摘要:

Calculated valve area depicts anatomical stenosis but does not quantify hemodynamic impairment. We propose that hemodynamic resistance, defined as the mean pressure gradient across the valve divided by mean flow rate during systolic ejection, gives a better indication of hemodynamic obstruction. This index was compared with Gorlin valve area in 40 patients with aortic stenosis. Calculated area ranged from 0.22 to 1.26 cm2, and mean transvalvular resistance ranged from 117 to 1,244 dyne. sec. cm−5. In general, resistance varied inversely with calculated area, but there was substantial variation about the mean relation. All of the variation could be accounted for by variations in the pressure gradients at each value of calculated area. Resistance was higher in proportion to area when flow and pressure gradient were high. Analysis of five published studies of a total of 83 valves showed that calculated area changed at least three times more than resistance when pressure gradient was varied. The utility of resistance as an index of stenosis is demonstrated by example calculations that show how during exercise a stenotic valve increases the ventricular work rate out of proportion to the work done on the peripheral resistance. These calculations are possible because hemodynamic resistance defines functional impairment in units commonly used for quantification of opposition to flow. Furthermore, resistance appears to be less dependent than area on conditions of measurement and does not require an empirical constant.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Resistance of large arteries appears to be greater in the cerebral circulation than in other vascular beds. Large arteries contribute importantly to total cerebral vascular resistance and are major determinants of local microvascular pressure. Recent studies have shown that resistance of large arteries and cerebral microvascular pressure are affected by several physiological stimuli, including changes in systemic blood pressure, increases in cerebral metabolism, activity of sympathetic nerves, and humoral stimuli such as circulating vasopressin and angiotensin. Stimuli such as sympathetic stimulation and vasopressin produce selective responses of large arteries and, thereby, regulate microvascular pressure without a significant change in cerebral blood flow. These findings lead to the new hypothesis that the brain may be sensitive to changes in cerebral microvascular pressure, resulting in activation of compensatory neurohumoral mechanisms. Important changes occur in large cerebral arteries under pathophysiological conditions. Chronic hypertension increases resistance of large cerebral arteries, which protects the microcirculation against hypertension. Atherosclerosis potentiates constrictor responses of large cerebral arteries to serotonin and thromboxane, which may contribute to vasospasm and transient ischemic attacks.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effects of hemostatic substances on the vascular tone in porcine coronary arteries and the influence of low density lipoprotein on tension were investigated. Thrombin induced a marked concentration-dependent relaxation in prostaglandin F2α-precontracted strips with intact endothelium, whereas it produced a modest constriction in endothelium-denuded arteries. Methylene blue abolished the relaxation, but indomethacin did not affect it significantly. An exposure of the intact strips to low density lipoprotein resulted in a marked inhibition of the relaxation to thrombin but did not interfere with vasodilation by sodium nitroprusside. The inhibition by low density lipoprotein was reversed completely by washing. In contrast, high density lipoprotein lacked such inhibitory effects. Adenosine diphosphate, calcium ionophore A23187, and platelet-activating factor also produced relaxation in the intact strips. An exposure of the strips to low density lipoprotein almost abolished relaxation to these substances. The inhibition was also reversible. Heat treatment or acid treatment of low density lipoprotein resulted in a complete loss of the inhibitory effects, but diisopropyl fluorophosphate treatment did not alter the effect. It is concluded that low density lipoprotein may play a new pathological role in promotion of coronary vasospasm through rapid and reversible inhibition in endothelium-dependent relaxation to hemostatic substances.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Phosphatidylethanolamine (PtdEtn)N-methyltransferase activities were studied in rat heart sarcolemmal and sarcoplasmic reticular fractions after a single intraperitoneal injection of isoproterenol (0.5–5.0 mg/kg). Three active sites (I, II, and III) for PtdEtnN-methylation were assayed by measurement of [3H]methyl group incorporation from 0.055, 10, and 150 μMS-adenosyl-l-[methyl-3H]methionine into membrane PtdEtn molecules. Total methylation activity for catalytic site I of both sarcolemma and sarcoplasmic reticulum was stimulated within 2 minutes by isoproterenol in a dose-dependent manner. Although the increased methyltransferase activity in sarcoplasmic reticulum was normalized at 10 minutes, the enzyme activity in sarcolemma was normalized at 5 minutes but was again increased at 10–30 minutes after isoproterenol injection. No changes in response to isoproterenol were seen for site II and IIIN-methylation activities in either membrane. IndividualN-methylated phospholipids (phosphatidyl-N-monomethylethanolamine, phosphatidyl-N, N-dimethylethanolamine, and phosphatidylcholine), which specifically formed at each site, showed similar behavior. Pretreatment of the animals with a β-blocking drug, atenolol, for 2 days prevented the isoproterenol-induced changes in hemodynamic parameters and sarcolemmal methylation without affecting the enhanced methylation activities in sarcoplasmic reticulum. In vitro addition of cyclic AMP-dependent protein kinase (catalytic subunit) plus Mg-ATP enhanced methyltransferase activities in sarcolemma and sarcoplasmic reticulum from control hearts by 2.7- and 2.3-fold, respectively; however, under the same in vitro conditions, only about 20% activation was seen in both subcellular membranes isolated from the heart of isoproterenol-injected animals. These results suggest that both cardiac sarcolemmal and sarcoplasmic reticular methyltransferase activities are rapidly activated by isoproterenol while the underlying mechanism may be different. This study also indicates that cyclic AMP-dependent protein kinase catalyzed phosphorylation can stimulate the methyltransferase system in both sarcolemmal and sarcoplasmic reticular membranes.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Residual stress in an organ is defined as the stress that remains when all external loads are removed. Residual stress has generally been ignored in published papers on left ventricular wall stress. To take residual stress into account in the analysis of stress distributions in a beating heart, one must first measure the residual strain in the no-load state of the heart. Residual strains in equatorial cross-sectional rings (2–3 mm thick) of five potassium-arrested rat left ventricles were measured. The effects of friction and external loading were reduced by submersing the specimen in fluid, and a hypothermic, hyperkalemic arresting solution containing nifedipine and EGTA was used to delay the onset of ischemic contracture. Stainless steel microspheres (60–100 μm) were lightly imbedded on the surface of the slices, and the coordinates of the microspheres were digitized from photographs taken before and after a radial cut was made through the left ventricular free wall. Two-dimensional strains computed from the deformation of a slice after one radial cut were defined as the residual strains in that slice. It was found that the distributions of the principal residual stretch ratios were asymmetric with respect to the radial cut: in areas where substantial transmural strain gradients existed, the distributions of strain components were different on the two sides of the radial cut. A second radial cut produced deformations significantly smaller than those produced from the first radial cut. Hence, a slice with one radial cut may be considered stress free. Our results show that the circumferential residual strain was negative in the endocardial region (stretch ratios were significantly less than 1.00,p<0.001 for five slices), while those in the epicardial region were either positive or negative with a much smaller magnitude. This residual strain distribution suggests that, in general, there is compressive circumferential residual stress at the inner layers of the ventricle. A residual stress distribution of this nature may reduce the endocardial peak in circumferential tensile stress at end diastole predicted by analytical models using nonlinear material properties.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Endothelin is a 21-residue peptide formed during incubation of isolated porcine endothelial cells. Due to its pronounced vasoconstrictor activity, endothelin has been proposed to play a role in the regulation of vascular tone. We studied the effects of synthetic endothelin (0.1–10 nM) on coronary flow, mechanical performance, myocardial oxygen uptake, and formation of purines, and outflow of 6-ketoprostaglandin F1α(metabolite of prostacyclin) in rabbit hearts perfused with saline by the Langendorff method. Endothelin dose-dependently decreased the coronary flow, at 10 nM, by about 75%. Heart rate, ventricular contractility, myocardial oxygen uptake, and purine release were affected by endothelin no more than by a corresponding mechanical reduction of the coronary flow. In contrast, the diastolic relaxation appeared to be directly diminished by endothelin. The concentration of 6-ketoprostaglandin F1αin the cardiac effluent was dose-dependently elevated by about 14 times by endothelin (10 nM) (p<0.001). A corresponding mechanical restriction of the coronary flow insignificantly affected the effluent concentration of 6-ketoprostaglandin F1α. The calcium channel blocker nifedipine (1 μM) completely abolished the decrease in diastolic relaxation induced by endothelin and markedly counteracted the peptide-induced increase in effluent concentration of 6-ketoprostaglandin F1α, but did not affect the vasoconstrictor activity. These data demonstrate that endothelin induces vasoconstriction and facilitates the outflow of prostacyclin in the rabbit heart. In addition, the peptide appears to affect diastolic relaxation in this organ.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

