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1. |
Transsinusoidal Fluid Dynamics in Canine Liver during Venous Hypertension |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 317-323
GLEN LAINE,
JEFF HALL,
SUSAN LAINE,
HARRIS GRANGER,
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摘要:
We studied arterial pressure, portal pressure, inferior vena caval pressure, hepatic interstitial pressure (implanted capsule technique), prenodal lymph flow, and the protein concentration in plasma and lymph in the anesthetized dog under normal conditions and during graded venous hypertension resulting from inferior vena caval occlusion. Under control conditions, portal, interstitial, and inferior vena caval pressures were 7.0, 5.8, and 2.0 mm Hg, respectively, and the lymph-plasma protein concentration ratio was 0.95. During acute venous hypertension, 64% of the inferior vena caval pressure increase was transmitted to the hepatic interstitium, and lymph flow increased 63% for every 1 mm Hg increment in interstitial pressure. The lymph-plasma protein concentration ratio did not change significantly during venous hypertension, indicating that: (1) the reflection coefficient of the sinusoidal wall for the major plasma proteins is close to zero, and (2) protein transport across the microvascular wall is due mainly to bulk flow. Using portal, interstitial, and inferior vena caval pressures as limits for possible values of sinusoidal pressure, our data suggest that (1) control sinusoidal pressure was between 5.8 and 7.0 mm Hg, and (2) approximately 90% of the increase in inferior vena caval pressure was transmitted to the sinusoids. The results indicate that changes in interstitial pressure, lymph flow, and surface transudation rate are major compensatory mechanisms operating in the liver to limit interstitial engorgement during venous hypertension. CireRea 45:317-323, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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2. |
Rate of Rise of Myocardial PCO2 during Early Myocardial Ischemia in the Dog |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 324-330
ROBERT CASE,
ALEXIS FELIX,
FRANK CASTELLANA,
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摘要:
We have investigated the rate of rise of myocardial Pco2(Pmco2) after coronary artery occlusion using a new method for this measurement. Previous studies of Pmcch have been limited by the slow response of the only available method, and no increase in Pmcoi prior to 3 minutes after occlusion has been found. We have implanted a miniature PcOj electrode, with a 63% response time of 14 seconds, into the left ventricle of 14 open-chest dogs. After abrupt coronary occlusion, Pmcoi began to rise in 13.6 ± 1.1 seconds in heparinized dogs and in 7.5 ± 0.7 seconds in unheparinized dogs. The subsequent magnitude of the increase in Pmco2was 24, 88, 171, and 222 mm Hg at 2, 5, 10, and 15 minutes after occlusion. The rate of rise of Pmco2was essentially linear from 1 minute to 10 minutes at a rate of 18.3 mm Hg/min. The rate of rise was slower during the first 30 seconds after occlusion (6.1 mm Hg/min) and also from 30 seconds to 1 minute (9.7 mm Hg/min). This rate of rise is much greater than that previously observed and reflects the severe myocardial acidosis developing during ischemia. A rise in Pmco, is one of the earliest metabolic changes that has been observed during myocardial ischemia. Ore Res 45:324-330, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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3. |
Effect of Sympathetic Stimulation on Permeability of the Blood‐Brain Barrier to Albumin during Acute Hypertension in Cats |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 331-338
DONALD HEISTAD,
MELVIN MARCUS,
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摘要:
Most studies concerning effects of neural stimuli on the cerebral circulation have focused on changes in cerebral blood flow (CBF). The purpose of this study was to examine effects of sympathetic nerves on permeability of the blood-brain barrier (BBB) to albumin, using a quantitative method, and to relate changes in blood flow to changes in permeability of the BBB. Permeability of the BBB was evaluated by measuring the accumulation ofulI-labeled serum albumin (RISA) in brain. RISA was injected intravenously, and the ratio of brain RISA to blood RISA was used as an index of permeability of the BBB. In normotensive cats, the BBB index in the cerebrum was 0.12 ± 0.04% (mean ± BE). During acute hypertension produced by intravenous norepinephrine, the BBB index in the cerebrum increased to 0.91 ± 0.20% (P< 0.05). Sympathetic stimulation during hypertension attenuated the increase in BBB index: the BBB index was 0.38 ± 0.10% and 1.01 ± 0.26% on the stimulated and unstimulated sides of the cerebrum, respectively (P < 0.05). CBF increased more than threefold during severe hypertension; sympathetic stimulation attenuated the increase in flow. Increases in flow and disruption of the BBB were most marked in cortical gray matter, and responses to sympathetic stimulation were also largest in cortical grey matter. Disruption of the BBB during hypertension was minimal in subcortical grey and white matter, and sympathetic stimulation had no detectable effect in these areas. In summary, these studies provide the first quantitative evidence that acute hypertension increases the permeability of the BBB to albumin and that sympathetic stimulation reduces disruption of the barrier. The regions of the brain that were most susceptible to disruption of the BBB were most responsive to the protective effect of sympathetic stimulation. Cine Res 45: 331-338, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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4. |
