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Biomedical subjects

J T Lie

Publications and source records attributed to J T Lie.

At least 271 records · Page 15Linked to original sources
PubMed1976

Ultrastructure of ischemic contracture of the left ventricle ("stone heart").

Myocardial biopsies from two patients who had developed "stone heart" (myocardial rigor mortis; ischemic contracture of the left ventricle) were studied by electron microscopy. The ultrastructure of tissue in stone heart, though ischemic in nature, differed from that of classic myocardial infarction in some respects. Apart from depletion of glycogen and distension of the sarcoplasmic reticulum and T-tubules, myofibrillar degeneration was much more widespread. Mitochondrial degeneration with active lysosomal autodigestion, disruption of the microcirculation, and lymphedema were prominent changes also observed. In the light of known clinical and experimental observations, our findings suggest that stone heart is an accelerated form of ischemic injury occurring in vulnerable (hypertrophied) hearts and is probably related to ischemia-triggered release of endogenous catecholamines.

Capillaries↗
PubMed1976

Energy dose for ventricular defibrillation of children.

Transthoracic direct current shock is the recommended treatment for ventricular fibrillation in children as in adults. To determine the appropriate energy dose, data were collected from 71 defibrillation attempts in 27 children. Sixty-three of the 71 shocks (89%) were successful in terminating fibrillation. Fifty-seven shocks were within 10 watt-seconds (w-sec) above or below an energy dose of 2 w-sec/kg of body weight. Fifty-two (91%) of these were effective and five (9%) were ineffective. In every case, fibrillation was ultimately terminated by a shock of 4 w-sec/kg or less. The results of these studies suggest that an energy dose of 2 w-sec/kg (or approximately 1 w-sec/lb) is adequate to defibrillate most children weighing under 50 kg. We currently use 2 w-sec/kg and double the energy dose if the first defibrillation attempt is unsuccessful.

Adolescent↗
PubMed1975

Juvenile temporal arteritis. Biopsy study of four cases.

Two young adults (aged 21 and 22 years) and two children (aged 7 and 8 years) complained of an unsightly, soft, painless unilateral nodule in the temporal region, ranging from 0.5 to 1.5 cm in diameter, clinically diagnosed as lipoma, sebaceous cyst, or dermoid cyst. In each instance, the patient had no evidence of systemic disease or history of trauma, and the nodule was excised for cosmetic reasons. Histologic examination of the lesions showed non-giant-cell granulomatous inflammation of the temporal arteries with intimal proliferation and microaneurysmal disruption of the media. Whether the lesions represent a juvenile form of temporal arteritis, an unusual form of localized polyarteritis nodosa, or Kimura disease (subcutaneous angiolymphoid hyperplasia with eosinophilia) remains conjectural.

Adult↗
PubMed1975

Histopathology of the conduction system in sudden death from coronary heart disease.

Sudden cardiac death (SCD) has been attributed to the development of lethal dysrhythmias in coronary heart disease victims, and several recent autopsy surveys showed that 10 to 50% of SCD patients had unsuspected acute myocardial infarction (AMI). The present study concerned histopathological findings of the conduction system in 49 SCD (within six hours of the onset of acute symptoms) patients; 39 with established AMI (group A) and ten without (group B). Both groups showed high incidence of cardiomegaly, significant coronary artery disease affecting one or more vessels, and acute myocardial ischemia detectable by specific histological criteria. Stenosis of nutrient vessels of the conduction system was present in about 50% of the atrioventricular (A-V) node arteries and about 25% of the sinoatrial (SA) node arteries in both groups of SCD patients. Nonspecific "degenerative" changes (fibrosis, fatty infiltration, or both) of the conduction tissue, which might or might not represent results of old ischemic injury, also occurred with similar frequencies. Acute changes (infarction, hemorrhage) of the A-V node and bundle branches were found only in two group A patients, both had massive septal infarction. Thus, the conduction tissue appeared more resistant to ischemic injury and was overtly damaged only on rare occasions in fatal AMI. The scarcity of acute lesions in the conduction system itself suggested that lethal dysrhythmia in SCD was probably due to electrical instability of the acutely ischemic contractile myocardium rather than a direct injury to the specialized tissue of the heart.

