Eric A. Schenk

HISTOCHEMICAL METHODS FOR SEPARATE, CONSECUTIVE AND SIMULTANEOUS DEMONSTRATION OF ACETYLCHOLINESTERASE AND NOREPINEPHRINE IN CRYOSTAT SECTIONS

Techniques for the separate, consecutive and simultaneous demonstration of acetylcholinesterase and norepinephrine in cryostat sections are described and discussed. The results, obtained in a variety of tissues from different animal species, are as satisfactory—in terms of sensitivity and sharpness of localization—as those obtained by previously described methods. The simultaneous visualization of both acetylcholinesterase and norepinephrine in the same section provides hitherto unavailable data relative to the exact interrelationship of cholinergic and adrenergic components of the peripheral autonomic nervous system.

Autonomic innervation of the rat vagina, cervix, and uterus and its cyclic variation

Specific histochemical methods for norepinephrine and for acetylcholinesterase have been used to delineate the pattern of autonomic innervation of the rat vagina, cervix, and uterus. A dual innervation is present in the adventitia, muscularis, and mucosa of these structures, and plexuses of varying complexity are associated with smooth muscle, blood vessels, and glands. Cholinergic fibers are seen in the surface epithelium. Adrenergic and cholinergic ganglion cells are present within ganglia and as isolated cells. The density of the adrenergic and cholinergic innervation has been found to be most prominent during estrus and least so during diestrus.

Cardiovascular Effects of Sustained Norepinephrine Infusions. II. Morphology

The major toxic effect of norepinephrine (NE) infusion in dogs, cats, and rabbits in doses relatively comparable to those used clinically has been shown to be on the heart. Noncardiac lesions were those of congestion, and were seen in animals receiving the higher doses. The dogs in these dose groups showed evidence of progressive deterioration of cardiac function. All dogs which developed cardiac lesions also developed an acute adrenalitis. The cardiac lesions in all animals consisted of focal degeneration and necrosis of myofibers, and subendocardial hemorrhage. These lesions healed within two weeks by fibrosis.

Human anticentromere antibodies: Distribution, characterization of antigens, and effect on microtubule organization

Properties of human anticentromere autoantibodies were analyzed. In intact cells or isolated cell fractions, these sera stain the centromeres of mitotic chromosomes and discrete speckles (prekinetochores) in nuclei. Staining is also retained in matrix preparations from nuclei or chromosomes. Immunoprecipitation or immunoblotting demonstrates protein antigens of 14, 20, 23, and 34 kd in HeLa nuclei and chromosomes; immunoprecipitates of nuclei also contain a protein of 15.5 kd. Matrix preparations contain only the 20, 23, and 34 kd species. Absorption of the anticentromere serum with any one of the four nuclear antigens immobilized on nitrocellulose is sufficient to eliminate centromere staining. Using a lysed cell model for microtubule nucleation, anticentromere sera are shown to inhibit specifically the organization of microtubules at the kinetochore.

Dual innervation of arteries and arterioles

SummarySpecific histochemical techniques for the demonstration of acetylcholinesterase and of norepinephrine have been used to study the distribution of cholinergic and adrenergic nerve fibers to arteries and arterioles in various organs of cats and dogs, including the male genital apparatus, tongue, skeletal muscle, heart and gastrointestinal tract. Arteries and arterioles in all of these organs showed both cholinergic and adrenergic nerve fibers, although the relative number of each of the types of fiber was variable. The findings provide morphologic evidence for a widespread and generalized dual adrenergic and cholinergic innervation of arteries and arterioles.

Tricuspid candida endocarditis complicating a permanently implanted transvenous pacemaker

Abstract The first reported case of tricuspid candida endocarditis which developed in association with a permanently implanted transvenous pacemaker is described. The patient died ten months after pacemaker implantation, and his terminal illness was characterized by congestive heart failure, fever, leukocytosis, and seven negative blood cultures. At autopsy, a large monilial vegetation was attached to the right atrial wall, involved and partially obstructed the tricuspid valve, and extended into the inferior vena cava. Histologic examination of the vegetations, the heart, the lung, and the kidney revealed the presence of candida organisms.

Pepsin secretion, pepsinogen, and gastrin in "Barrett's esophagus." Clinical and morphological characteristics.

