Thyroid hormones differentially affect sarcoplasmic reticulum function in rat atria and ventricles

We have recently reported that the short-acting anesthetic and analgesic drug midazolam can produce analgesia and decrease morphine tolerance and dependence in the rat by interacting with the opioid system. This study was designed to investigate the effect of midazolam, morphine, and both together on met-enkephalin levels in the rat. Male Sprague-Dawley rats were divided into four groups: (1) saline-saline; (2) saline-morphine; (3) midazolam-saline, and (4) midazolam-morphine groups. First, a saline or midazolam injection was given intraperitoneally and after 30 min a second injection of saline or morphine was given subcutaneously once daily for 11 days. Animals were sacrificed on the 11th day 60 min after the last injection to measure met-enkephalin by radioimmunoassay. Morphine tolerant animals showed a significant increase in met-enkephalin levels in the cortex (137%) and midbrain (89%), and a significant decrease in met-enkephalin levels in the pituitary (74%), cerebellum (34%) and medulla (72%). Midazolam treated animals showed a significant decrease in met-enkephalin levels in the pituitary (63%), cortex (39%), medulla (58%), kidneys (36%), heart (36%) and adrenals (43%), and a significant increase in met-enkephalin levels in the striatum (54%) and pons (51%). When morphine and midazolam were injected together, midazolam antagonized the increase in met-enkephalin levels in cortex and midbrain region and the decrease in met-enkephalin level in the medulla region observed in morphine tolerant animals. These results indicate that morphine tolerance and dependence is associated with changes in the concentration of met-enkephalin in the brain. Midazolam may inhibit morphine tolerance and dependence by reversing some of the changes induced in met-enkephalin levels in brain by morphine in morphine tolerant and dependent animals.     

Modification and abolition of re-entry within the His-Purkinje system in man by diphenylhydantoin

The phenomenon of macrore-entry (Re) within the His-Purkinje system (HPS) was consistently observed in 10 of 19 patients during retrograde refractory period studies. Effects of intravenous infusion of diphenylhydantoin (DPH) on Re were studied in these 10 patients 10 minutes after completion of infusion (mean plasma level equal to 17.0 microgram/ml). Diphenylhydantoin modified determinants of Re in seven patients (group I) and abolished Re in the remaining three patients (group II). In group I, DPH shortened the critical V1 V2 from 310.0 +/- 30.5 to 292.9 +/- 25.6 msec (P less than 0.025) and critical V2 H2 intervals for Re from 201.4 +/- 18.4 to 185.0 +/- 13.8 msec (P greater than 0.05). In group II, DPH abolished Re in two of three patients by precluding attainment of critical V2 H2 intervals whereas Re was abolished in the remaining one patient despite attainment of critical V2 H2 intervals (vs control). For both groups, DPH significantly shortened functional and effective refractory periods of the HPS (P less than 0.001 and less than 0.01, respectively) without significantly affecting the effective refractory period of the ventricular muscle. Diphenylhydantoin either completely abolished or significantly shortened the retrograde gap zones in the HPS. It is concluded that diphenylhydantoin significantly shortens His-Purkinje system refractoriness, abolishing Re in the patients with higher degree of improvement in refractoriness.     

Intractable paroxysmal tachycardia caused by a concealed retrogradely conducting Kent bundle. Demonstration by epicardial mapping and cure of tachycardias by surgical interruption of the His bundle

Electrophysiological and epicardial mapping studies are described in a patient without pre-excitation who had intractable recurrent paroxysmal supraventricular tachycardia. Electrophysiological studies revealed fixed VA conduction times during both rapid ventricular pacing and coupled ventricular stimulation. Catheter mapping of atrial activation during retrograde conduction and during induced paroxysmal supraventricular tachycardia revealed early distal coronary sinus activation (posterior left atrium) relative to the low septal, low lateral, and high lateral right atrium. These studies suggested the presence of a concealed left-sided bypass tract. The patient underwent surgical interruption of the His bundle for control of paroxysmal supraventricular tachycardia. Epicardial mapping of the atria (during ventricular pacing) confirmed the presence of a concealed left-sided bypass tract. Surgery produced antegrade av block (while retrograde conduction was maintained) and total cure of paroxysmal supraventricular tachycardia. This is the first reported case of a concealed retrograde extranodal pathway documented by epicardial mapping.     

Changing activation sequence in the embryonic chick heart. Implications for the development of the His-Purkinje system

Viruses that establish persistent infections in their host, such as herpesviruses, adenoviruses or HIV, express proteins designed to pre-empt or evade recognition and elimination by MHC class I restricted CD8+ T lymphocytes. Notable discoveries during the annual period of review have demonstrated that, in principle, each single step within the MHC class I pathway of antigen processing and presentation is fair game for manipulation by viral functions. The viral factors that are natural inhibitors of this pathway have been instrumental for the elucidation of the distinct molecular mechanisms that are exploited by viruses. The viral stealth strategies that downregulate MHC class I protein surface expression may lead, however, to a higher susceptibility of virus-infected cells to natural killer cell activity. Strikingly, there is evidence that some viruses counteract increased natural killer cell recognition by expressing viral MHC class I homologues that function as surrogate inhibitors of natural killer cell activity.     

