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At least 145 records · Page 8Linked to original sources

The effect of chronic cardiac volume overload on regional myocardial blood flow in the dog.

1. Regional myocardial blood flow was studied in the anaesthetized, open-chest dog with a large chronic aorto-caval fistula, using carbonized microspheres of 7-10 mum diameter. The results from fourteen dogs with fistulae of 4-84 days duration were compared to those from nine normal animals. 2. Myocardial blood flow to all areas of both ventricles was increased to between 180 and 250% of the normal despite lower aortic diastolic (coronary diastolic) pressure. Myocardial blood flow in the right ventricle was lower than in the left in both groups of dogs although the increase above normal in dogs with fistulae was relatively greater in the right ventricle. Increased myocardial blood flow is attributed to coronary autoregulation resulting from increased myocardial oxygen consumption due to increase in myocardial tension development. 3. Although absolute blood flow to the inner left ventricular wall was markedly increased in all dogs with fistulae, in those with aortic diastolic pressure below 55 mmHg the ratio of flow in the inner to that in the outer free left ventricular wall was significantly less than in those with aortic diastolic pressure above 55 mmHg (P less than 0 with 02). Low aortic diastolic pressurere and diastolic coronary perfusion pressure probably resulted in relative ischaemia of the inner left ventricular wall.

Animals↗

Mitogen-activated protein kinases (p38 and c-Jun NH2-terminal kinase) are differentially regulated during cardiac volume and pressure overload hypertrophy.

Chronic pressure overload (PO) and volume overload (VO) result in morphologically and functionally distinct forms of myocardial hypertrophy. However, the molecular mechanism initiating these two types of hypertrophy is not yet understood. Data obtained from different cell types have indicated that the mitogen-activated protein kinases (MAPKs) comprising c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 play an important role in transmitting signals of stress stimuli to elicit the cellular response. We tested the hypothesis that early induction of MAPKs differs in two types of overload on the heart and associates with distinct expression of hypertrophic marker genes, namely ANF, alpha-myosin heavy chain (alpha-MHC), and beta-MHC. In rats, VO was induced by aortocaval shunt and PO by constriction of the abdominal aorta. The PO animals were further divided into two groups depending on the severity of the constriction, mild (MPO) and severe pressure overload (SPO), having 35 and 85% aortic constriction, respectively. Early changes in MAPK activity (2-120 min and 1 to 2 d) were analyzed by the in vitro kinase assay using kinase-specific antibodies for p38, JNK, and ERK2. The change in expression of hypertrophy marker genes was examined by Northern blot analysis. In VO hypertrophy, the activity of p38 was markedly increased (10-fold), without changing the activity of ERK and JNK. However, during PO hypertrophy, the activity of JNK was significantly increased (two- to sixfold) and depended on the severity of the load. The activity of p38 was not changed in MPO hypertrophy, whereas it was slightly elevated (50%) in hearts with SPO. Similarly, ERK activity was not changed in hearts with MPO, but a transient rise in activity was observed in hearts with SPO. The expression of ANF and beta-MHC genes was elevated in both PO and VO hypertrophy; however, this change was much greater in hearts subjected to PO than VO hypertrophy. Alpha-MHC expression was downregulated in PO but remained unchanged in VO hypertrophy hearts. Thus, these results demonstrate differential activation of MAPKs in two types of cardiac hypertrophy and this, in part, may contribute to differential expression of cardiac muscle gene expression, giving rise to unique cardiac phenotype associated with different hemodynamic overloads.

Animals↗

Comparison of the angiotensin II type 1-receptor antagonist YM358 and the angiotensin-converting enzyme inhibitor enalapril in rats with cardiac volume overload.

We evaluated the effects of chronic oral administration of an angiotensin II type 1 (AT1)-receptor antagonist YM358 and an angiotensin converting enzyme inhibitor enalapril on hemodynamics and cardiac hypertrophy in rats with volume overload-induced heart failure. We assessed changes of cardiac hemodynamics and cardiac hypertrophy at 2 and 4 weeks after administration of YM358 (3, 30 mg/kg per day) or enalapril (30 mg/kg per day) in abdominal aortocaval shunt rats. YM358 (30 mg/kg) attenuated increases of left ventricle (LV)/body weight (BW), left atrium (LA)/BW, right ventricle (RV)/BW and heart/BW ratios, but did not affect cardiac hemodynamics in shunt rats. Enalapril also reduced the increased LV/BW and heart/BW ratios together with significant reductions of systolic blood pressure, left ventricular systolic pressure and the first derivative of left ventricular pressure. These data suggest that the effects on attenuation of the development of cardiac hypertrophy are not different for YM358 and enalapril, although the effects on cardiac hemodynamics are different for the same dosages. The attenuating action of YM358 on cardiac hypertrophy was independent of the action on hemodynamics and indicated the direct action of the AT1 receptor on the heart.

