in left ventricular (LV) pressure-overload hypertrophy and failure, in a given LV we examined ventricular mechanics, sarcomere mechanics, and free tubulin and microtubule levels in control dogs and in dogs with aortic stenosis both with LV hypertrophy alone and with initially compensated hypertrophy that had progressed to LV muscle failure. In comparing initial values with those at study 8 weeks later, dogs with hypertrophy alone had a very substantial increase in LV mass but preservation of a normal ejection fraction and mean systolic wall stress. Dogs with hypertrophy and associated failure had a substantial but lesser increase in LV mass and a reduction in ejection fraction, as well as a marked increase in mean systolic wall stress. Cardiocyte contractile function was equivalent, and unaffected by microtubule depolymerization, in cells from control LVs and those with compensated hypertrophy. In contrast, cardiocyte contractile function in cells from failing LVs was quite depressed but was normalized by microtubule depolymerization. Microtubules were increased only in failing LVs. These contractile and cytoskeletal changes, when assayed longitudinally in a given dog by biopsy, appeared in failing ventricles only when wall stress began to increase and function began to decrease. Thus, the microtubule-based cardiocyte contractile dysfunction characteristic of pressure-hypertrophied myocardium, originally described in the RV, obtains equally in the LV but is shown here to have a specific association with increased wall stress.
Non-NASA Center↗
Metabolic and cardiovascular adaptation, monkey. NASA SMD 3, project 76, experiment 44 conducted at NASA/JSC, 14-25 May 1977
The biomedical results from an experiment on a monkey subjected to space flight conditions are reported. A background history of the development and testing of an experiment system designed to permit measurement of physiological parameters in subhuman primates during continuous, comfortable, couch restraint for periods of up to 30 days is reviewed. Of major importance in the experimental design of the system was the use of a fiberglass pod, which could be sealed and subdivided into upper and lower parts, to monitor and control the physiological responses for various parts of the animal's body. The experiment was conducted within the Spacelab Simulator for a period of 11 days. Data recorded includes: Spacelab Simulator cabin temperature; ventilation rate; pod internal temperature; fraction percent oxygen; fraction percent carbon dioxide; oxygen consumption rate; carbon dioxide production rate; respiratory quotient; intrathoracic temperature; heart rate; mean aortic pressure; mean ventricular pressure; diurnal variation of parameters measured; comparison of mean preflight, flight, and postflight values of the parameters measured; and correlation matrix for the parameters measured.
Pace, N.↗
Chronic mitral regurgitation and Doppler estimation of left ventricular filling pressures in patients with heart failure
Previous studies relating Doppler parameters and pulmonary capillary wedge pressures (PCWP) typically exclude patients with severe mitral regurgitation (MR). We evaluated the effects of varying degrees of chronic MR on the Doppler estimation of PCWP. PCWP and mitral Doppler profiles were obtained in 88 patients (mean age 55 +/- 8 years) with severe left ventricular (LV) dysfunction (mean ejection fraction 23% +/- 5%). Patients were classified by severity of MR. Patients with severe MR had greater left atrial areas, LV end-diastolic volumes, and mean PCWPs and lower ejection fractions (each P <.01). In patients with mild MR, multiple echocardiographic parameters correlated with PCWP; however, with worsening MR, only deceleration time strongly related to PCWP. From stepwise multivariate analysis, deceleration time was the best independent predictor of PCWP overall, and it was the only predictor in patients with moderate or severe MR. Doppler-derived early mitral deceleration time reliably predicts PCWP in patients with severe LV dysfunction irrespective of degree of MR.
NASA Discipline Cardiopulmonary↗
Mitral inertance in humans: critical factor in Doppler estimation of transvalvular pressure gradients
The pressure-velocity relationship across the normal mitral valve is approximated by the Bernoulli equation DeltaP = 1/2 rhoDeltav(2) + M. dv/dt, where DeltaP is the atrioventricular pressure difference, rho is blood density, v is transmitral flow velocity, and M is mitral inertance. Although M is indispensable in assessing transvalvular pressure differences from transmitral flow, this term is poorly understood. We measured intraoperative high-fidelity left atrial and ventricular pressures and simultaneous transmitral flow velocities by using transesophageal echocardiography in 100 beats (8 patients). We computed mean mitral inertance (M) by M = integral((DeltaP)-(1/2 x rho v(2))dt/integral(dv/dt)dt and we assessed the effect of the inertial term on the transmitral pressure-flow relation. ranged from 1.03 to 5.96 g/cm(2) (mean = 3.82 +/- 1.22 g/cm(2)). DeltaP calculated from the simplified Bernoulli equation (DeltaP = 1/2. rhov(2)) lagged behind (44 +/- 11 ms) and underestimated the actual peak pressures (2.3 +/- 1.1 mmHg). correlated with left ventricular systolic pressure (r = -0.68, P < 0.0001) and transmitral pressure gradients (r = 0.65, P < 0.0001). Because mitral inertance causes the velocity to lag significantly behind the actual pressure gradient, it needs to be considered when assessing diastolic filling and the pressure difference across normal mitral valves.
