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Skeletal muscle fibers are capable of regeneration following ischemia, traumatic injury, or transplantation. Although the time course of the regenerative process has been studied in detail histologically, little is known about the time of activation of myogenic precursor cells which are primarily responsible for muscle regeneration. This study was designed to determine the initiation, peak proliferative activity, and cessation times of muscle precursor replication in small skeletal muscle transplants. Forty-eight young male BALB/c mice had the extensor digitorum longus muscles of both hind legs autotransplanted to a different site in the same leg. At various time intervals after transplantation (from 24 hours to 14 days), mice were injected once with a small dose of tritiated thymidine in order to label proliferating myogenic precursor cells. The transplants were allowed to regenerate for 14 days, before being removed, processed for autoradiography, and analysed by light microscopy. The presence of labelled myotube nuclei in regenerated transplants showed that myogenic precursors had been replicating at the time of tritiated thymidine injection. Myogenic precursor replication was initiated late on the second day (42-48 hours) after transplantation, peaked after 6 days, and was complete within 10 days.
Anat Rec 1989 May
PMID:Initiation and duration of myogenic precursor cell replication in transplants of intact skeletal muscles: an autoradiographic study in mice. 272 11

In a recent study (Nitz et al., Exp Neurol 94:264-279, 1986) the validity of a rat animal model to examine effects of tourniquet compression and vascular occlusion on limb motor function, leg girth, and electrophysiologic changes was established. Here we report observations on sciatic nerve morphologic and morphometric alterations of these same animals. The hindlimbs of 90 rats were compressed by a pneumatic tourniquet at clinically relevant pressures (200 to 400 mm Hg) for 1 to 3 hours, and the sciatic nerve was assessed by light and electron microscopy at 1, 3, and 6 weeks post compression. The nerves were also examined from five additional animals at each of these time intervals following arterial ligation and sciatic nerve epineurectomy (30 rats). Percentage of degenerating myelinated nerve fibers and volume fraction of mast cells and fibroblasts were quantified morphometrically. The percentage of degenerating myelinated nerve fibers after moderate to severe tourniquet compression and vascular manipulation was similar and ranged from 15% to 45%. Tourniquet compression, but not vascular occlusion, resulted in an increase of mast cells and fibroblasts and disruption of endothelial cells of endoneurial vessels. The results suggest that clinically relevant tourniquet compression causes a secondary increase in vascular permeability, intraneural edema, and subsequent prolonged tissue ischemia, resulting in nerve degeneration.
Anat Rec 1989 Sep
PMID:Structural assessment of rat sciatic nerve following tourniquet compression and vascular manipulation. 277 14

The 40-minute infusion of norepinephrine (NE) into the renal artery of dogs produces a reversible ischemic model of acute renal failure. While the physiology of this model has been extensively studied, no complete description of the pathology exists. This study uses light microscopy and transmission electron microscopy to describe and quantitate the structural and ultrastructural changes which occur in the kidneys of dogs 1, 3, and 24 hours after the intrarenal infusion of 0.75 mg/kg/minute of NE. One hour after a 40-minute NE infusion the majority of convoluted and straight proximal tubules showed apical blebs, loss of brush border, microvillar whorl formation, and mitochondrial condensation and high-amplitude swelling with flocculent densities. Necrotic cells were occasionally seen at 1 hour. The injury was progressive after 3 hours and by 24 hours animals had either complete or partial patchy necrosis of all regions of the proximal tubule. The percentages of injured and necrotic proximal tubules in outer, mid-, and inner cortical regions are presented. We conclude that the extent and pattern of injury seen after NE infusion differs significantly from the renal artery clamping model of ischemia.
Anat Rec 1986 Apr
PMID:Morphology of norepinephrine-induced acute renal failure in the dog. 370 79

This study compares the ultrastructure of beating canine hearts with that of hearts subjected to different clinically common forms of cardiac arrest. The contraction state per test field was ascertained according to a specially developed classification. The volume density of myofibrils and the surface to volume ratio of mitochondria were used as parameters for cellular and mitochondrial swelling. Contraction bands were not found in any of the differently pretreated hearts. Following immersion fixation, contractions as well as over- and hypercontractions in beating, fibrillating, and St. Thomas-arrested hearts are significantly more pronounced than in HTK-arrested hearts. Cellular and mitochondrial volumes were similar in beating and fibrillating hearts. St. Thomas-perfusion significantly decreased cellular and mitochondrial volume compared to beating hearts, but these values were in the same range as in fibrillating hearts. Only HTK-solution actually led to a strong reduction of these compartments. Compared to immersion, perfusion fixation after coronary perfusion with cardioplegic solutions led to comparable cellular volumes, but significantly elevated the percentage of relaxed sarcomeres and significantly reduced mitochondrial swelling. The best structural preservation of myocytes was found after HTK-perfusion and perfusion fixation. Such ultrastructural quantitative and morphometrical parameters are powerful tools since results confirm that the degree of myocardial preservation depends on the method of cardiac arrest. This forms the basis for the choice of preconditions for subsequent ischemia. Furthermore, significant alterations of myocardial ultrastructure depend on a combination of the functional state of the heart, the method of cardioplegia, and the technique of fixation.
Anat Rec 1993 Mar
PMID:Preservation of cardiac myocytes subjected to different preconditions: a comparative morphometric study of beating, fibrillating, and cardioplegically arrested canine hearts. 843 Sep 12