For investigation of late potentials seen on the signal-averaged electrocardiogram, intracardiac and thoracic distributions of terminal activity were analyzed in 16 patients undergoing cryosurgery for ventricular tachycardia after remote myocardial infarction. The body surface potentials measured with 63 time-averaged unipolar leads were compared with epicardial and endocardial potential maps in six patients without and 10 patients with bundle-branch block. Intracardiac post-QRS activity, defined as extending beyond the thoracic QRS offset, was found in five of six patients without bundle-branch block (83%) and in five of 10 patients with bundle-branch block (50%), corresponding to 4±5% of the total number of electrograms in each patient. Fragmentation, double deflections, and single deflections were observed in 27%, 34%, and 39%, respectively, of these post-QRS electrograms. Post-QRS activation patterns that were stable from beat to beat showed slow propagation around or within areas of conduction block. Post-QRS activity was most often observed on both epicardial and endocardial surfaces (five of 10 patients). In the six patients without post-QRS activity, an area of late activity displaying low-amplitude deflections that were masked by the terminal activation of the normal myocardium was identified. Isopotential maps of the high-pass-filtered (55-Hz) thoracic and intracardiac signals demonstrated a close spatial correlation between the location, amplitude, and orientation of the potential extrema observed over the thoracic, epicardial, or endocardial surfaces during post-QRS activity. The thoracic patterns were generally dipolar with close extrema for anteroseptal or apical sites of post-QRS activity and more distant extrema for other sites. We concluded that the spatial domain analysis of intracardiac and thoracic potential distributions contributes to the understanding of the electrogenesis and electrocardiographic measurement of late potentials.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