NASA Discipline Cardiopulmonary↗
Effects of 12 days exposure to simulated microgravity on central circulatory hemodynamics in the rhesus monkey
Central circulatory hemodynamic responses were measured before and during the initial 9 days of a 12-day 10 degrees head-down tilt (HDT) in 4 flight-sized juvenile rhesus monkeys who were surgically instrumented with a variety of intrathoracic catheters and blood flow sensors to assess the effects of simulated microgravity on central circulatory hemodynamics. Each subject underwent measurements of aortic and left ventricular pressures, and aortic flow before and during HDT as well as during a passive head-up postural test before and after HDT. Heart rate, stroke volume, cardiac output, and left ventricular end-diastolic pressure were measured, and dP/dt and left ventricular elastance was calculated from hemodynamic measurements. The postural test consisted of 5 min of supine baseline control followed by 5 minutes of 90 degrees upright tilt (HUT). Heart rate, stroke volume, cardiac output, and left ventricular end-diastolic pressure showed no consistent alterations during HDT. Left ventricular elastance was reduced in all animals throughout HDT, indicating that cardiac compliance was increased. HDT did not consistently alter left ventricular +dP/dt, indicating no change in cardiac contractility. Heart rate during the post-HDT HUT postural test was elevated compared to pre-HDT while post-HDT cardiac output was decreased by 52% as a result of a 54% reduction in stroke volume throughout HUT. Results from this study using an instrumented rhesus monkey suggest that exposure to microgravity may increase ventricular compliance without alternating cardiac contractility. Our project supported the notion that an invasively-instrumented animal model should be viable for use in spaceflight cardiovascular experiments to assess potential changes in myocardial function and cardiac compliance.
NASA Discipline Cardiopulmonary↗
Viscoelastic properties of pressure overload hypertrophied myocardium: effect of serine protease treatment
To determine whether and to what extent one component of the extracellular matrix, fibrillar collagen, contributes causally to abnormalities in viscoelasticity, collagen was acutely degraded by activation of endogenous matrix metalloproteinases (MMPs) with the serine protease plasmin. Papillary muscles were isolated from normal cats and cats with right ventricular pressure overload hypertrophy (POH) induced by pulmonary artery banding. Plasmin treatment caused MMP activation, collagen degradation, decreased the elastic stiffness constant, and decreased the viscosity constant in both normal and POH muscles. Thus, whereas many mechanisms may contribute to the abnormalities in myocardial viscoelasticity in the POH myocardium, changes in fibrillar collagen appear to play a predominant role.
NASA Discipline Cardiopulmonary↗
Microtubule depolymerization normalizes in vivo myocardial contractile function in dogs with pressure-overload left ventricular hypertrophy
BACKGROUND: Because initially compensatory myocardial hypertrophy in response to pressure overloading may eventually decompensate to myocardial failure, mechanisms responsible for this transition have long been sought. One such mechanism established in vitro is densification of the cellular microtubule network, which imposes a viscous load that inhibits cardiocyte contraction. METHODS AND RESULTS: In the present study, we extended this in vitro finding to the in vivo level and tested the hypothesis that this cytoskeletal abnormality is important in the in vivo contractile dysfunction that occurs in experimental aortic stenosis in the adult dog. In 8 dogs in which gradual stenosis of the ascending aorta had caused severe left ventricular (LV) pressure overloading (gradient, 152+/-16 mm Hg) with contractile dysfunction, LV function was measured at baseline and 1 hour after the intravenous administration of colchicine. Cardiocytes obtained by biopsy before and after in vivo colchicine administration were examined in tandem. Microtubule depolymerization restored LV contractile function both in vivo and in vitro. CONCLUSIONS: These and additional corroborative data show that increased cardiocyte microtubule network density is an important mechanism for the ventricular contractile dysfunction that develops in large mammals with adult-onset pressure-overload-induced cardiac hypertrophy.
