Left Ventricle Of Human Heart Research Articles

Enhanced Clearance of Specifically Bound Digoxin from Human Myocardial and Skeletal Muscle Samples by Specific Digoxin Antibody Fragments

The effect of digoxin antibody fragments (Fab) on clearance of specifically bound digoxin from its specific receptor (Na, K-ATPase) was studied in human heart left ventricle (LV) and vastus lateralis skeletal muscle (SK) samples obtained postmortem. Initially, [3H]digoxin was bound to samples at conditions giving high relative occupancy of receptor. Half-life (t1/2) for its net release from LV in buffer was 32.2, 6.7, and 0.9 h at 0 degrees, 30 degrees, and 37 degrees C, respectively. For SK, t1/2 was 5.4 h in buffer at 30 degrees C. Inhibition of rebinding of digoxin by addition of specific digoxin Fab (5 x 10(-7) M) or excess unlabeled digoxin (1 x 10(-4) M) to buffer at 30 degrees C increased net release rate for specifically bound digoxin 2.5- to 3.0-fold in heart and SK. [3H]Digoxin was also bound to samples at conditions giving low relative occupancy. Samples were subsequently washed in buffer containing 5 x 10(-7) M specific digoxin Fab for 16 h at 30 degrees C. This wash reduced occupancy of receptors by digoxin from 10 to 0.5% in LV and from 9 to 0.3% in SK, respectively. At variance with wash at 37 degrees C, this procedure allowed subsequent vanadate-facilitated complete quantification of Na,K-ATPase by [3H]ouabain binding; values were 378 +/- 13 and 370 +/- 12 pmol/g wet weight (p greater than 0.6) in LV and 309 +/- 19 and 315 +/- 16 pmol/g wet weight (p greater than 0.7) in SK with and without previous wash, respectively (mean +/- SEM, n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic digitalization: No upregulation of digitalis glycoside receptor (Na,K-ATPase) concentration in human heart left ventricle samples obtained postmortem

Chronic digitalization: No upregulation of digitalis glycoside receptor (Na,K-ATPase) concentration in human heart left ventricle samples obtained postmortem

Cooperative Heart Study Cardiac Volume Analysis

The diagrams and photographs represent the present state of development of the Aerospace/Loma University School of Medicine cooperative effort to measure the volume of the human heart left ventricle directly from 35 cineoangiograms. A cineoangiogram is obtained by photographing the output of an image amplifier when blood soluble radio opaque contrast media is passed through the heart. The physician passes a catheter through the circulatory system into the vicinity of the heart. At the same time, he raises the voltage on his x-ray, starts the cinecamera, and gives a high speed injection of the contrast media which is heavily loaded with Iodine is used because the very high molecular weight shows up well against the x-rays. Also, the kidneys tolerate the iodine reasonably well when it comes to removing the iodine from the blood stream. Most contemporary procedures are framed at anywhere from 40 to 80 frames per second, although some research efforts go as high as 200 frames per second.

The vascularized cardiac thrombus as a possible vicarious source of blood supply in ischemic human hearts

A thrombus in the heart undergoes much the same evolutionnary change as elsewhere. It is covered by endothelium, and organized by fibroblasts and capillaries. In time, a more or less vascular connective tissue replaces part or all of the clot. In large vessels, the invasion of the thrombus by capillaries proceeds from the wall of the vessel involved, and from the patent parts of the lumen. New cappillaries which originate from one of these sources may connect with those derived from the other 1,2. Through communications thus established, blood from the lumen of the vessel may enter the vasa vasorum. It appeared possible that new vascular channels formed in the cardiac thrombus may similarly convey blood from the lumen of the heart to the myocardium. Our aim was to test this hypothesis anatomically. The study reported upon here was confined to thrombi associated with infarcts in the left ventricle of human hearts, and deals with the presence or absence of vascular intercommunications between the lumen of the left ventricle, the thrombus, and the myocardium. We have been unable to find reference to similar studies on record. A detailed account of the vascularization of thrombi in various chambers of hearts with and without infarcts will be given in a subsequent report.

Creatine Content of Human Hearts

Even before the important rôle of phosphocreatine in muscular contraction was recognized, Constabel noted that there was a decreased total creatine content in those human hearts that showed either clinical or post-mortem evidence of damage. Recently Cowan has examined a larger group of hearts, and found that myocardial failure is accompanied by a creatine content that is markedly below normal. Seecof, Linegar and Myers, whose method for determining myocardial creatine we have employed, have also examined a series of human hearts, emphasizing particularly the higher creatine concentration in the left ventricular muscle as compared to the right ventricle. In our laboratory we have approached from several experimental angles the question of the chemical changes that initiate or accompany heart failure. Since our primary interest is clinical, we have also analyzed muscle from the left ventricle of human hearts, as this material became available from time to time. In Table I we have summarized creatine determinations on 105 additional human hearts. The total creatine has been determined, the total solids, and from this calculated the percentage of creatine on a dry basis. The normal values have been determined in hearts from patients that died a traumatic or surgical death, and in hearts from those who died from an infectious disease, yet showed no gross or microscopic evidence of myocardial involvement. We list the mean value, with the standard deviation from the mean. In hypertrophied hearts, which have not failed, the values for total creatine are elevated; in those with myocardial change secondary to coronary sclerosis, the averages are low. The creatine content of hearts that have failed is reduced, averaging 30% below normal. Low values were also obtained in hearts that showed microscopic changes, inflammatory or degenerative, from patients that had died of infectious disease.