With the inhalation of smoke, there are both cardiopulmonary changes and elevated levels of carbon monoxide (CO). We hypothesize that these changes in cardiopulmonary function are the result of a histotoxic hypoxia associated with CO poisoning. This hypothesis was tested in chronically instrumented sheep (n=19). Piezoelectric crystals were attached to the left ventricle for the measurement of its external minor and major diameters in addition to wall thickness. A pressure transducer was placed in the left ventricle via the apex. The caudal-mediastinal lymph node was also cannulated. After a five-day recovery period, six sheep (smoke group) were insufflated with four series of 16 breaths (700 mllbreath) of cotton smoke, and five sheep (control group) were insufflated with air using a modified bee smoker (smoke group: COHb, 90±6%; control group: COHb, 6±1%). Eight sheep (CO group) were ventilated with 2% CO in air to reach a COHb of 90% (COHb, 92±1%). In the smoke group, lung lymph flow reached 42±10 ml/hr at 24 hours after smoke insufflation (baseline, 6±1 ml/hr). The maximum elastance of the left ventricle (end-systolic pressure-volume ratio), a sensitive index of myocardial contractility, was significantly decreased from a baseline of 6.5±0.9 to 3.3±0.7 mm Hg/ml. In the control and CO group, neither lung lymph flow nor maximum elastance varied from the baseline value. We conclude that the cardiopulmonary dysfunction after smoke inhalation does not occur after a similar exposure to CO. Initial CO poisoning alone is not a causative factor of cardiopulmonary dysfunction after smoke inhalation.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Atrial pressure, atrial natriuretic factor (ANF), the renin-angiotensin-aldosterone system, and renal hemodynamic functions were examined during and after right ventricular pacing in anesthetized dogs (n=9). Mean arterial pressure, cardiac output, and renal blood flow decreased during tachycardia while right and left atrial pressures increased. ANF markedly increased during tachycardia but urinary and fractional excretion of sodium were unchanged from control. Plasma renin activity was not increased during pacing despite the decrease in renal perfusion pressure. After tachycardia and restoration of mean arterial pressure to control, ANF declined but remained elevated above control despite a return of atrial pressure to control level. After tachycardia, urinary and fractional sodium excretion increased significantly in the absence of an increase in glomerular filtration rate. These findings support the following conclusions: 1) tachycardia increases ANF in association with increased atrial pressure; however, an elevation of ANF persists following tachycardia despite the absence of the persistent stimulus of elevated atrial pressures; 2) the increase in ANF during tachycardia may contribute to the absence of a decrease in sodium excretion and activation of the renin-angiotensin system that occurs with reduction in renal perfusion pressure; and 3) tachycardia-induced natriuresis may be dependent on an increase in ANF and the maintenance of renal perfusion pressure.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

We evaluated cardiac muscle development in the absence of hemodynamic work load but in the presence of host factors including blood vessels, nerves, and circulating neurohumoral agents by transplanting 12-day fetal rat ventricle into the anterior eye chamber of adult host rats. Implants were studied by electron microscopy at intervals from 1 to 14 weeks in oculo. For comparison with myocardium developing in oculo, 12-day fetal tissue and 3-, 8-, and 28-day-old normally growing rats were also studied. At 1 week in oculo, myofibrils were laterally located and more frequent than in the 12-day fetus. Fibrils had clear Z bands and H bands, but no M bands. At 10 days in oculo (comparable to birth in normally growing animals), myocyte mitoses were present and tritiated thymidine autoradiography revealed many labeled myocyte nuclei. By 5 weeks in oculo, cells were filled with mature myofibrils with clear M bands and lateral connections between adjacent Z bands. However, myofibril bundles sometimes coursed at sharp angles to each other within single cells. Except for the relative lack of fibrillar polarization and small cell size, ultrastructure of myocytes developing in oculo for 5 or more weeks appeared very similar to myocytes developing in normally growing rats. By 10 weeks in oculo, when in situ growing hearts are clearly in a hypertrophic phase of growth, no mitoses or tritiated thymidine-labeled nuclei were present in myocytes, although labeled nonmyocyte nuclei were present. Morphometric evaluation revealed no change in myocyte diameter or nuclear-to-cytoplasmic ratio from 1 to 3 weeks in oculo, consistent with continued hyperplastic growth. Binucleated cells were present by 3 weeks in oculo and later, and the cytoplasm per nucleus increased fourfold between 3 and 5 weeks in oculo, suggesting conversion to hypertrophic cell growth. We concluded that cells proliferated and differentiated in the absence of a hemodynamic load, but that polarized alignment of myocytes and myofibrils was incomplete.

ISSN:0009-7330    

出版商:OVID    

年代:1990

数据来源: OVID