Myocardial morphology in fibrillation and defibrillation of the heart ventricles

The morphology of the contractile myocardium was studied experimentally in fibrillation and defibrillation of the ventricles on 30 rabbits. Morphology of the contractile myocardium appears as vacuolated dystrophy of the cardiomyocytes, destruction of mitochondria and contracture lesions of the myofibrils. The latter with progressing fibrillation become irreversible. Myocardial changes are related both to the mechanical lesions of cardiomyocytes and the haemodynamic disorders, developing as a result of ventricular fibrillation, which leads to marked myocardial hypoxia. The changes in the microcirculatory bed contribute to the development of the latter. Hyperfunction of the intracellular structures, especially of mitochondria and myofibrils, taking place under unfavourable conditions leads to a rapid energy depletion, which is one of the main causes of development of the acute cardiac insufficiency in this type of arrhythmias. Studies of cardiac defibrillation enabled one to elicit the dynamics of morphological changes, appearing in the myocardium as related to the duration of ventricular fibrillation.     

NADPH diaphorase-positive neurons in the intracardiac plexus of human, monkey and canine right atria

Distribution of nitric oxide synthase in intracardiac ganglion cells located in human, monkey and canine right atria was histologically investigated using the reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase method and acetylcholinesterase histochemistry. In the intracardiac ganglion, many large neurons exhibited both positive reactions, whereas some of the NADPH diaphorase-positive small neuronal cells were shown with negative acetylcholinesterase reaction.     

Newly occurring stenocardia: the clinical picture, diagnosis, treatment and prognosis

The article analyses the results of treatment of 77 patients with primarily emerged stenocardia. Three variants of clinical course of illness were distinguished: primarily emerged stenocardia at the state of exertion, primarily emerged progressive stenocardia at the state of exertion, primarily emerged stenocardia at rest state. As for primarily emerged stenocardia at the state of exertion, the changes at the final part of QRS complex were disclosed in 56% of patients, and abnormalities in the mobility of the left ventricle walls in 32%. The contractive function of left ventricle was unchanged. The myocardial infarction developed in 8% of patients in the course of one month, and in 4% in the course of one year. Stenocardia attacks disappeared in 16% of patients. As for primarily emerged progressive stenocardia, the ECG changes were marked in 74% of cases. The whole sphygmic fraction in 65% of patients was 55% lower. The myocardial infarction developed in 12% of patients in the course of one month and in 10.7% in more remote period. 52% of patients with the primarily emerged stenocardia at rest had ECG changes. In ECG daily monitoring 33% of patients had characteristic changes of coronary artery spasm. Myocardial infarction occurred in 8% of patients in the course of the first year. Stenocardia attacks disappeared in 25% of patients.     

Experimental and clinical data on the state of the atria in postinfarct cardiosclerosis

In 16 rabbit experiments with macrofocal postinfarction cardiosclerosis and 8 control intact animals delayed electron microscopy of myocardium portions from the left ventricle and atria was undertaken, and in 76 clinical observations of patients who had survived a myocardial infarction 1 to 10 years before the examination the indices of the haemodynamic and electrical activity of the atria were compared with those of the contractile function of the left ventricular myocardium under bicycle exercise tests of a growing intensity (with the data of the left ventricular ultrastructure--in the experimental cases). The changes in the left atrium were found to be of an adaptational nature, the right atrium entering the pathogenetic chain when the compensatory capacities of the left atrium got exhausted in the course of the disease, this being a prognostically alerting sign.     

Incorporation of 3H-thymidine into the cells of the heart conduction system (sinoatrial and atrioventricular nodes, bundle of His) during cardiogenesis in mice

The number of DNA synthesizing myocytes in the conductive system, as compared with the working myocardium, was determined by means of light autoradiography. At the same time the number of mitosing cells was counted. The indices of labelled nuclei in the sinoatrial and atrioventricular nodes of the embryos after the single and repeated 3H-thymidine injections were significantly lower than in the working ventricle and atrium. During the postnatal development (3-11 days) only in the sinoatrial node the index of labelled nuclei was significantly lower than in the working ventricle. The proliferative activity in all the myocardium parts fell markedly by the 13th day of development. Following 10 3H-thymidine injections with 12 hrs intervals, the indices of labelled nuclei varied from 0.03 to 0.67% in the working ventricle and atrium and from 0.13 to 1.0% in the conductive system of adult mice. During the embryogenesis the index of labelled nuclei in the sinoatrial node was significantly higher than in the atrioventricular one and during the postnatal development-vice versa.     