Non-NASA Center↗
Single-channel pressure telemetry unit.
Single channel pressure telemetry unit for chronic implantation into cardiac chambers or major blood vessels in unrestrained animals for measuring ventricular pressure
Datnow, B.↗
Action of acetylstrophanthidin on experimental myocardial infarction.
An experimental animal model with acute myocardial infarction of a size insufficient to produce profound heart failure or shock was used to study the effects of acute infarction on digitalis tolerance and the hemodynamic changes produced by moderate and large doses of acetylstrophanthidin. With acute myocardial infarction, digitalis toxic arrhythmias could be precipitated with significantly lower doses of digitalis than in animals without myocardial infarction. There was no precise correlation between the size of infarction and the toxic dose of glycoside. Coronary artery ligation produced a stable but relatively depressed circulatory state, as evidenced by lowered cardiac output and stroke volume and elevated systemic vascular resistance and left atrial mean pressure. When digitalis was infused, the following significant changes were observed at nontoxic doses: (1) elevation of aortic and left ventricular pressures; (2) further decline in cardiac output; and (3) decreased left atrial mean pressure.
Nola, G. T.↗
Assessment of the time constant of relaxation: insights from simulations and hemodynamic measurements
The objective of this study was to use high-fidelity animal data and numerical simulations to gain more insight into the reliability of the estimated relaxation constant derived from left ventricular pressure decays, assuming a monoexponential model with either a fixed zero or free moving pressure asymptote. Comparison of the experimental data with the results of the simulations demonstrated a trade off between the fixed zero and the free moving asymptote approach. The latter method more closely fits the pressure curves and has the advantage of producing an extra coefficient with potential diagnostic information. On the other hand, this method suffers from larger standard errors on the estimated coefficients. The method with fixed zero asymptote produces values of the time constant of isovolumetric relaxation (tau) within a narrow confidence interval. However, if the pressure curve is actually decaying to a nonzero pressure asymptote, this method results in an inferior fit of the pressure curve and a biased estimation of tau.
NASA Discipline Cardiopulmonary↗
Coronary flow and left ventricular function during environmental stress.
A canine model was used to study the effects of different environmental stresses on the heart and coronary circulation. The heart was surgically instrumented to measure coronary blood flow, left ventricular pressure, and other cardiovascular variables. Coronary flow was recorded by telemetry. Physiologic data were processed and analyzed by analog and digital computers. By these methods the physiologic response to altitude hypoxia, carbon monoxide, hypercapnia, acceleration, exercise, and the interaction of altitude hypoxia and carbon monoxide were described. The effects of some of these stresses on the heart and coronary circulation are discussed.
Erickson, H. H.↗
Effect of varying differentiator frequency response on recorded peak dP/dt
Dogs were used to study the effects of varying the differentiator cutoff frequency on the recorded peak first derivative of left ventricular pressure with respect to time (dP/dt), using high-precision solid-state pressure transducers and recording equipment. In canine hearts with a basic periodicity of 1 to 3 Hz, the differentiator frequency response required to record an accurate peak dP/dt is found to be influenced by the value of peak dP/dt. At peak dP/dt ranging from 1500 to 9000 mm Hg/sec (200 and 1200 kPa/sec), a differentiator cutoff frequency of at least 90 Hz was required to record accurately peak dP/dt.
