PubMed Health⌕ Search

Biomedical subjects

H Feinberg

Publications and source records attributed to H Feinberg.

At least 91 records · Page 5Linked to original sources
PubMed1978

Potassium cardioplegia. An alternate method of intraoperative myocardial protection.

Potassium-induced cardioplegia was studied in 38 mongrel dogs supported by normothermic cardiopulmonary bypass and subjected to 60 minutes of aortic cross clamping followed by 30 minutes of reperfusion. A study of preischemic and postischemic ventricular function and myocardial high-energy phosphate compounds, lactate, and glycogen showed substantial preservation of high-energy phosphates and ventricular performance when potassium cardioplegia was used. However, the substantial depression in contractility observed following ischemia nad reperfusion suggests that potassium cardioplegia alone does not provide adequate intraoperative protection of the myocardium.

Adenosine Diphosphate↗
PubMed1978

Intraoperative protection of the myocardium.

It appears obvious that in evaluating gross mortality and morbidity, clinical statistics are insufficient to demonstrate which form of a myocardial protective measure is safest. Previous studies indicate that significant ischemic injury may not be detectable by routine measurements of contractility. Only microscopic examination of the heart at a later period will allow detection of the patchy ischemic injury. In patients, loss of cardiac reserve as measured by postoperative catheterization, particularly compliance studies, and stress testing may be the final clinical arbiter of this controversy.

Aorta↗
PubMed1977

Movement of sodium into human platelets induced by ADP.

1. In normal human platelets the concentrations of Na+ and K+ were 42.1 +/- 4.3 and 98.8 +/- 3.7 mequiv/l of platelet water respectively (mean +/- S.E. of 22 samples). 2. When platelet-rich plasma was incubated with 22Na+ at 37 degrees C for 2-3 h an increase in platelet Na+ concentration was found which was significant after 210 min. Platelet K+ concentration did not change significantly. The platelet 22Na+ radioactivity increased faster than did the total Na+ suggesting a Na+o-Na+ exchange process in unactivated platelets. 3. Addition of ADP to platelet-rich plasma resulted in platelet aggregation and a rapid rise (within seconds) in 22Na+-radioactivity within the platelets and after 300 s this increase diminished toward control levels. 4. Under the same experimental conditions, ADP did not bring about an increase of 36Cl- in the platelets. 5. Ouabain (10-(6) M) added to platelet-rich plasma induced an increase in Na+ concentration and 22Na+ radioactivity in the platelets, as well as a decrease in K+ concentration. ADP produced a further increase in 22Na+, which did not return toward control values, in the presence of ouabain. 6. The association of an increase in 22Na+ but not of 36Cl- accompanying aggregation by ADP suggests a selective mechanism for the movement of Na+ into platelets rather than a movement of NaCl together with water under an osmotic gradient.

Adenosine Diphosphate↗
PubMed1977

Does intermittent coronary perfusion offer greater myocardial protection than continuous aortic cross-clamping?

There has been considerable controversy concerning the relative merits of intermittent coronary perfusion vs. continuous aortic cross-clamping for cardiac procedures requiring ischemic arrest. Using the isovolumic ventricular balloon model and "stop-freeze" biopsy techniques, myocardial contractility (LV dp/dt max, length-tension, and force-velocity relationships) and metabolism (adenine nucleotides, creatine phosphate, and glycogen) were studied in 46 intact dogs supported by normothermic cardiopulmonary bypass and subjected to either 60 minutes of continuous ischemic arrest or to four 15-minute intervals of ischemia each followed by 5 minutes of reperfusion. Following ischemia the hearts were reperfused for 30 minutes and defibrillated after the first 10 minutes. There were no significant differences in either metabolic parameters or contractile function between the groups. Although partial regeneration of adenosine triphosphate and glycogen occurred during reperfusion, only creatine phosphate achieved normal values and the end result was no difference between the two techniques. These data indicate that 5 minutes of coronary reperfusion between consecutive episodes of ischemic arrest affords no greater intraoperative protection of the myocardium than does continuous aortic cross-clamping.

Adenine Nucleotides↗
PubMed1975

Biochemical changes of ischemia.

Normothermic ischemic arrest by aortic cross-clamping, a widely used clinical technique, is associated with metabolic changes in the myocardium that are incompletely understood. The effects of aortic cross-clamping on glycolytic pathways as well as associated morphological changes are discussed. Emphasis is placed on the conservation of high-energy phosphate moieties during the period of cross-clamping as well as during reperfusion. A marked reduction in total high-energy phosphates (62%) and glycogen (63%) and an increase in lactate production (243%) denote a shift to anaerobic metabolism during the period of arrest. Despite reperfusion, total high-energy nucleotides remained depressed. The data suggest that persistent abnormal myocardial carbohydrate metabolism and low levels of high-energy nucleotides prevent recovery of contractility following normothermic ischemic arrest and reperfusion.