Angiotensin Receptor Antagonists↗

[Is brain blood supply affected by changes in cardiac volume? Measurements of brain blood supply in healthy subjects during volume overload and in patients with artificial pacemaker by changing the pacing rate].

A constant cerebral blood flow (CBF) in the presence of systemic blood pressure changes and cardiac output (CO) alterations during physiological conditions are postulated by the mechanism of cerebral autoregulation. The aim of the present study is the analysis of CBF in pacemaker (PM) patients with unspecific neurological symptoms. CBF was measured in 9 controls and 23 pacemaker patients with 133xenon, CO using Doppler echocardiography or impedance cardiography. Mean and individual CBF in controls remained unchanged when a CO increase of 28% induced by volume overload was observed. In PM patients a mean CO increase of 38% induced by an increase of basic pacing rate caused different effects of CBF. CBF increased or decreased by about 10% or remained constant. In summary, the data suggest an impairment of cerebrovascular function in those patients with concomittant CBF changes due to CO alterations (15/23 approximately equal to 65%). Thus, the analysis of brain perfusion in PM patients with unspecific neurological symptoms is possibly a new diagnostic feature in the future. It can be discussed whether or not indication and optimizing of pacemaker therapy has to be additionally analyzed by determination of endorgan perfusion.

Adult↗

Angiocardiographic evaluation of ventricular septal defect--pre- and post-operative cardiac volume characteristics.

The characteristics of the left and the right heart volume in isolated ventricular septal defect were investigated in 62 patients before surgery and in 17 after corrective surgery, which was undergone at ages ranging from 0.5 to 13. Postoperative cardiac catheterization was performed one to two months after surgery. Preoperatively, the right atrial maximal volume increased in accordance with the pulmonary to systemic pressure ratio, and the left ventricular end-diastolic volume, the left atrial maximal volume and the right ventricular end-diastolic volume increased in accordance with the degree of the left-to-right shunt. These volumes decreased considerably after surgery, although they still remained above normal. The left ventricular mass also increased in accordance with the degree of the left-to-right shunt preoperatively and did not decrease postoperatively. The left and the right ventricular ejection fractions were close to or within normal limits preoperatively and remained so after surgery. On the basis of our results and the findings previously published in the literature, factors which may influence the postoperative cardiac function in ventricular septal defects were discussed.

Adolescent↗

An investigation of the estimation of ejection fractions and cardiac volumes by a quantitative gated SPECT software package in simulated gated SPECT images.

BACKGROUND: The purpose of this investigation was to determine the accuracy of the estimation of ejection fractions (EFs) and left ventricular volumes from a commercially available software package (Quantitative Gated SPECT [QGS]) as a function of different true EFs, count level in the acquisitions, severity and location of perfusion defects, increasing hepatic activity, and modified wall motion. METHODS AND RESULTS: The dynamic mathematic cardiac-torso digital phantom was used to create three-dimensional source and attenuation maps representing the distribution of a technetium-99m-labeled cardiac perfusion agent in the chest. Three hearts with varying end-systolic volumes were used to investigate different EFs. Perfusion defects were created as localized uptake within selected portions of the cardiac walls, scaled to the desired fraction of the normal wall uptake, and subtracted from the normal distribution. The hepatic uptake was increased up to five times of the normal heart uptake to investigate the influence of a "hot" liver. Alteration of lateral wall motion was also investigated. A three-dimensional projector that included the influence of distance-dependent spatial resolution and nonuniform attenuation was then used to create projection images. The projections were scaled to the desired acquisition count level, and Poisson noise was added. Automatic determination of EF slightly overestimated the true EF for normal count levels by 3% to 7% of the true EF and underestimated the true EF by up to 9% for very low count levels for 180-degree reconstructions. The accuracy for determining the volumes was not as high as for the EFs (an average error of 12% was observed). The calculated EFs were relatively accurate for perfusion defects of 50% or less. When perfusion defects exceeded 50%, extracardiac counts were included in the heart contours, causing larger underestimations of EF. With removal of the extracardiac counts, the EFs increased. With a hepatic uptake of two or more times the heart uptake, no meaningful EF could be obtained. Either drawing a single region of interest for every slice or use of the manual mode with constrain option could remarkably improve the estimation. The accuracy of the calculation of EF and volumes for the heart with stationary wall was fairly high but decreased significantly when coupled with perfusion defects. CONCLUSION: It is concluded that the QGS program evaluates the functional parameter of EF accurately. The biggest limitations occurred in determining the appropriate cardiac contour if areas with very high extracardiac counts were present in the heart slices, and when a greater than 50% decrease occurred in uptake for perfusion defects.

