Peter V. Moulder
University of Chicago
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Featured researches published by Peter V. Moulder.
American Journal of Cardiology | 1968
Su-chiung Chen; RenéA. Arcilla; Peter V. Moulder; Donald E. Cassels
Abstract The electrocardiograms of 60 patients with atrial septal defect, aged 23 months to 37 years, were obtained after open heart surgery and analyzed. The over-all incidence of conduction abnormalities was 60 per cent; excluding first degree A-V block, it was 52 per cent. There was no significant difference in incidence between cases of secundum and primum atrial septal defect, or between those with patch repair and suture repair. Arrhythmia after total body perfusion lasting over one hour was not significantly higher than that following shorter perfusion times. The incidence of the various conduction disturbances was: A-V block, 28 per cent; right bundle branch block, 30 per cent; A-V junctional rhythm, 20 per cent; supraventricular tachycardia, 5 per cent; and atrial flutter, 2 per cent. As a rule, the arrhythmias were benign. Excluding right bundle branch block, they also tended to be transient. However, postoperative complete A-V block has persisted in 1 child for over a year. The P-R interval in the immediate postoperative period increased, decreased, or remained essentially unchanged; that observed several weeks later did not differ significantly from the preoperative level. Surgically induced right bundle branch block resulted in a distinct increase of the RS ratio in V 1 . This regressed after disappearance of block. The possible mechanisms for the postoperative A-V block and right bundle branch block are discussed.
Circulation | 1967
Friedrich A. O. Eckner; Jona C. Thaemert; Peter V. Moulder; Eugene H. Blackstone
Full-thickness biopsies of ventricular dog myocardium, beating and in arrest, have been studied by conventional fixation (immersion in fixative solution), by the use of cryostat sections thawed on slides, and by freeze drying of tissue blocks. Three types of artifacts were found and could be related (1) to cutting into the beating heart, (2) to thawing of frozen sections on slides, and (3) to the failure of fixative solutions to immobilize still reactive myocardium immediately. The method described yields a biopsy specimen of sufficient diameter to delineate the cutting artifacts. For histological preparation freeze drying appears to be the method of choice.
American Journal of Cardiology | 1968
Ramon E. Acevedo; Otto G. Thilenius; Peter V. Moulder; Donald E. Cassels
Abstract Pseudocoarctation and coarctation of the aorta in a 7 year old boy are reported. This association is very unusual, particularly in a young child. A possible pathogenetic relation between these two anomalies is discussed.
Histochemistry and Cell Biology | 1969
Friedrich A. O. Eckner; Brigitte H. Riebe; Peter V. Moulder; Eugene H. Blackstone
SummaryBiochemical methods for demonstration of enzyme activity are test tube models outside the organization of cell. Their application to the complicated organization of the cell present problems to histochemistry. The morphological and chemical preservation of tissue which is desirable in histochemistry leads to a multiplicity of reactions when “test tube” methods are applied. For example, the histochemical phosphorylase and glycosyltransferase reactions rest on the assumption that one can distinguish between preexisting glycogen and newly formed polysaccharides. We used frozen dried canine myocardium and liver for examination of the authenticity of histochemical phosphorylase and glycosyltransferase (branching enzyme, UDPG-glycogen transglycosylase) reactions as described in histochemical reference books. We were unable to distinguish between preexisting glycogen and supposedly newly formed polysaccharides with methods presently used for this purpose (Iodine stain, differential digestion with amylases, acid hydrolysis). Tissue without PAS stainable glycogen remained so after substrate incubation. When preexisting glycogen was present, the amounts of stainable polysaccharides after incubation were invariably less. Therefore, we could not prove beyond doubt that any polysaccharide synthesis due to enzyme reaction had oceured. The prescribed controls, perhaps adequate for biochemical “test tube” reactions, have to be redefined for meaningful histochemical procedures.