Animals↗
PubMed1975

Protection of the myocardium with high-energy solutions.

An approach to intraoperative protection of the myocardium is described that attempts to increase glucose utilization by infusion of high-energy solutions during aortic cross-clamping. Infusion of hypertonic glucose or glucose plus insulin prior to aortic cross-clamping has enhanced contractility and increased high-energy phosphate moieties in animals with induced ischemia. Recent pilot experiments in our laboratory suggest that infusions of creatine may result in increased production of creatine phosphate, which in turn induces phosphorylation of adenosine diphosphate to adenosine triphosphate, possibly enhancing myocardial contractility. The intraoperative clinical benefits of these infusions remain to be proved, however.

Adenosine Triphosphate↗
PubMed1975

Postbypass treatment.

Ischemia induced by cross-clamping the aorta during open-heart operations initiates progressive metabolic derangement. If the duration of ischemia is short, these derangements are easily reversed by restoring the flow of blood containing oxygen and substrate. If ischemia is prolonged, treatment designed to ameliorate ischemic damage may be necessary. Three problems are discussed: (1) loss of adenine nucleotides, particularly adenosine triphosphate, (2) impairment of calcium sequestration, and (3) formation of microemboli in coronary vessels. The rationale for postbypass treatment is presented.

Cardiopulmonary Bypass↗
PubMed1975

Binding of adenosine diphosphate to intact human platelets.

1. Human platelet-rich plasma was incubated at 37 degrees C with [8-14C]ADP and with human serum albumin labelled with 125I. The platelets were rapidly separated by centrifugation through silicone oil. From radioactivity determinations of plasma and platelet pellets the uptake of ADP, without or with break-down products, by the platelets was calculated on the assumption that the 125I radioactivity in the pellet represented trapped plasma. 2. ADP radioactivity was taken up by platelets within 10 sec and increased with time of incubation. The uptake of other nucleotide diphosphates was less initially and increased much more slowly. 3. Radioactivity added as ADP was recovered as ATP to the extent of 60%; as ADP of 30%; and as AMP of 10%. 4. Prostaglandin E1 which inhibited platelet aggregation had no effect on the initial or subsequent uptake or on this distribution of radioactivity. 5. The rate of rise in uptake was much slower when platelets were resuspended in plasma heated to 56 degrees C for 30 min. 6. Unlabelled adenosine inhibited the later, but not the initial, uptake while unlabelled ADP inhibited both. Dipyridamole, which blocks adenosine uptake, prevented the later but not the initial uptake. 7. [alpha-32P]ADP radioactivity was taken up at the earliest sampling time and the extent of uptake did not further increase. 8. Guinea-pig platelets, which do not take up adenosine, took up [8-14C]ADP radioactivity from purine-labelled ADP initially. 9. It was concluded that the initial uptake represented binding of ADP and that the later uptake represented labelled adenosine originating as a break-down product of ADP. 10. A Scatchard plot of ADP uptake indicated more than one type of binding site. There were approximately 88,000 high affinity sites per platelet which had an affinity constant of 5-41 X 10(5) M-1.

Adenosine↗
PubMed1975

Anoxia-induced release of prostaglandins in rabbit isolated hearts.

We investigated the relationship between prostaglandin release and the coronary vasodilation evoked by anoxia. Isolated rabbit hearts were perfused via the aorta with Krebs-Ringer's solution. The coronary effluent was bioassayed continuously in terms of prostaglandin E2 for prostaglandinlike substance which was present (at less than 1 ng/ml) in 60 of 66 hearts. This basal release was abolished by the prostaglandin synthetase inhibitor, indomethacin (1-2 mug/ml), a result which adds further to the identity of the prostaglandinlike substance as a prostaglandin. Anoxia increased coronary flow sometimes by 100% and evoked prostaglandin release shortly thereafter. Ablolition of prostaglandin synthesis by indomethacin pretreatment did not affect nor did infusion of exogenous prostaglandin mimic the anoxia-induced flow increment; thus, we conclude that prostaglandin release cannot account for the anoxia-induced vasodilator response. Furthermore, the failure of indomethacin to alter resting coronary blood flow suggests that a local prostaglandin release is not responsible for either the maintenance or the modulation of coronary flow in this preparation.

Animals↗