Anterolateral muscle bundle of the left ventricle, bulboventricular flange and subaortic stenosis

Materials of an experimental study on allergenic properties of prolonged-action sulfanilamides and their semi-products are presented. Investigations involved the use of express-methods with intradermal administration of the substance into the ear and introduction of the agents together with the Freind adjuvant into the hind paw pad of a guinea pig. Experiments ascertained satisfactory dermal-allergic responses to the introduction of allergens differing in their strength by employing the above methods, as express ones for primary evaluation tof allergenic properties of drugs and their semi-products in conducting toxicological investigations.     

Parallel study of the fibrillation and excitation thresholds in the cardiac ventricles in experimental animals

To find the fibrillation threshold under rapidly changing conditions a method of its determination with long-lasting stimuli (100--300 msec) far exceeding the period of the highest vulnerability is described. The figures of the fibrillation threshold found by way of stimulating the heart with short and long impulses were partically identical. Intravenous administration of 4 mg/kg Lidocaine resulted in an increase of the fibrillation threshold in the experimental dogs, without changing the projection of the stimulus producing the fibrillation onto the force-interval curve and at the same time increasing the excitability of the myocardium. Intravenous 1 mg/kg Propranolol elevated the fibrillation threshold causing a parallel rightward shift in the projection of the stimulus on the force-interval curve and decreasing the exitability of the heart.     

Dorsal noradrenergic bundle and selective attention in the rat.

Tested the role for the dorsal noradrenergic bundle (DNB) in selective attention and stimulus filtering in 4 experiments with 138 male Wistar rats. The DNB was damaged by stereotaxically guided injection of 4 μg of the neurotoxin 6-hydroxydopamine (6-OHDA). The latent inhibition effect was blocked by 6-OHDA-induced depletion of forebrain noradrenaline, whereas nonreversal shift performance was better in noradrenaline-depleted Ss than controls. Data indicate that Ss with DNB lesions are impaired in ignoring irrelevant stimuli. In situations in which control Ss did not learn to ignore irrelevant stimuli, no lesion-induced difference was found. Thus, controls and DNB lesioned Ss learned equally about each of 2 dimensions of a multiple-redundant discrimination task. This was assessed both by interpolated trials with only 1 dimension present and by shifts in which only 1 of the previous 2 dimensions remained relevant. It is concluded that the DNB lesion does not increase stimulus sampling globally but that it impairs performance only in those cases in which normal rats learn to ignore irrelevant stimuli. (53 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A case of synchronous triple early cancer occurring in the stomach, colon and gallbladder

Tissue expansion is one of the most important armamentaria for aesthetic scalp reconstruction after burn; however, the proper way to employ this technique for the scalp reconstruction usually presents a challenge to the plastic surgeon, especially in the case of a "sideburn" scenario or a large lesion, as with, for example, hemiscalp alopecia. In this article, 11 patients, with different degrees of hair-bearing scalp loss as a result of burn, and including four patients with hemiscalp alopecia were successfully treated by using tissue expansion. The results show that tissue expansion is a simple, safe, and efficient technique for aesthetic scalp reconstruction. Versatile design of the expanded scalp flap can distribute the expanded hair-bearing scalp properly in the reconstructed recipient site.     

Multifascicular block in cardiomyopathy. Incidence, localization by His bundle study and prognosis

The comparison of Histocompatibility Testing in 82 MS Patients and 368 controls is presented. The increase in HL-A7 and decrease in HL-A12 are confirmed. A significant increase in HL-A8 is reported. Mixed Lymphocyte Reaction confirms the LD7a increase (19 out of 24 Multiple Sclerosis patients tested); 100% of the patients bearing the HL-A7 determinant are found to be LD7a. The presence of specific Immune Response genes in Multiple Sclerosis is discussed.     

Influence of acetylcholine, isoproterenol, quinidine and ouabain on effective refractory periods of atrial and ventricular myocardium in the dog

Acetylcholine-, isoproterenol-, quinidine- and ouabain-induced variations of the effective refractory periods (E.R.P.) of the non-specialized atrial and ventricular tissue have been explored in the dog by the extra-stimulus method during total cardiopulmonary by-pass. Acetylcholine significantly shortens the E.R.P. of atrial fibers, but does not provoke any change in the ventricular tissue, whereas a parallel decrease of atrial and ventricular E.R.P. is noted with isoproterenol. Quinidine induces a larger increase of the E.R.P. in the atrium than in the ventricle. The ouabain-induced shortening of the E.R.P. in the atrium is more marked than in the ventricle but is followed by a secondary increase which depends on both time after injection and dose. Hypotheses about the mechanisms of these effects, their importance in fibrillation and their relation to clinical uses are discussed.