Histochemistry and Cell Biology | 1968
Friedrich A. O. Eckner; Brigitte H. Riebe; Peter V. Moulder; Eugene H. Blackstone
SummaryCytochrome oxidase, succinic dehydrogenase, phosphorylase and branching enzymes were consistently demonstrated in frozen dried paraffin embedded dog myocardium if the appropriate solvent for deparaffinization was used. No modification of the incubating medium was necessary for cytochrome oxidase. For succinic dehydrogenase a 0.8 M succinate solution was used instead of the usual 0.2 M solution and phenazine methosulfate had to be added to the incubating medium. No primer or activators were necessary for demonstration of phosphorylase and branching enzyme activities.
Circulation Research | 1966
Peter V. Moulder; Lillian Eichelberger; James J. Rams; A. G. Greenburg
The water, nitrogen, and electrolyte content of the normal canine myocardium partitioned as right ventricle, septum, and left ventricle are presented on a connective tissue-free basis as well as fat-free and blood-free. Considering the tissue on a fat-free, blood-free, connective tissue-free basis, the extracellular phase (expressed as g/kg heart muscle) of the left ventricle was 86% that of the right ventricle; that of the septum was 91% that of the right ventricle. In all three segments, cell water was constant at 77%. One kilogram of myocardial cells contains 29.7 g of noncollagenous protein nitrogen, 116 mEq of potassium, 26 mEq of magnesium, and is associated with 0.3 (septum and left ventricle) and 0.53 (right ventricle) mEq of calcium.
Experimental Biology and Medicine | 1956
Peter V. Moulder; Richard G. Thompson
Conclusions 1. Total circulatory occlusion alone does not slow the rate of the normother-mic or hypothermic heart. 2. Intracoronary acetylcholine will profoundly decrease the cardiac rate in the occluded heart. The duration of this effect is short at normal body temperatures but quite prolonged during hypothermia (24–27°C). 3. Intracoronary atropine readily reverses the acetylcholine effect on the heart. 4. Cardiac slowing or arrest affords an added protection to the hypothermic heart during total circulatory occlusion.
The Journal of Pediatrics | 1962
Klara J. Prec; Donald E. Cassels; Murray Rabinowitz; Peter V. Moulder
Patent ductus arteriosus in infants under 1 year of age can lead to cardiac failure in the presence or in the absence of a high pulmonary vascular resistance, as exemplified by the findings in 2 infants 8 weeks and 5 months of age. Possible reasons for the development of pulmonary hypertension in one of these infants are discussed. It is suggested that chronic anoxia, resulting from postmaturity with associated placental dysfunction, might be an important etiologic factor in producing alterations of the pulmonary vessels.
American Journal of Cardiology | 1967
Pat O. Daily; Klaus Ranniger; James J. Rams; Peter V. Moulder
Abstract The medical treatment of the acute phase of dissecting hematoma using the therapeutic regimen of Wheat et al. has been described. The apparent resolution of most of the extensive dissection process with this therapy is emphasized and demonstrated angiographically.
Experimental Biology and Medicine | 1949
J. Garrott Allen; Peter V. Moulder; Charles L. McKEEN; Willadene Egner; Richard M. Elghammer; Burton J. Grossman
Summary 1. The platelet concentration influences the sensitivity of bloods and plasmas to the effect of added heparin. The anticoagulant potency of heparin is also enhanced by prothrombin deficiency. The potentiated effect of heparin in thrombocytopenic bloods may be due to reduced thromboplastin (cephalin) activity. 2. The protamine titration may be increased when the platelet count is normal and it may be normal in the presence of thrombocytopenia. It is influenced by heparin, heparinoid substances, prothrombin deficiency, hemophilia, and possibly other factors. 3. Increased protamine titrations may occur in bleeding patients who have no other apparent clotting defects, including the whole blood clotting time. Many of these patients cease bleeding when given intravenous toluidine blue. The protamine titration under these conditions can be returned to or toward normal regardless of the platelet level.