Atrioventricular Node↗
PubMed1975

Modification of ventricular fibrillation latency following coronary artery occlusion in the conscious pig.

Abrupt occlusion of the left anterior descending coronary artery was performed on 45 unanesthetized farm pigs in order to evaluate the relative effects on the latency to ventricular fibrillation (VFL) of 1) adaptation of the animals to the laboratory, and 2) beta-receptor blockade by propranolol. Compared to control values, VFL was greatly lengthened (i.e., VF delayed or prevented) by adaptation (P smaller than 0.01), was shortened by large (2 MG/KG) doses of racemic propranolol in unadapted animals (P smaller than 0.02), and was again increased while under the influence of the drug, by adaptation (P smaller than 0.051). Neither a lower (0.02 mg/kg) dose of racemic propranolol, 2 mg/kg of dextropropranolol, nor ventricular pacing to a higher heart rate had an effect on VFL. The results suggest that reduced psychological stress was very effective in retarding or preventing the onset of VF, that low doses of propranolol were ineffective, and that higher doses were deleterious in unadapted animals.

Adaptation, Physiological↗
PubMed1975

Time course and zonal variations of ischemia-induced myocardial cationic electrolyte derangements.

Myocardial cationic electrolytes were determined at regular time intervals up to 24 hours after coronary artery ligation in the dog. Replicate electrolyte ratios were computed for different areas of the heart at each time interval. For purposes of statistical analysis, ratios from two border areas and four areas remote from the infarct were pooled as values for ZONE B and ZONE N, respectively, and compared with those from the infarct proper, ZONE I. Ischemia-induced tissue Mg++/Ca++ changes paralleled those of K+/Na+ with respect to time course and zonal variations. In ZONE I, both K+/Na+ and Mg++/Ca++ fell precipitously during the first hour, and the falls became more gradual thereafter, approac hing those of extracellular fluid at 24 hours. Changes in ZONE B, which appeared normal histologically, followed a similar downward trend but differed in magnitude from those in ZONE I (P smaller than 0.01). Changes in ZONE N were small but did not always overlap values in sham-operated dogs. It was concluded that lowered tissue K+/Na+ and Mg++/Ca++ were sensitive, but not specific, indices of myocardial ishemia, and multiple samplings of ionic ratios were essential for proper interpretation of ischemia-induced myocardial electrolyte derangements.

Animals↗
PubMed1975

Extracellular glomerular microparticles in nephrotic syndrome of heroin users.

Intracellular and extracellular glomerular microparticles (GMP) have been described in diverse human glomerulopathies. We have recently detected extracellular GMP in two heroin abusers with nephrotic syndrome. Most of the GMP were approximately 100 nm in diameter (range, 56 to 178 nm), and consisted ultrastructurally of an electron-dense central core surrounded by a concentric, lucent area and an electron-dense limiting membrane. Incomplete forms of GMP and residual laminated membranes without a central core were also present. The distribution of extracellular GMP was both intramembranous and subepithelial; they did not resemble virions morphologically. As these GMP have been observed in human glomerulopathies that are etiologically and morphologically varied, they probably represent nonspecific markers of glomerular injury. The prevalence of GMP in the nephrotic syndrome of heroin abusers awaits cumulative experience.

Adult↗
PubMed1975

Macroscopic enzyme-mapping verification of large, homogeneous, experimental myocardial infarcts of predictable size and location in dogs.

