ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID

摘要:

SUMMARYCalcium binding at 0°C to a purified sheep kidney Na+,K+-ATPase was described by linear Scatchard plots. Binding at saturating free calcium was 65–80 nmol/mg of protein, or 30–40 mol of calcium/mol of enzyme. Aqueous emulsions of lipids extracted from Na+,K+-ATPase yielded dissociation constants and maximum calcium-binding values that were similar to those for native Na+,K+-ATPase. Phospholipase A treatment markedly reduced calcium binding. Pretreatment of native Na+,K+-ATPase with ouabain increased the dissociation constant for calcium binding from 131 ± 7 to 192 ± 7 &mgr;M without altering maximum calcium binding. Ouabain pretreatment did not affect calcium binding to extracted phospholipids, ouabain-insensitive ATPases, or heat-denatured Na+,K+-ATPase. Na+and K+(5–20 mM) in-creased the dissociation constants for calcium, which suggests competition between the monovalent cations and calcium for the binding sites. At higher concentrations of monovalent cations, ouabain increased the apparent affinity of binding sites for calcium. Extrapolation to physiological cation concentrations revealed that the ouabain-induced increase in apparent affinity for calcium may be as much as 2- to 3-fold. These results suggest: (1) calcium binds to phospholipids associated with Na+,K-ATPase; (2) ouabain interaction with Na+,K+-ATPase induces a perturbation that is transmitted to adjacent phospholipids, altering their affinity for calcium; and (3) at physiological concentrations of Na+or K+, or both, ouabain interaction with Na+,K+-ATPase may lead to an increased pool of membrane-bound calcium.

ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID

摘要:

SUMMARYThe purpose of this investigation was to differentiate primary cardiac participation in systemic anaphylaxis from a cardiac reaction secondary to respiratory distress. Hemocyanin-sensitized guinea pigs were anesthetized with sodium pentobarbi-tal and artifically ventilated. The chest was opened and the left ventricle cannulated. The electrocardiogram, bronchial resistance, arterial blood pressure, and left ventricular pressure and its first derivative were recorded. Following intravenous administration of antigen, the sinus rate increased by about 50–60 beats/min, left ventricular dP/dt increased by a factor of 3, and mean arterial pressure doubled. Conduction disturbances occurred in all of the experiments and ventricular fibrillation in four of six. These changes were concomitant with a 4-fold rise in bronchial resistance. To separate the cardiac and respiratory components, antigen was administered directly into the left ventricle to expose the heart to antigen before the lungs. The intracardiac challenge resulted in increases in sinus rate and left ventricular and arterial pressures quantitatively similar to changes recorded from guinea pigs after the intravenous challenge. However, all these changes preceded the rise in bronchial resistance by 60 seconds. Arrhythmias occurred as frequently as with the intravenous challenge. Our findings show that by use of an appropriate route for administration of antigen, cardiovascular and respiratory components of systemic anaphylaxis can be separated. Our data also indicate that anaphylactic cardiovascular changes can be dissociated temporally into two sets of events: an initial primary cardiac reaction caused by intracardiac release of histamine and a subsequent cardiovasular reaction secondary to systemic release of mediator.

ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID

摘要:

SUMMARY.Right ventricular papillary muscles from normal rabbits and rabbits with sustained pulmonary artery constriction (67% decrease in external diameter) were studied at several resting muscle lengths and at an early instant in the isometric twitch. Instantaneous force-velocity data were obtained at 30-38% of time to peak tension (TPT) and at 96%, 98%, and 100% of the resting muscle length at which active twitch tension was maximal. Unloaded shortening velocity (Vmax) was estimated with a linearized form of the Hill hyperbolic formula, and was depressed in hypertrophy to 36% less than normal. We found that Vmaxdid not change with muscle length in the normal or hypertrophied muscles; therefore there was a length- and time-independent depression of contractile element shortening capacity that was consistent with previous work from this laboratory which demonstrated a depression of myosin and actomyosin ATPase activity in hypertrophy.

ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID

摘要:

SUMMARYHearts of late fetal mice were maintained in organ culture in the presence of 30–100 mM sucrose or mannitol. Activities of several lysosomal enzymes (cathepsin D, β-acetylglucosaminidase, acid phosphatase) were increased by up to 30% after 18–24 hours and by up to 50% after 48–72 hours, as compared to enzyme activities in litter-matched hearts maintained in control medium or medium supplemented with equimolar urea. Simultaneously, the ratio of nonsedimentable to sedimentable enzyme activity was significantly increased, suggesting increased lysosomal fragility. Light and electron microscopic examination of the hearts revealed marked vacuolization in myocytic, interstitial, and endothelial cells. The vacuoles were limited by single membranes, often contained particulate or amorphous cellular debris resulting from autophagocytosis, and in cytochemical preparations frequently exhibited an electron-dense reaction product indicative of acid phosphatase activity. Hydrocortisone failed to prevent the marked lysosomal activation induced by the sugars. In conclusion, prolonged exposure to nonmetabolizable sugars induces severe lysosomal derangements with prominent autophagy, in fetal mouse heart maintained in organ culture.

ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID

摘要:

SUMMARY Indomethacin inhibits the synthesis of prostaglandin and the release of renin.These effects were studied in normal rabbits and rabbits with two-kidney Goldblatt hypertension (2KGH) and one-kidney Goldblatt hypertension (1KGH) by giving daily intravenous injections of indomethacin (3 mg/kg after two initial doses of 9 mg/kg), and in appropriate control rabbits given diluent phosphate buffer without indomethacin. In normal rabbits, indomethacin significantly decreased immunoreactive plasma prostaglandin E-like substance (IPGE) and plasma renin activity (PRA). Indomethacin did not change plasma creatinine (PCr) or mean blood pressure but it decreased renal blood flow (RBF) and glomerular filtration rate (GFR). In 2KGH rabbits, responses depended on the level of renal function and, to a lesser extent, on the level of PRA. In six of 10 2KGH rabbits in which hypertension developed without significant changes in PRA, IPGE, PCr, RBF, and GFR, indomethacin produced changes similar to those seen in normals. In the other four rabbits, development of 2KGH was accompanied by increased PRA, increased IPGE, and decreased RBF and GFR, and indomethacin produced renal failure, oliguria, malignant hypertension, and death within 5 days. In 1KGH rabbits, indomethacin decreased IPGE, PRA, and renal function but increased mean blood pressure. These observations suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.

ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID

摘要:

SUMMARY.This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe reduction of cardiac norepinephrine stores (normal, 1.42 &mgr;g/g: RVH, 0.11&mgr;g/g; CHF, 0.01 &mgr;g/g)-After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.

ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID

摘要:

SUMMARYThe intrinsic innervation of the heart has been described anatomically but seldom, functionally. These experiments were designed to verify and to evaluate the influence of intrinsic neural activation on the contractility of the atria and ventricles. Nine mongrel dogs underwent total cardiac denerva-tion using the Geis two-stage technique. Following recovery, they were placed on total cardiopulmonary bypass. Balloons were inserted into each cardiac chamber, filled with saline, and used to record atrial and ventricular isovolumic pressures in response to intracoronary drug injections. The hearts were paced to avoid rate changes. Acetylcholine (ACh) (0.05–1.0 &mgr;g) was given to assess direct effects on the myocardium; nicotine (NIC) (25–200 &mgr;g) was used to produce indirect inotropic effects. d-Tubocurare (dTC) (1.0–2.5 mg) and tetrodotoxin (TTX) (10–30 &mgr;g) were used to differentiate the direct and the indirect effects. Both ACh and NIC produced qualitatively similar negative inotropic responses in both atria and ventricles. dTC usually produced a significantly greater blockade of responses to NIC than to ACh. TTX administered to 12 other denervated dogs to differentiate direct and neurally mediated responses, completely blocked NIC- induced negative inotropy but did not change responses to ACh. The data show that (1) the intrinsic cardiac innervation can exert significant negative inotropic effects on atria and ventricles (10 to >30%); (2) there is no functional evidence of participation by chromaffin cells in the inotropic responses to intrinsic nerve activation; (3) the negative inotropy produced by NIC is sensitive to dTC and, especially, TTX blockade. This is consistent with the mechanism of action being intrinsic neural stimulation.

ISSN:0009-7330    

出版商:OVID    

年代:1977

数据来源: OVID