Decreased Myocardial Contractility in Papillary Muscles from Atherosclerotic Rabbits |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 338-346
DARWIN PETERSON,
DAVID GRIFFITH,
CHARLES NAPOLITANO,
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摘要:
To determine the effect atherosclerosis has on myocardial contractility, we studied the contractile properties of right ventricular papillary muscles from 34 atherosclerotic and 17 control rabbits. We produced atherosclerosis by feeding for 2 to 8 months a diet of 5% lard, 5% peanut oil, 0.5% cholesterol, and 89.5% rabbit pellets. The controls received only rabbit pellets during the same time interval. Contracting isometrically 12 times per minute at 25°C, muscles from the atherosclerotic rabbits developed tension at a lower ma-rimum rate (max dT/dt), had a longer latency, and required longer to develop tension at the maximum rate and to develop peak tension. In isotonic contractions, they shortened with lower mmiimim velocities and required longer to accelerate to muTimiim velocity and to shorten maximally. We found no evidence that developed tension or distance shortened differed between the two groups of muscles. Raising the contraction frequency to 24 contractions ner minute brought performance of the two groups of muscles closer in both types of contraction. Norepinephrine (1.5 x 10-6M) nearly abolished differences between performance of the two groups. The loss of contractility correlates poorly with coronary and aortic atherosclerosis. It occurred early in the feeding of the atherogenic diet. We think it was due to a lipid-induced defect in the cardiac cell's handling of calcium. Circ Res 45: 338-346, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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5. |
Normal Levels of Fibrinopeptide A in Patients with Primary Hyperlipidemia |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 347-350
HYMIE NOSSEL,
FRANK REESSMITH,
ALAN SEPLOWITZ,
RALPH DELL,
ROBERT SCIACCA,
CLARENCE MERSKEY,
DEWITT GOODMAN,
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摘要:
Fibrinopeptide A (FPA) levels were measured in a group of 130 controls and patients with various types of primary hyperlipidemia to investigate whether an increased steady state level of thrombin activity is present in hyperlipidemic patients. In a subset of 56 subjects, levels of clotting factors n, VTL and X were measured as well. FPA levels in hyperlipidemic patients were not significantly different from those of control subjects. Furthermore, on multiple regression analysis, no significant relationships were found between FPA levels and the concentrations of serum cholesterol or triglyceride, or log triglyceride levels. Statistically significant relationships were found between all three clotting factor levels and triglyceride concentration. The correlation coefficients for these relationships, however, were low, so that the correlations are of questionable pathophysiological significance. A weak relationship also wan found between the plasma levels of cholesterol and of factor II. Thus, although small increases in various clotting factors may be found in patients with hyperlipidemia, plasma FPA levels are normaL These data indicate that hyperlipidemia is not associated with a steady state of increased thrombin activity in vivo in humans.CircRet45: 347-350, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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6. |
Quantitative Effects of Sodium Nitroprusside on Coronary Hemodynamics and Left Ventricular Function in Dogs |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 351-359
D. PENNINGTON,
MICHAEL VEZERIDIS,
GILLIAN GEFFIN,
DENNIS O'KEEFE,
DEMETRIOS LAPPAS,
WILLARD DAGGETT,
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摘要:
We studied the effects of nitroprusside on left ventricular contractility, coronary blood flow, and coronary vascular resistance in dogs during right heart bypass in which stroke volume, aortic pressure, and heart rate were controlled. Intravenous nitroprusside increased coronary blood flow and decreased coronary vascular resistance but did not change left ventricular end-diastolic pressure or Tim-rimnm dP/dt when aortic pressure was held constant. When aortic pressure was allowed to fall during intravenous nitroprusside infusion, coronary flow increased slightly as coronary resistance decreased, but left ventricular contractility increased (left ventricular end-diastolic pressure fell at constant maximum dP/dt). After βadrenergic blockade, intravenous nitroprusside decreased maximum dP/dt, coronary flow, and coronary resistance when aortic pressure fell during intravenous nitroprusside infusion. When the coronary and systemic circulations were separated and coronary pressure was kept constant, intravenous nitroprusside did not change coronary flow or coronary resistance, but maximum dP/dt decreased when aortic pressure felL Conversely, intracoronary nitroprusside increased coronary flow and decreased coronary resistance but did not change left ventricular end-diastolic pressure or maximum dP/dt. We conclude that nitroprusside dilates coronary arteries but has no direct effect on left ventricular contractility. When mean aortic pressure is decreased by nitroprusside, β-adrenergic stimulation results in increased left ventricular contractility and indirect coronary dilation. Ore Ret 45: 351-359, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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7. |
Pulmonary Vascular Response to Nitroprusside in Dogs |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 360-365
EDWARD SIVAK,
BARRY GRAY,
H. MCCURDY,
ARDIS PHILLIPS,
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摘要:
Although the effects of nitroprusside (NP) on myocardial function have been studied extensively, the effects of this vasodilator on the pulmonary vasculature have received less attention. In closed-chest anesthetized dogs, we used indicator dilution measurements of pulmonary blood volume (PBV), along-with measurements of pulmonary artery (Ppa) and left atrial (Pla) pressures, to address this problem in three experimental protocols. In protocol I, NP at 10-30 μg/kg per min in volume-expanded dogs reduced Ppa by 20% and Pla by 44% but produced no consistent change in PBV. In protocol II, NP at 1.8-5.4 μg/kg per min accompanied by autologous blood transfusion, sufficient to return Pla to the control level, resulted in no change in Ppa, but an increase in PBV from 8.8 to 9.9 ml/ kg (P < 0.05). In protocol m, NP at 2-6 μ/kg per min was compared to decreased venous return produced by partial occlusion of the inferior vena cava (TVC). With IVC occlusion adjusted to yield Pla equal to that during NP infusion, there was no difference in Ppa, but PBV was greater during NP infusion (10.5 ml/kg), compared to IVC occlusion (7.6 ml/kg, P < 0.05). In some experiments NP produced an increase in PBV when Pla and Ppa were reduced. In protocols II and m, NP decreased pulmonary vascular resistance by 40-50% (P < 0.05) at equal levels of Ppa. We conclude that NP shifts the pressure-volume curve of the pulmonary vasculature so that greater volume and flow are accommodated at the same pressure and, under some conditions, may produce a paradoxical increase in PBV while reducing pulmonary vascular pressure. Ore Res 45: 380-366, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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8. |
Effects of Ischemia on Tissue Metabolites in Red (Slow) and White (Fast) Skeletal Muscle of the Chicken |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 366-373
RICHARD KLABUNDE,
STEVEN MAYER,
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摘要:
Brief periods of ischemia have been shown to produce marked reactive hyperemia in both red (slow) and white (fast) skeletal muscle. However, evidence is lacking for specific vasodilator metabolites which are rapidly produced in ischemic skeletal muscle. The present study examined the effects of 1 and 3 minutes of ischemia on creatdne phosphate (CrP), adenine nucleotide metabolism, and anaerobic glycolysis in red anterior (ALD) and white posterior latissimus dorsi (PLD) muscles of the chicken. Tissue metabolite concentrations were determined from perchloric acid or trichloroacetic acid extracts using enzymatic assay or high pressure liquid chromatography. CrP or adenine nucleotldeg were not significantly altered in either muscle following 1 or 3 minutes of ischemia. However, adenosine increased by 611% in the ALD at 1 minute. Following 3 minutes of ischemia, adenosine concentrations were elevated by 439% and 201% in the ALD and PLD, respectively. The PLD showed the greatest increases in inosine and IMP. Inorganic phosphate increased by 67% and lactate increased by 142% in the ALD at 3 minutes. The PLD, which is reported to have a high anaerobic glycolytic capacity, showed no increase in lactate. These results support the hypothesis that adenosine may be a mediator of skeletal muscle reactive hyperemia folio-wing short periods of ischemia. Circ Res 46: 366-373, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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9. |
Circus Movement in Canine Right Ventricle |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 374-378
JACQUES DE BARKER,
BERTHOLD HENNING,
WOLFGANG MERX,
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摘要:
The present study reports on the epicardial spread of excitation during premature beats and during the initial stages of ventricular fibrillation, both of which were induced by single-test stimuli during regional ischemia or local hypothermia. Simultaneous recording of the activity at 48 epicardial sites on the right ventricle of dog hearts enabled us in some instances to demonstrate a circus movement. Ore Res 45: 374-378, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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10. |
Characterization of the Extravascular Component of Coronary Resistance by Instantaneous Pressure‐Flow Relationships in the Dog |
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Circulation Research,
Volume 45,
Issue 3,
1979,
Page 378-390
RONNEY PANERAI,
JEREMY CHAMBERLAIN,
BRUCE SAYERS,
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摘要:
To investigate the mechanical effects of the myocardium on the blood perfusion of the canine left ventricle, phasic total left ventricular (LV) coronary blood flow, perfusion pressure, LV pressure, aortic flow rate, and LV segment length were recorded continuously in an open-chested dog heart preparation. These variables were analyzed on a digital computer and time synchronized so that coronary pressure-flow curves could be drawn for various instants in the cardiac cycle. During diastole, the pressure-flow relationship is linear, changing to a nonlinear curve with the onset of systole. To estimate phasic patterns of coronary resistance and intramyocardial pressure (IMP), a model based on the vascular waterfall mechanism was developed and fitted to the experimental data. The results of this operation show inferred coronary resistance patterns that increase during ejection and remain constant during diastole and isovolumic contraction. Assuming LV pressure to represent endocardial IMP, the estimated epicardial IMP signal averages 42.1 ± 13.3% of peak LV pressure at this instant of peak pressure. Furthermore, increases in end-diastolic volume reduced the changes in inferred coronary resistance taking place during ejection, but the epicardial IMP signal remained practically unchanged. Circ Res 45: 378-390, 1979
ISSN:0009-7330
出版商:OVID
年代:1979
数据来源: OVID
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