[A case of pulmonary papillomatosis (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Iijima.
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The effects of noradrenaline (NA), L-3, 4-dihydroxyphenylalanine (L-DOPA), 5-hydroxydopamine (5-OHDA), 6-hydroxydopamine (6-OHDA), and reserpine (RES) on the uptake, accumulation, and release of amines in catecholamine-containing specific endothelial granules (SEG) of carp cerebral veins and their mode of formation were examined by fluorescence histochemistry and electron microscopy. The intramuscular injection of NA (4 mg/kg) or L-DOPA (200 mg/kg) resulted in an increase in both the fluorescence and electron density of SEG. After the administration of false neurotransmitters. 5-OHDA (190 mg/kg) or 6-OHDA (200 mg/kg), the venous endothelial fluorescence almost completely disappeared but the SEG electron density increased. Following the injection of RES (15 mg/kg), the fluorescence intensity and SEG electron density showed no sign of decrease, as was expected, but in fact increased. It is suggested that the SEG are able to take up and accumulate exogeneous amines and that these mechanisms are RES-resistant. The electron density of SEG increased in proportion to the amount of amines in the SEG. The swelling and fragmentation of rough endoplasmic reticulum cisternae and the accumulation of dense material within the cisternae suggests the possible participation of these organelles in SEG formation.
Lamprey, Entosphenus japonicus, cerebral blood vessel autonomic nerve supply was studied with fluorescence and cholinesterase histochemistry and electron microscopy. Nerve fibers emitting a yellow fluorescence characteristic of serotonin (Exc./Em. max.; 380/530 nm) were found on the major cerebral and pial arteries, but not acetylcholinesterase (AChE)-positive ones. Single ganglion cells also emitting a strong yellow fluorescence were seen in the artery adventitia. On rare occasions these cells were observed in pairs. Terminal varicosities of central catecholamine-containing nerves (Exc./Em. max.; 410/475 nm) were observed on parenchymal capillaries, but not central AChE-positive nerve terminals. In ganglion cells, dense cored vesicles (ca. 130 nm in average diameter; DCV) were abundant in the Golgi area, suggesting their formation at this site. Two types of DCV were observed; one with a homogeneous dense core and the other with a granular core. DCV were numerous in axons as well, axons in which many small clear vesicles (40--60 nm in diameter) as well as DCV were occasionally observed. The question of whether the small clear vesicles or the DCV contained serotonin could not be resolved.
The role of the hypothalamic beta-adrenoceptors in the depressor response and bradycardia induced by stimulation of the anterior hypothalamus was studied in cats. In chloralose and urethane anaesthetized cats the anterior hypothalamus was superfused with artifical cerebrospinal fluid through a push-pull cannula. Electrical stimulation of the anterior hypothalamus with the tip of the cannula elicited a fall of systemic blood pressure and a decrease in heart rate. Superfusion of the anterior hypothalamus with isoprenaline did not change the depressor response and bradycardia induced by electrical stimulation of the anterior hypothalamus. Superfusion with atenolol or butoxamine also failed to modify the responses. Superfusion with (+/-)-propranolol significantly suppressed the responses. However, superfusion with (+)-propranolol suppressed the responses to the same extent. The resting systemic blood pressure and heart rate were not significantly changed by superfusion of the hypothalamus with these drugs. These results suggest that beta-adrenoceptors of the anterior hypothalamus are not involved in the depressor response and bradycardia elicited by hypothalamic stimulation.
Chromosomal DNA of Bacillus subtilis 168 (trpC2) prepared from defective phage P BSX was digested by restriction endonuclease Eco RI and ligated in vitro with DNA fragments of page phi 105C digested by the same endonuclease. The ligated DNA was used to transform a competent culture of B. subtilis (trpC2 lys3 metB10) which was lysogenic for phi 105, and transformants of the auxotroph markers were selected. The bacterial DNA ligated to the phage DNA fragments could be integrated into the prophage genome by transformation. The transformants in toto were treated with mitomycin C and the lysate was used to transduce B. subtilis (trpC2 lys3 metB10). Among metB+ transductants, one clone appeared to be a double lysogen carrying both plaque forming and metB+ transducing phage genomes. The latter defective phage was designated phi 105dmetB. Physical mapping of these phages was carried out by agarose gel electrophoresis of the restriction endonuclease digests and also by electron microscopic analysis of heteroduplex DNA. These results indicate that two adjacent fragments Eco RI-G and E of phi 105 DNA had been substituted with a foreign fragment Eco RI-M in phi 105dmetB DNA. Transformation experiments showed that the metB+ gene resided on the fragment Eco RI-M. This fragment was found to have a BamHI-sensitive site. The transforming activity for the metB marker, however, was not affected by the treatmment with BamHI.