Difficulty is frequently experienced in producing a large homogeneous myocardial infarct in the dog heart because of the extensive network of coronary anastomoses. This problem may be overcome by combining the ligation of the left anterior descending coronary artery with agar injection into the distal coronary vasculature to obliterate anastomotic channels. All infarcts produced in this manner occupied a constant area in the anterior wall of the left ventricle. From our results in 25 dogs, the individual infarct averaged 12.3 Gm. in weight (range 9.4 to 13.5), representing 25 to 30 per cent of the total left ventricular muscle mass. The homogeneity of the infarct was verified by a simple, macroscopic enzyme-mapping technique based on the inability of the ischemic (dehydrogenase-deficient) myocardium to reduce triphenyl tetrazolium chloride and by detailed histologic studies. Apart from providing ample raw material for comprehensive morphologic, chemical, histochemical, and radioisotopic analyses, a large myocardial infarct also serves as a useful experimental model for various physiological and hemodynamic studies of cardiogenic shock and left ventricular akinesis.

Agar↗
PubMed1975

Pathology of the myocardium and the conduction system in sudden coronary death.

This review summarizes previously unpublished and recently published autopsy findings of prehospital sudden coronary death (SCD) in four different counties (Olmsted, Minnesota; Albany, New York; Dade, Florida; and San Francisco Bay Area, California), totaling 868 patients. The prevalence of cardiomegaly and significant coronary atherosclerosis, and the relative infrequency of acute coronary thrombosis in prehospital SCD, well documented in the past, have been reaffirmed in current studies. Differences in the patient populations and laboratory techniques notwithstanding, these independent autopsy studies showed that 62% to 74% of cases of SCD had either acute or old myocardial infarction (MI); the incidence of acute MI ranged from 12% to 47%, and that of old MI from 22% to 53%. The prospective autopsy study of 120 Olmsted County SCD cases showed that among those with established acute MI, subendocardial lesions outnumbered transmural lesions by the ratio of 2:1, and the infarcts ranged in histological age from less than 24 hours to 4 weeks. Evidence of acute myocardial ischemia, as determined by the histological criteria of myofibrillar degeneration, sinuous fibers, and positive HBFP staining, was present in 52% to 81% of patients. Such high incidence of myocardial ischemia is compatible with the proposed mechanism of the terminal event in SCD, namely ventricular fibrillation or asystole, and underscores the importance of presymptomatic diagnosis of coronary heart disease. The lack of specific or acute anatomical lesions in the conduction system in SCD, however, does not preclude the possibility of bradyarrhythmias occurring shortly before death.

Acute Disease↗
PubMed1975

Lipoproteins in atherosclerotic lesions. Localization by immunofluorescence of apo-low density lipoproteins in human atherosclerotic arteries from normal and hyperlipoproteinemics.

Using immunofluorescence techniques, apoLDL, the major protein component of human plasma low and very low density lipoproteins was localized in athersclerotic lesions from the aorta, coronary, and carotid arteries in human normolipoproteinemic, type II, and type IV hyperlipoproteinemics. Although no apoLDL was detected in uninvolved arteries, atheromas from advanced lesions as well as certain collagen and elastic fibers from both fatty streaks and advanced lesions were positive for apoLDL. This localization pattern was the same in each lipemic group, except for the presence of apoLDL in some intimal cells from type II cases. However, extensiveness of apoLDL localization was greatest in the type II group, but equal in the normolipemic and type II group. This may be explained by the high concentration gradient between plasma and tissue for apoLDL in the type II group.

Adult↗
PubMed1975

The fate of internal mammary arterial implants and bypass conduits for myocardial revascularization. Experimental angiographic, histologic, and ultrastructural observations.

Experimental angiographic, histologic, and ultrastructural observations were obtained from dogs to determine the fate of internal mammary artery (IMA) implants and aorta-coronary bypass (ACB) conduits in the 3 month postoperative period. Angiographic implant patency and evidence of implants forming collaterals with the coronary circulation did not accurately reflect anatomic luminal narrowing. Subendothelial fibrocellular proliferation similar to that described in saphenous vein grafts occurred with regularity in all IMA implants and ACB conduits. The intimal changes were much more severe in the IMA implants as compared to the ACB conduits: There was 25 to 95 per cent liminal narrowing in the IMA implants, whereas the ACB conduits rarely showed greater than 25 per cent luminal narrowing. Both reduced flow and surgical trauma appeared to be influential determining factors of the intimal proliferative process, whereas devascularization alone seemed less important.

Animals↗