Cardiac Volume↗

Real-time, volumetric echocardiography: usefulness of volumetric scanning for the assessment of cardiac volume and function.

BACKGROUND: A novel imaging system has been introduced which uses a dedicated two-dimensional echo probe for rapid beam forming to scan a pyramidal volume in real time. Real-time volumetric echocardiography has the potential to determine accurate cardiovascular anatomy, volume and function in the beating heart without reconstructions. The results of animal and human studies using volumetric echocardiography are evaluated for the potential for clinical applications. IMAGING METHODOLOGY: A new type of ultrasound imaging, high-speed volumetric scanning based on phased array principles permits real-time three-dimensional, volumetric echocardiography (real-time 3-DE). The system requires no off-line reconstruction techniques, thus enabling dynamic three-dimensional visualization and quantification of the heart in real time using a transthoracic approach. Real-time 3-DE uses a 2-D matrix phased array transducer. Image formation employs 16:1 parallel processing to scan a pyramidal volume composed of multiple steering directions in the azimuth dimension and in the elevation dimension. The finished transducer is mounted in a hand-held case with a circular aperture of 16 mm diameter. The array consists of approximately 1,600 elements, operating at 2.5 MHz. Real-time 3-DE permits simultaneous, multiple plane display of two sector arcs (B-scans) and C-scan (parallel to the transducer face or inclined) on a single monitor, conveying the three-dimensional nature of the ultrasound data. This system also allows these planes to be angled for extra diagnostic flexibility. The motion of all the structures during the cardiac cycle can be evaluated in dynamic mode. METHODS: Real-time 3-DE was assessed for accuracy of volume measurement by measuring the volume of balloons of different size and shape, and the hearts of 15 closed chest dogs with myocardial contrast enhancement, and compared to the volumes measured by left ventricular angiography in the dogs. Real-time 3-DE was used to evaluate the endocardial border determination of the entire left ventricle by injecting contrast agent in 12 patients. The endocardial border determination of each segment was scored, and the endocardial border score index calculated. Both real-time 3-D images and cine magnetic resonance imaging (MRI) were performed in 16 patients to assess the accuracy of volume measurement of the left ventricle in humans. The endocardial border of the left ventricle was manually traced, and the volumes calculated by Simpson's rule. RESULTS: The volumes measured by real-time 3-DE correlated well with the true volumes for different sizes of balloon and for asymmetric balloons. The end-diastolic volume and end-systolic volume linear correlation of real-time 3-DE versus angiography measurements using manual tracing in vivo also gave a good correlation (r = 0.97, p < 0.001; r = 0.92, p < 0.01). Fifty-eight of 192 segments were rated as good at baseline and 143 rated as good after Levovist injection. Endocardial border determination was improved by Levovist injection in 100 of 137 segments (74.6%). The endocardial border score index was significantly higher after Levovist administration than at baseline (p < 0.003). The end-diastolic volume and end-systolic volume of the left ventricle measured by real-time 3-DE in humans correlated well with those measured by MRI (end-diastolic volume: r = 0.97, p < 0.001; end-systolic volume: r = 0.96, p < 0.001). CONCLUSIONS: Transthoracic real-time, volumetric echocardiography opens a new and exciting field of echocardiography. The results of these studies demonstrate that this system can accurately measure the ventricular volume and function without use of geometric assumptions. This volumetric mode or V-mode scanning is a new imaging modality that provides a practical methodology to investigate important clinical and research questions.

Animals↗

Pulmonary tissue volume, cardiac output, and diffusing capacity in sustained microgravity.

In microgravity (microG) humans have marked changes in body fluids, with a combination of an overall fluid loss and a redistribution of fluids in the cranial direction. We investigated whether interstitial pulmonary edema develops as a result of a headward fluid shift or whether pulmonary tissue fluid volume is reduced as a result of the overall loss of body fluid. We measured pulmonary tissue volume (Vti), capillary blood flow, and diffusing capacity in four subjects before, during, and after 10 days of exposure to microG during spaceflight. Measurements were made by rebreathing a gas mixture containing small amounts of acetylene, carbon monoxide, and argon. Measurements made early in flight in two subjects showed no change in Vti despite large increases in stroke volume (40%) and diffusing capacity (13%) consistent with increased pulmonary capillary blood volume. Late in-flight measurements in four subjects showed a 25% reduction in Vti compared with preflight controls (P < 0.001). There was a concomittant reduction in stroke volume, to the extent that it was no longer significantly different from preflight control. Diffusing capacity remained elevated (11%; P < 0.05) late in flight. These findings suggest that, despite increased pulmonary perfusion and pulmonary capillary blood volume, interstitial pulmonary edema does not result from exposure to microG.

