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Biomedical subjects

K Goto

Publications and source records attributed to K Goto.

At least 811 records · Page 45Linked to original sources

[Neuronal and adrenomedullary catecholamine response to cardiopulmonary bypass: with special reference to comparative studies based on functional classification].

Plasma epinephrine (E) and norepinephrine (NE) levels during cardiopulmonary bypass (CPB) were studied in thirty-eight cardiac patients with various grades of NYHA classification. Striking increases of both E and NE levels after release of aortic cross clamp (stage 4) were noted. A thirteen fold increase in E (from 0.05 +/- 0.05 ng/ml to 0.62 +/- 0.48 ng/ml) and sixfold increase in NE (from 0.21 +/- 0.18 ng/ml to 1.26 +/- 0.78 ng/ml) occurred from prebypass (stage 1) to stage 4. The values of E and NE were peaked at stage 4 and rapidly decreased after heart beating (stage 5). At chest closure (stage 7), E returned to close to prebypass control (stage 1) value, however NE remained still in moderately high level. Patients were divided into three groups: The mild group (NYHA class I and II, fourteen patients), the ill group (NYHA class III and IV, nineteen patients) and the IABP group (IABP support since prior to CPB due to unstable angina and ventricular septal perforation, five patients). Whereas E value at either stage 4 or stage 5 in the mild group was statistically significantly higher (p less than 0.05) than each E value at corresponding stages in the ill group. NE value at each stage 3 (prior to aortic cross clamp), stage 4 or stage 5 in ill group significantly higher than each NE value at same stages in the mild group respectively. These data suggest that depletion of E and compensatory increase of NE in the ill group may be occurred during CPB.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Cardiac rhabdomyoma associated with tuberous sclerosis. An autopsy case of newborn infant died of cardiac failure.

An autopsy case of cardiac rhabdomyoma associated with tuberous sclerosis in a 27-day-old infant is presented. He was born with severe cyanosis. Echocardiogram revealed the presence of multiple mass lesions, some of which protruded into the left ventricle at the level of subaortic valve. From the age of 4 days, cardiac arrhythmia developed and lasted until his death. The arrhythmia started as WPW syndrome and atrial extrasystoles and then additional paroxysmal supraventricular tachycardia, ventricular fibrillation, sinus arrest, and S-A block occurred. Computed tomographic scanning of the brain revealed the presence of symmetric high-density spots around the central part of lateral ventricle. Before his death paroxysmal supraventricular tachycardia occurred frequently which changed to ventricular fibrillation and he collapsed without urination and then died. Autopsy examination revealed the presence of generalized congestion, multiple nodules of cardiac rhabdomyoma, some of which causing subaortic stenosis, and tuberous sclerosis in the brain. From the clinical and autopsy findings, the direct cause of death was attributable to the cardiac rhabdomyoma.

Heart Neoplasms↗

The contractile activities of neurokinin A, B and related peptides on smooth muscles.

The contractile activities of neurokinin A (NKA), neurokinin B (NKB) and related peptides on the guinea-pig ileum, rat vas deferens and rat duodenum were compared to the activity of substance P (SP). The potencies of NKA and NKB on the guinea-pig ileum (SP-P tissue) were nearly the same as that of SP. NKA was approximately 250-400 times more potent than SP on the rat vas deferens (EC50 = 59.5 nM; SP, EC50 = 1500 nM) and rat duodenum (EC50 = 1.8 nM; SP, EC50 = 674 nM) (SP-E tissues). NKB also showed high contracting activity on the rat duodenum (EC50 = 3.1 nM) but was 10 fold less active than NKA on the rat vas deferens. These results suggest that neurokinin peptides are possible endogenous agonists for the SP-E tissues. The contractile potency of NKA and NKB remained nearly complete after removal of N-terminal tripeptide portions, i.e., His-Lys-Thr and Asp-Met-His from the native peptides, respectively. However, the removal of the Asp residue from both NKA7 and NKB7 decreased activity until it was similar to that of SP.

Amino Acid Sequence↗

Synthesis of hydrocarbons under presumed prebiotic conditions using high-frequency discharge.