Cholinergic influence on atrioventricular (AV) junctional rhythm via its intervention in the intracardiac autonomic nerves was investigated in the canine, blood-perfused AV node preparation. Large amounts of acetylcholine (ACh) injected into the anterior septal artery (ASA) caused a rapid increase in the rate of automaticity superimposed on a slow increase. Nicotine given in the ASA caused to a rapid increased superimposed on a slow increase. Large amounts of ACh injected into the posterior septal artery (PSA) caused a slow increase, which was superimposed by a rapid icrease in the presence of l-hyoscyamine. The rapid and slow increases were abolished by dl-propranolol given in the PSA and ASA, respectively. Both types of increases were suppressed by tetrodotoxin (TTX). Nicotine given in the PSA caused a decrease superimposed by a rapid increase, both of which were abolished by TTX. These reslts indicate that cholinergic excitatory intervention induces AV junctional tachycardia via norepinephrine release from sympathetic nerve endings, distributing widely from the proximal to distal portion of the AV junctional area.
Effects of ouabain on atrioventricular (AV) conduction were studied by using the canine excised, blood-perfused AV node preparations. Ouabain was continuously infused either selectively into the AV node artery (I) of systematically i.v. into the pentobarbital-anesthetized (II) and the pithed donor dog. (III). AV conduction in the isolated AV node preparation was interrupted by AV block in the half of I and II and in all of III after prominent prolongation of AV conduction time. In the remaining half of I and II, AV conduction was interrupted by accelerated prematures. The prematures continued to increase. After AV block ventricular rate decreased in the half of I and II and the inherent automaticity was sustained in all of III. PQ interval of the donor dog was interrupted by accelerated prematures in all of II and two thirds of III. In one third of III, AV block was induced. Interrupting doses of ouabain in the isolated AV node preparation of II and III and in the pithed donor dog heart were almost similar, all of which were significantly larger than that in pentobarbital-anesthetized dog heart. It is concluded that ouabain depresses directly AV conduction but this effect was modified by sympathetic nerve activity in the nerve-intact animals and also by inherent characteristics of the AV nodal cells.
The effects of N,N-diethyl-5-methyl[1,2,4]triazolo[1,5-alpha]pyrimidine-7-amine (trapidil) on the electrical activities of canine right ventricular muscle were studied using standard microelectrode techniques. Trapidil (10(-4) and 10(-3) mol/l) increased the plateau amplitude and shortened the duration of the action potential without changing the resting membrane potential and the maximum rate of rise of the action potential. Trapidil (10(-3) mol/l) restored regenerative action potentials (the slow response) in the ventricular muscle depolarized by elevation of extracellular K+ concentrations to 30 mmol/l. The slow response induced by trapidil was not affected by pindolol (10(-7) mol/l) which abolished that elicited by isoprenaline (10(-6) mol/l). These results indicate that the action of trapidil on the cardiac cell membrane is to increase the slow inward current during the action potential independently of stimulation of beta-adrenoceptors. Taken together with the results obtained by previous investigations the present results suggest that the increase in slow inward current during the action potential would be responsible for the positive inotropic effect of trapidil and would probably be related to its inhibitory action on cyclic AMP phosphodiesterase.
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Adrenergic and cholinergic innervation of the cerebral blood vessels were studied in the carp using fluorescence and cholinesterase histochemistry. Most of the major cerebral and pial arteries were densely innervated with both nerves. Moreover, both nerves, being probably of central origin, were observed frequently on the walls of parenchymal arterioles and capillaries in the sections of the inferior lobe but were only rarely found in the other brain sections.