Subarachnoid hemorrhage (SAH) resulting from the rupture of a cerebral aneurysm represents one major cause of stroke. SAH may be followed by a spontaneous severe contraction of major cerebral arteries, a condition referred to as cerebral vasospasm. Vasospasm may result in brain ischemia or actual tissue death. This constrictive vascular state is devastating, remains largely untreatable, and is a major cause of morbidity and mortality in SAH patients. Approximately 30,000 Americans are affected by this condition each year. The overall death rates are 25%, and significant neurological complications occur in 50% of individuals who survive the initial bleed. This report highlights some of the important aspects of this vascular disease.
Anat Rec 1998 04
PMID:Stroke: anatomy of a catastrophic event. 960 61

Early graft dysfunction after lung transplantation is a significant and unpredictable problem. Our study aimed at a detailed investigation of structure-function correlations in a rat isolated heart-lung model ofischemia/ reperfusion injury. Variable degrees of injury were induced by preservation with potassium-modified Euro-Collins solutions, 2 hr of cold ischemia, and 40 min of reperfusion. Pulmonary artery pressure (Ppa), pulmonary vascular resistance (PVR), peak inspiratory pressure (PIP), and perfusate gases (deltaPO2, deltaPCO2) were recorded during reperfusion. Right lungs were used to calculate W/D-weight ratios. Nineteen experimental and six control left lungs were fixed for light and electron microscopy by vascular perfusion. Systematic random samples were analyzed by stereology to determine absolute and relative volumes of lung structures, the amount of interstitial and intraalveolar edema, and the extent of epithelial injury. Lectin- and immunohistochemistry using established epithelial cell markers were performed in three animals per group to reveal sites of severe focal damage. Experimental lungs showed a wide range in severity of ischemia/ reperfusion injury. Intraalveolar edema fluid amounted to 77-909 mm3 with a mean of 448+/-250 mm3 as compared with 22+/-22 mm3 in control lungs (P<0.001). Perfusate oxygenation (deltaPO2) decreased from 30.5+/-15.2 to 21.7+/-15.2 mm Hg (P=0.05) recorded after 5 and 40 minutes of reperfusion. In experimental lungs, a surface fraction of 1% to 58% of total type I pneumocyte surface was damaged. Intraalveolar edema per gas exchange region (Vv ape,P) and deltaPO2 were related according to deltaPO2 = 96 - 60 x log10(Vv ape,P) [mm Hg]. The extent of epithelial injury did not correlate with deltaPO2 nor with intraalveolar edema, but increased significantly with PVR. Lectin- and immunohistochemistry revealed focal severe damage to the alveolar epithelium at the border of perivascular cuffs.
Anat Rec 1999 05 01
PMID:Pulmonary ischemia/reperfusion injury: a quantitative study of structure and function in isolated heart-lungs of the rat. 1032 96

Angiogenesis, the formation of vessels from pre-existing vessels, is of critical importance not only during normal growth, but also in pathological situations. In the latter, some diseases are enhanced by excessive vascular growth (e.g., tumors), whereas in others inadequate vascular growth contributes to morbidity and mortality (e. g., ischemic heart disease). Our current state of knowledge makes it clear that the cascade of angiogenic events depends on complex processes that include cell-cell interactions, various intracellular signaling pathways, and the appropriate extracellular microenvironment. The literature regarding angiogenesis has increased exponentially during the last decade. Progress in this area is largely a consequence of advances in our understanding of angiogenic growth factor and cytokine function, in part due to the determination of their complete amino acid sequences and cloning of their genes. Other factors also play key roles in angiogenesis, including the extracellular matrix, adhesion molecules and their inhibitors, and metabolic and mechanical factors. The potential for developing therapeutic protocols has been enhanced by data from both in vitro and in vivo studies and has provided the rationale for clinic trials. Angiogenic therapy strategies include inhibition of aberrant angiogenesis, as seen in tumors or diabetes, as well as stimulation of angiogenesis in conditions of ischemia, such as ischemic heart or peripheral vascular disease. Anat Rec (New Anat) 261:126-135, 2000.
Anat Rec 2000 06 15
PMID:Angiogenesis: new insights and therapeutic potential. 1086 30