Blood Gas Analysis↗

Determination of left ventricular cardiac volume by simultaneous radionuclide angiography and measurement of oxygen consumption at rest and during maximal exercise: a comparison of two non-invasive isotopic procedures.

The investigation of left ventricular contractile reserve usually requires the determination of left ventricular volume, but its measurement with radionuclide angiography is difficult. The aim of this study was to determine left ventricular volume directly during exercise by the simultaneous measurement of peak exercise left ventricular ejection fraction (LVEF) and oxygen consumption (VO2max) and to compare the results with another geometric method. In the absence of lung disease, the systemic arteriovenous oxygen difference (DAVmax) during maximal exercise converges to 0.13-0.14 ml O2 per ml blood. The measurement of VO2max allows maximal cardiac output (COmax) to be calculated as VO2max = COmax. DAVmax. By simultaneously determining LVEFex, exercise end-diastolic volume (EDVex) can then be expressed as a linear function of VO2max, maximal heart rate (HRmax), DAVmax and LVEFex. Then, the relationship between end-diastolic counts and true volume can be derived at rest. The two methods were closely correlated (r = 0.91, P < 0.001), despite the geometric method being less accurate when applied to low counting statistic acquisitions. We conclude that rest and exercise left ventricular volume can be determined non-invasively by the simultaneous measurement of VO2max and LVEFex. Furthermore, this method provides additional prognostic information which is clinically relevant in the staging of patients with heart failure.

Adult↗

Tidal volume, cardiac output and functional residual capacity determine end-tidal CO2 transient during standing up in humans.

In man assuming the upright position, end-tidal P(CO(2)) (P(ETCO(2))) decreases. With the rising interest in cerebral autoregulation during posture change, which is known to be affected by P(ETCO(2)), we sought to determine the factors leading to hypocapnia during standing up from the supine position. To study the contribution of an increase in tidal volume (V(T)) and breathing frequency, a decrease in stroke volume (SV), a ventilation-perfusion (V/Q) gradient and an increase in functional residual capacity (FRC) to hypocapnia in the standing position, we developed a mathematical model of the lung to follow breath-to-breath variations in P(ETCO(2)). A gravity-induced apical-to-basal V/Q gradient in the lung was modelled using nine lung segments. We tested the model using an eight-subject data set with measurements of V(T), pulmonary O(2) uptake and breath-to-breath lumped SV. On average, the P(ETCO(2)) decreased from 40 mmHg to 36 mmHg after 150 s standing. Results show that the model is able to track breath-to-breath P(ETCO(2)) variations (r(2)= 0.74, P P 0.05). Model parameter sensitivity analysis demonstrates that the decrease in P(ETCO(2)) during standing is due primarily to increased V(T), and transiently to decreased SV and increased FRC; a slight gravity-induced V/Q mismatch also contributes to the hypocapnia. The influence of cardiac output on hypocapnia in the standing position was verified in experiments on human subjects, where first breathing alone, and then breathing, FRC and V/Q were controlled.

Adult↗

Haemoglobin, blood volume, cardiac function, and aerobic power.

Alterations in [Hb], which are mediated through changes in arterial oxygen content, and alterations in BV, which are mediated through changes in cardiac output (Q), have a significant effect on both VO2max and aerobic performance. If BV is held constant, a decrease in [Hb] (anaemia) causes a decrease in VO2max and aerobic performance, while an increase in [Hb] (blood doping) causes an increase in VO2max and aerobic performance. If [Hb] is held constant, an increase in BV can cause and increase in both VO2max and aerobic performance, while a decrease in BV can cause a decrease in VO2max and aerobic performance. In addition, an increase in BV can compensate for moderate reductions in [Hb] through increase in Q, allowing VO2max to remain unchanged or even increase. Also, a large portion of the difference in the enhanced cardiovascular function of endurance athletes is due to their high BV and the resultant enhancement of diastolic function. Hence, optimizing both [Hb] and BV is a very important consideration for endurance performance.

Anemia, Iron-Deficiency↗