Four cases of Barretts esophagus are presented. Three cases presented with significant esophageal bleeding and one case presented with high esophageal stricture. Gastrointestinal panendoscopy was done in each case and multiple biopsies were taken. The biopsies were utilized for histomorphology, pepsinogen agar gel electrophoresis, and tissue gastrin assays. Tissue gastrin levels in esophageal mucosa were elevated in 2 cases when compared to controls with and without hiatus hernia. Pepsin and acid secretory studies were done by isolating the esophagus. Barretts esophagus was shown to produce pepsin by both chemical studies (2 cases) and agar gel electrophoresis at pH 5.7 (3 cases), and was also shown to produce acid. The mucosa contained either cathepsin or cathepsin and pepsinogens in all cases. Nissens fundoplication was performed in all of the patients. Of 3 patients who were bleeding, 2 who consented for this operation stopped bleeding after the operation. It is to be noted that the usual clinical treatment of antacids, bedrest, and raising the head end of the bed failed in all of the patients. The follow-up of 9 months to 3 years postoperatively has shown persistence of Barretts mucosa with no evidence for any reversion to normal esophageal type.

Ability of high-intensity ultrasound to ablate human atherosclerotic plaques and minimize debris size.

To investigate whether high-intensity ultrasound can destroy atherosclerotic plaques while sparing the normal arterial wall, 279 normal human aortic sites and 119 fibrous and 193 calcified plaques, obtained from 24 necropsies, were insonified in a water tank, at 20 kHz and at 5 different power intensities, ranging from 68 W/cm2 (P1) to 150 W/cm2 (P5). These intensities were associated with a total excursion of the ultrasound irradiation apparatus tip from 90 to 268 microns, respectively. Time to perforate normal aortic sites and fibrous and calcified plaques was recorded at each intensity. There was no difference in perforation time between normal aortic sites and fibrous and calcified plaques when high-power levels (P2 to P5) were used. However, at the lowest power (P1), perforation time for the normal aortic wall was significantly longer than for fibrous and calcified plaques: 30 +/- 18 seconds (166 observations), 14 +/- 7 seconds (p less than 0.001) (78 observations) and 12 +/- 8 seconds (p less than 0.001) (115 observations), respectively. When perforation times for normal vessel wall versus fibrous plaque and normal vessel wall versus calcified plaque from the same necropsy specimen were compared in a pairwise manner, the results were: 29 +/- 13 vs 16 +/- 7 (p less than 0.001) (48 paired observations) and 26 +/- 9 vs 10 +/- 5 seconds (p less than 0.001) (55 paired observations), respectively. Regardless of whether paired or unpaired comparison was applied, no significant difference was found in perforation time between fibrous and calcified plaques. The debris did not differ in size as measured separately for normal sites and fibrous and calcified plaques by a computer-interfaced Channelizer and Coulter Counter system.(ABSTRACT TRUNCATED AT 250 WORDS)

Ultrasonic Detection of Myocardial Infarction by Amplitude Analysis

Myocardial infarctions were produced in dogs by occluding the left anterior descending artery; the dogs were killed at varying times, from 30 minutes to 8 days. Prior to sacrifice, Thioflavin S was injected intravenously. The excised heart was scanned by a B-scanner interfaced with a computer that permitted quantification of signal amplitude. The heart was sectioned, photographed, and studied pathologically. Infarcted myocardium showed high ultrasonic reflectivity with average amplitudes 1.4--2.6 times that of normal muscle. Perfusion-histomorphologic evidence of infarction correlated best in infarcts of 24 hours or less; older infarcts were generally underestimated. Tissue changes, sources of false-positive and false-negative findings, signal processing, and potential clinical utility are discussed.

PRESSURE THRESHOLD FOR SHOCK WAVE INDUCED RENAL HEMORRHAGE

Studies were performed with an interest in determining a pressure threshold for extracorporeal shock wave induced renal damage. Histological evidence of intraparenchymal hemorrhage was used as an indicator of tissue trauma. Depilated C3H mice were anesthetized and placed on a special frame to enhance visualization and treatment of the kidneys in situ. A Wolf electrohydraulic generator and 9 French probe designed for endoscopic use were utilized to expose the kidneys to 10 double spherically divergent shock waves. Measurements of the shock waves revealed two positive pressure peaks of similar magnitude for each spark discharge. The kidneys were exposed to different peak pressures by choice of distance from the spark source and were removed immediately after treatment for histologic processing. A dose response was noted with severe corticomedullary damage apparent following 15 to 20 MPa shocks. Hemorrhage was more apparent in the medulla where evidence of damage could be seen following pressures as low as three to five MPa. When a latex membrane was interposed to prevent possible collapse of the initial bubble from the spark source against the skin surface, histological evaluation revealed substantial reduction of severe tissue damage associated with the highest pressures tested, 20 MPa. However, the threshold level for evidence of hemorrhage remained about three to five MPa. Hydrophonic measurements indicated that the membrane allowed transmission of the acoustic shock waves and suggested that collapse of the bubble generated by electrohydraulic probes may have local effects due to a cavitation-like mechanism.