Barry, W. H.↗
Effect of Actual and Simulated Microgravity on Cardiac Mass and Function in the Rat
The purpose of this study was to test the hypothesis that exposure to actual or simulated microgravity induces cardiac atrophy in male Sprague-Dawley rats. For the microgravity study, rats were subdivided into four groups: Preflight (PF, n = 12); Flight (FL, n = 7); Flight Cage Simulation (SIM, n = 6), and Vivarium Control (VIV, n = 7). Animals in the FL group were exposed to 7 days of microgravity during the Spacelab 3 mission. Animals in the simulated microgravity study were subdivided into three groups: Control (CON, n = 20); 7 day hindlimb unloaded (7HU, n = 10); and 28 day unloaded (28HU, n = 19). In a subset of CON (n = 7) and 28HU (n = 6) rats, a catheter was advanced into the left ventricle to measure the rate of rise in ventricular pressure (+dP/dt) during standing as an estimate of cardiac contractility. After completion of their respective treatments, hearts were removed and weighed. Animals in the PF group were sacrificed 24 hr prior to launch while the FL group was sacrificed 11- 17 hr after landing. The SM and VIV groups were sacrificed 48 and 96 hr after the FL group, respectively. Heart mass was unchanged in adult animals exposed to 7 days of actual microgravity (PF 1.33 +/- .03 g; FL 1.32 +/- 0.02 g; SIM 1.28 +/- 0.04 g; VIV 1.35 +/- 0.04 g). Similarly, heart mass was unaltered with hin~limb unloading (CON 1.40 +/- 0.04 g; 7HU 1.35 +/- 0.06 g; 28HU 1.42 +/- 0.03 g). Hindlimb unloading also had no effect on myocardial contractility (CON 8055 +/- 385 mmHg/sec; 28HU 8545 +/- 755 mmHg/sec). These data suggest that cardiac atrophy does not occur following short-term exposure to microgravity, and that neither short- nor long-term simulated microgravity alter cardiac mass or function.
Ray, Chester H.↗
Effect of short-term microgravity and long-term hindlimb unloading on rat cardiac mass and function
The purpose of this study was to test the hypothesis that exposure to short-term microgravity or long-term hindlimb unloading induces cardiac atrophy in male Sprague-Dawley rats. For the microgravity study, rats were subdivided into four groups: preflight (PF, n = 12); flight (Fl, n = 7); flight cage simulation (Sim, n = 6), and vivarium control (Viv, n = 7). Animals in the Fl group were exposed to 7 days of microgravity during the Spacelab 3 mission. Animals in the hindlimb-unloading study were subdivided into three groups: control (Con, n = 20), 7-day hindlimb-unloaded (7HU, n = 10), and 28-day hindlimb-unloaded (28HU, n = 19). Heart mass was unchanged in adult animals exposed to 7 days of actual microgravity (PF 1.33 +/- 0.03 g; Fl 1.32 +/- 0.02 g; Sim 1.28 +/- 0.04 g; Viv 1.35 +/- 0.04 g). Similarly, heart mass was unaltered with hindlimb unloading (Con 1.40 +/- 0.04 g; 7HU 1.35 +/- 0.06 g; 28HU 1.42 +/- 0.03 g). Hindlimb unloading also had no effect on the peak rate of rise in left ventricular pressure, an estimate of myocardial contractility (Con 8,055 +/- 385 mmHg/s; 28HU 8,545 +/- 755 mmHg/s). These data suggest that cardiac atrophy does not occur after short-term exposure to microgravity and that neither short- nor long-term simulated microgravity alters cardiac mass or function.
manned↗
Telemetry of left ventricular diameter and pressure measurements from unrestrained animals
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Patrick, T. A.↗
Effect of decreased gravity on circulation in the rat
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.
Popovic, Vojin P.↗
Body position does not affect the hemodynamic response to venous air embolism in dogs
Current therapy for massive venous air embolism (VAE) includes the use of the left lateral recumbent (LLR) position. This recommendation is based on animal studies, conducted 50 years ago, which looked primarily at survival. Little is known, however, about the concomitant hemodynamic response after VAE in various body positions. The purpose of this study was to investigate the hemodynamic and cardiovascular changes in various body positions after VAE. Twenty-two mechanically ventilated supine mongrel dogs received a venous air infusion of 2.5 mL/kg at a rate of 5 mL/s. One minute after the infusion, 100% oxygen ventilation was commenced and the body position of the dogs was changed to either the LLR (n = 6), the LLR with the head 10 deg down (LLR-10 deg; n = 6) or the right lateral recumbent (RLR; n = 5) position. Five dogs were maintained in the supine position (SUP; n = 5). One dog died in every group except in the SUP group, where all the dogs recovered. There were no significant differences among the various body positions in terms of heart rate, mean arterial pressure, pulmonary artery pressure, central venous pressure, left ventricular end-diastolic pressure, or cardiac output. The acute hemodynamic changes occurring during the first 5-15 min after VAE recovered to 80% of control within 60 min. Our data suggest that body repositioning does not influence the cardiovascular response to VAE. Specifically, our data do not support the recommendation of repositioning into the LLR position for the treatment of VAE.
Mehlhorn, Uwe↗