Various hydrocarbons were synthesized by high-frequency discharge in a primordial terrestrial model atmosphere. The products were extracted by benzene or methanol and analyzed by GC-MS. The mean carbon chain length of the hydrocarbons formed by the discharge through pure CH4 gas was less than 6. Benzene was also obtained. Some isomers were obtained for each of the hydrocarbons containing a given number of carbons. When a small amount of C2H2 was added to the CH4, longer chain compounds were formed, as compared with discharge in CH4 only. However, when the amount of C2H2 was increased, unextractable high molecular weight compounds were produced. The amounts of products decreased as the mixing ratio of CO2 to CH4 increased. No hydrocarbons were detected when the ratio of CO2/CH4 exceeded 1.

Acetylene↗

Preparation and characterization of two major isotypes of parvalbumins from skeletal muscle of bullfrog (Rana catesbeiana).

Two major isotypes of parvalbumins (PA1 and PA2) have been isolated from the skeletal muscle of bullfrog, Rana catesbeiana. The Mr values were estimated to be 10,100 (PA1) and 11,800 (PA2) by SDS/polyacrylamide gel electrophoresis, and the isoelectric points were determined to be 4.78 (PA1) and 4.97 (PA2) by polyacrylamide gel isoelectric focusing. The amino acid compositions and isoelectric points indicate that PA1 corresponds to Rana esculenta pI 4.50 and Rana temporaria pI 4.75 parvalbumins and PA2 to Rana esculenta pI 4.88 and Rana temporaria pI 4.97 parvalbumins, showing that PA1 is genetically a beta-parvalbumin and PA2 an alpha-parvalbumin. However, in terms of the amino acid compositions, PA1 and PA2 are distinctly different from the corresponding parvalbumins of Rana esculenta or Rana temporaria. The ultraviolet spectra of PA1 and PA2 are consistent with their amino acid compositions. An ultraviolet difference spectrum of the Ca2+-loaded form vs. metal-free form indicates that a Tyr and some Phe residues in PA1 are affected by a conformational change associated with the binding of Ca2+. On electrophoresis in polyacrylamide gel in 14 mM Tris and 90 mM glycine, the Ca2+-loaded form of PA1 migrated twice as fast as the Mg2+-loaded form. Both PA1 and PA2 show increased mobility in the Ca2+-loaded forms, like troponin C but different from calmodulin.

Amino Acids↗

Calcitonin gene-related peptide as potential neurotransmitter in guinea pig right atrium.

The potential neurotransmitter role of calcitonin gene-related peptide (CGRP) in cardioacceleratory nonadrenergic noncholinergic (NANC) nerves was examined in the guinea pig right atrium in vitro. In the presence of atropine, a muscarinic antagonist, and atenolol, a beta-adrenoceptor antagonist, transmural nerve stimulation (TNS) of the isolated right atrium caused a positive chronotropic response, which is slow in both onset and decay. This TNS-induced slow response was assumed to be mediated by NANC nerves in the right atrium since tetrodotoxin inhibited the response. Dense distribution of CGRP-like immunoreactive (CGRP-I) nerves was demonstrated in the sinus node. Exogenously applied CGRP exerted a positive chronotropic effect on the isolated right atrium in a dose-dependent manner. Both CGRP-I nerves and NANC response induced by TNS were not affected by surgical sympathectomy and reserpine pretreatment but were abolished by the pretreatment of animals with capsaicin. The results suggest that CGRP is the neurotransmitter of cardioacceleratory NANC nerves in the right atrium of the guinea pig.

Animals↗

Peripheral angiotensin II stimulates release of vasotocin in conscious chickens.