Two types of sinus nodal cells were responsible for the main differences in the literature concerning the ultrastructure of the sinuatrial node: the intercalated clear cells and pale cells. Canine hearts were arrested by (1) aortic cross clamping, (2) coronary perfusion with the cardioplegic solution St. Thomas, and (3) coronary perfusion with the cardioplegic solution HTK (Custodiol(R)). After fixation by immersion or perfusion the sinus node tissue was prepared for electron microscopy. Following cardioplegic arrest and perfusion fixation, three nodal cell types in the non-ischemic sinuatrial node were observed: typical nodal cells, transitional cells, and intercalated clear cells. Less than 1% of the non-ischemic sinuatrial cells were intercalated clear cells, surrounded by typical nodal cells or transitional cells. The contractile apparatus of the intercalated clear cells was extremely poorly developed. Great structural variations in the mitochondria were observed in intercalated clear cells, variations that would not appear under conditions of ischemia. In contrast, after 15-25 min of ischemia at 25 degrees C the appearance of the sinus nodal cells was strikingly different from that of the non-ischemic sinuatrial cells. More than 10% of the nodal cells showed typical ischemic alterations, e.g., mitochondrial swelling, clumping of nuclear chromatin, loss of glycogen particles, and cell swelling in varying degrees. Because they look very pale, these nodal cells have been described as pale cells in the literature. Intercalated clear cells appear mainly in non-ischemic nodal tissue. Pale cells are ischemically damaged sinus nodal cells.
Anat Rec 2000 09 01
PMID:Intercalated clear cells or pale cells in the sinus node of canine hearts? An ultrastructural study. 1096 34

It has been shown that QT dispersion (QTD) increases during episodes of myocardial ischemia or infarction. However, no extensive data on the relation between the diseased coronary artery or the localization of stenosis and the QTD are available. The aim of the study was to examine the relation between QTD and diseased coronary artery and lesion localization during exercise stress test in patients with single coronary artery disease without prior myocardial infarction. One hundred nineteen patients with single coronary artery disease and 53 patients with normal coronary arteries were enrolled in study. All patients underwent exercise stress test with modified Bruce protocol, and QT interval parameters were measured at rest and at minute 2 of the recovery (rec-2) period. QT dispersion at rest was found higher in all single-vessel disease groups compared with that in the control group, and corrected QT dispersion at rec-2 period was also markedly higher in left anterior descending, circumflex, and right coronary artery groups compared with that in the control group. No relation was found between QT dispersion and diseased coronary artery or the lesion localization. In conclusion, no qualitative difference was found between QT dispersion and diseased coronary artery or proximal or distal lesion localization. However, it was observed that patients with single-vessel disease had wider baseline QT dispersion as compared with that in the control group, which further increased significantly with exercise. This finding supports the idea that severity of localized ischemia rather than extent of coronary artery disease would be expected to have a greater effect on inducible QT dispersion.
 ...
PMID:QT dispersion in single coronary artery disease: is there a relation between QT dispersion and diseased coronary artery or lesion localization? 1120 30

Alterations in pulmonary surfactant have been reported to be associated with ischemia/reperfusion injury in experimental and clinical lung transplantation. It is unknown whether these alterations are due to damage to surfactant synthesizing type II pneumocytes during hypothermic ischemic storage. The aim of the present study was to examine the effects of hypothermic ischemic storage of the lung on canine type II pneumocytes by means of conventional (CTEM) and energy filtering TEM (EFTEM) and stereology. The lungs of 18 dogs were fixed for TEM immediately after cardiac arrest (6 double lungs) and after storage in Tutofusin at 4 degrees C for 20 min, 4 hr, 8 hr, and 12 hr (6 single lungs, respectively). Using a systematic uniform random sampling scheme, type II pneumocytes were analyzed qualitatively and stereologically. The relative phosphorus content of cell organelles, especially the surfactant containing lamellar bodies, was investigated by EFTEM. By CTEM, no major qualitative alterations could be observed in type II pneumocytes of the experimental groups. Stereologically, no significant changes in the volume densities or the volume-to-surface ratios of type II pneumocytes and their lamellar bodies were found. By EFTEM, the highest intracellular phosphorus signals were recorded over lamellar bodies in all experimental groups. No changes in the phosphorus signals were observed during ischemia. These results indicate that the ultrastructure of canine type II pneumocytes and their lamellar bodies is not affected by hypothermic ischemia of the lung up to 12 hr. Structural preservation of intracellular surfactant is possible during prolonged ischemic lung storage.
Anat Rec 2001 06 01
PMID:Ultrastructure of canine type II pneumocytes during hypothermic ischemia of the lung: a study by means of conventional and energy filtering transmission electron microscopy and stereology. 1136 Feb 29


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