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Specific histochemical techniques for the demonstration of catecholamine and acetylcholinesterase have been used to study the distribution of adrenergic and cholinergic nerves on the cerebral blood vessels of bullfrog, Rana catesbeiana. The adrenergic nerve meshworks on the cerebral arteries of bullfrog were less dense, had a more elongate appearance along the arterial axis as compared with those of mammals and were rather similar to those of snakes. The nerve plexuses on the cerebral carotid artery and its main branches were somewhat denser than those on the basilar artery. The most characteristic feature of innervation in the bullfrog cerebral vessels was that no acetylcholinesterase-positive fibres were observed on the extraparenchymal arteries, whereas, in all higher vertebrates investigated so far, the cerebral arteries have been found to be dually innervated although differences in the density of innervation of the two nerves may exist. This suggests that the peripheral adrenergic innervation on the cerebral blood vessels appeared earlier than the cholinergic one in the evolution of vertebrates. On the other hand, both adrenergic and acetylcholinesterase-positive fibres were observed in close contact with parenchymal arterioles and capillaries suggesting the possible existence of a dual central innervation. This feature, however, was by no means common. Thus, the central neurons have a significant influence on the cerebral circulation in the bullfrog is somewhat equivocal. Most of the pial and the parenchymal small vessels and the parenchymal capillaries exhibited a heavy acetylcholinesterase activity on the vascular walls. Although the significance of the enzyme is obscure as yet, this has to be considered in relation to the regulatory mechanism of the cerebral circulation.
The maximal rate of rise (Vmax) of the embryonic chick ventricular action potential increased about 2-fold from 112 +/- 6 V/sec and 113 +/- 5 V/sec on the 4th and 6th incubation days, respectively, to 217 +/- 7 V/sec on the 12th incubation day. Neither the steady state inactivation (hinfinity) of Vmax, the temperature-dependent shift of hinfinity, nor the time constant for recovery (tauRec) of Vmax changed significantly when Vmax had doubled. Inhibition of Vmax by tetrodotoxin (TTX) was the same in hearts from the 4th, 6th, and 18th incubation days. The relation between Vmax and TTX concentration could be described by a one-to-one binding curve with an apparent dissociation constant of 2 X 10(-8) M. The increase of Vmax, a valid measure of the early inward Na+ current (iNa) during the rising phase of the cardiac action potential, can be attributed to an elevated maximal Na+ conductance (-gNa) during ontogenesis. These results indicate that the physicochemical properties of the gNa unit responsible for the rapid rising phase of the action potential and of the TTX binding site associated with it may remain constant during a period of embryonic development when -gNa increased significantly.
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The formaldehyde-induced fluorescence technique and the argentaffin reaction with ultra-thin sections were applied to the vessels of carp to demonstrate the presence of a catecholamine. After formaldehyde gas treatment for 30 minutes at 50 degrees C, the venous endothelia emitted a greenish-yellow fluorescence suggesting the presence of a primary catecholamine. In the endothelial cells of veins, the specific granules, consisting predominantly of spherical granules with a diameter of about 0.3 micrometer, showed heavily to moderately positive argentaffin reaction. Granules also occurred in the endothelial cells of arteries. However, these granules stained weakly or not at all with ammoniacal silver solution. It is concluded that the specific endothelial granules in veins of carp contain a primary catecholamine.
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In open-chest dogs the heart rate was controlled at 150 beats/min and drugs were given intravenously. Propranolol (30 microgram/kg--1 mg/kg) prolonged the atrioventricular (A-V) conduction time and functional refractory period of the A-V conduction system (FRP) by blockade of the existing tone of the sympathetic nerves to the heart. The prolongation of the two parameters by the non-specific depressant action of propranolol was evident only at 3 mg/kg. Propranolol (3--30 microgram/kg) shortened the A-V conduction time in the heart deprived of the vagal and sympathetic tone, suggesting some sort of sympathomimetic effect. Pindolol in a wide range of doses (0.3--300 microgram/kg) exerted virtually no effect on the A-V conduction time and FRP, and its non-specific depressant action was apparent only at 3 mg/kg. Carteolol slightly prolonged the A-V conduction time and FRP only in low doses (1--10 microgram/kg), and in high doses (30 microgram/kg--1 mg/kg) it shortened the two parameters, reflecting its predominant sympathomimetic action.