In mammals, intracranial or peripheral administration of angiotensin II (ANG II) has a number of actions, including the release of antidiuretic hormone (ADH). Relatively little is known of the interactions between the renin-angiotensin and ADH systems in birds. In the present study [Asp1, Val5]ANG II (fowl ANG II) was infused intravenously into conscious White Leghorn cockerels to determine whether peripheral ANG II influences the release of arginine vasotocin (AVT), the avian ADH. Cannulas were inserted into a wing artery and vein under local anesthesia. ANG II was dissolved in 0.154 M NaCl and administered intravenously at 0, 2, 20, and 200 ng X kg-1 X min-1. In a second series of experiments, ANG II was infused in 0.1 and 1.0 M NaCl (200 ng X kg-1 X min-1) to examine the effect of the peptide on osmotic release of ADH. In the three groups administered ANG II in 0.154 M NaCl, plasma AVT before intravenous infusion averaged between 1.8 +/- 0.46 to 2.6 +/- 0.30 microU/ml. In these birds, infusion of ANG II at 2, 20, and 200 ng X kg-1 X min-1 caused plasma AVT to increase over preinfusion means by 39, 78, and 300%, respectively. The changes in AVT occurred in the absence of differences in plasma osmolality, electrolyte composition, or arterial blood pressure among the groups. In chickens that were administered ANG II in 0.1 and 1.0 M NaCl, significantly higher plasma AVT levels were observed compared with a control group receiving the saline infusions alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

Pharmacological studies of imidazoline derivatives. I. A comparison of the effect on pre- and postsynaptic alpha-adrenoceptors in the rat vas deferens.

The effects of 8 imidazoline derivatives on pre- and postsynaptic alpha-adrenoceptors and [3H]norepinephrine release were investigated in the rat vas deferens and were compared with those of reference drugs, yohimbine, phentolamine, tolazoline, and prazosin. K-6341 and K-6343 activated postsynaptic alpha 1-adrenoceptor and were antagonized by prazosin. The order of potency series as alpha 1-antagonist, prazosin greater than phentolamine greater than yohimbine greater than K-4011 greater than K-3827 greater than K-4300, tolazoline was found in antagonism against phenylephrine. Many derivatives exhibited an antagonistic action against clonidine, and the potency series as alpha 2-antagonist was revealed as follows: phentolamine greater than yohimbine greater than K-3827 greater than K-4011 greater than K-6341 greater than K-6343 greater than K-4300, tolazoline greater than prazosin greater than K-4299. The antagonistic effect was more selective on presynaptic (alpha 2) than postsynaptic (alpha 1) adrenoceptor and the rank order of selectivity (KB-post/KB-pre) was K-3827 greater than yohimbine greater than K-4011 greater than tolazoline, K-4300 greater than phentolamine greater than prazosin. Imidazoline derivative increased [3H]norepinephrine release, the actions of K-3827, K-6341 and K-4300 being particularly potent. From these results, the structure-activity relationship was summarized. First, when 2',3'-methylenedioxyphenyl group is connected with the imidazoline ring via an amino or methylene residue, these compounds become alpha 1-agonist. Secondly, when the methylenedioxyphenyl group and the imidazoline ring are connected via an amino residue, these compounds show a weak agonistic and potent antagonistic characteristics at the presynaptic alpha 2-adrenoceptor. Thirdly, an addition of a methylenedioxy radical to the phenyl ring increased the affinity of the compounds to presynaptic alpha 2-receptor.

Animals↗

Depletion of calcitonin gene-related peptide (CGRP) by capsaicin in cerebral arteries.

Effects of capsaicin in vivo and in vitro on calcitonin gene-related peptide (CGRP)-containing nerves were examined in cerebral arteries. CGRP-like immunoreactive (CGRP-I) nerves were demonstrated in cerebral arteries of rats, guinea pigs and rabbits. The overall distribution of CGRP-I nerves was similar to that of substance P-containing nerves. Since the distribution of CGRP-I nerves of cerebral arteries among these species was the densest in guinea pigs, this animal was used to study the effect of several treatments on CGRP-I nerves. Catecholamine (CA)-fluorescence but not CGRP-I nerves was abolished by surgical sympathectomy or reserpine pretreatment. Pretreatment of the animal with capsaicin abolished CGRP-I nerves of cerebral arteries. CGRP-like immunoreactivity disappeared from cerebral arteries by in vitro incubation with capsaicin. Capsaicin treatment in vivo and in vitro did not affect CA-fluorescence nerves in these arteries. Since capsaicin selectively affects primary afferent nerves, it is suggested that CGRP is contained in sensory nerves. Capsaicin may be a valuable tool in elucidating the physiological or pathophysiological role of CGRP in cerebral circulation.

Animals↗