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Biomedical subjects

I Ninomiya

Publications and source records attributed to I Ninomiya.

At least 127 records · Page 7Linked to original sources
PubMed1987

An alternative metabolic pathway of 11-deoxycorticosterone in bovine adrenal in vitro: evidence for the presence of a pathway of 11-deoxycorticosterone oxidation at 19-position.

Comparative studies of 11 beta-, 18-, and 19-hydroxylation activities of 11-deoxycorticosterone (DOC) by bovine adrenal mitochondria revealed that an appreciable level of hydroxylation rate was observed in 19-hydroxylation (0.32 nmol/min/mg mitochondrial protein), as well as in 11 beta- and 18-hydroxylations (4.7 and 0.27 nmol/min/mg mitochondrial protein, respectively), at saturated substrate concentration in vitro. Also, the rates of the oxidation reactions of 19-hydroxy-11-deoxycorticosterone (19-OH-DOC) and 19-oxo-11-deoxycorticosterone (19-oxo-DOC) at the 19-position were about 5 times higher than the 19-hydroxylation rate of DOC. Although the affinities of 19-OH-DOC and 19-oxo-DOC for the enzyme(s) involved in the C-19 oxidation were about one-fifth those of DOC, these results strongly suggest the presence of the following pathway in bovine adrenal in vitro: DOC----19-OH-DOC----19-oxo-DOC----19-oic-DOC. This was further confirmed by a dynamic study of the formation and subsequent decay of the C-19 oxidized metabolites produced from DOC. At maximum concentrations of 19-OH-DOC and 19-oxo-DOC, the rates of production of, respectively, 19-oxo-DOC and 19-oic-DOC reached maximum. Furthermore, at the beginning of the incubation (1-4 min), an induction period in the formation of 19-oxo-DOC and 19-oic-DOC was observed and the formation of 19-oxo-DOC always preceded the appearance of 19-oic-DOC. These observations strongly support the existence of the pathway of the C-19 oxidation of DOC as mentioned above. It was also established that reduced pyridine nucleotide (NADPH) and molecular oxygen were required for these oxidation reactions. In addition, these three oxidation reactions were uniformly inhibited by the presence of carbon monoxide or metyrapone (0.01-1.0 microM), which is known to bind specifically with cytochrome P-450, while potassium cyanide (0.01-0.1 mM) did not affect them. These results suggest the possibility of the involvement of cytochrome P-450 in the C-19 oxidation reactions of DOC, 19-OH-DOC, and 19-oxo-DOC. We also showed that 19-oic-DOC is not further metabolized to other steroids such as 19-nor-11-deoxycorticosterone in bovine adrenal cortex.

Adrenal Glands↗
PubMed1987

Changes in renal sympathetic nerve activity, heart rate and arterial blood pressure associated with eating in cats.

1. Renal sympathetic nerve activity, heart rate and arterial blood pressure were simultaneously measured in thirteen awake cats before, during and after eating which was evoked by presenting food for a period of 10-15 s. 2. With food presentation, eating behaviour occurred in 93% (191) of 205 trials, and renal sympathetic nerve activity significantly increased in 65% of the 191 trials. On the other hand, in many of food presentation trials when no eating occurred, or with presentation of an empty food box, renal sympathetic nerve activity did not change significantly. 3. Eating started 1-8 s after the food presentation. The increase in renal sympathetic nerve activity was closely related to the beginning of eating but not to the onset of food presentation. Renal sympathetic nerve activity and heart rate increased with a slight time lag of 0.5-1.5 s from the onset of eating, whereas an increase in arterial blood pressure followed the onset of eating by 5.5 s. After the beginning of eating, renal sympathetic nerve activity, heart rate and arterial blood pressure increased at a maximum of 61 +/- 18% (mean +/- S.E. of mean), 26 +/- 4.0 beats/min, and 17 +/- 4.9 mmHg from the control values at 1.0, 5.5 and 11.5 s, respectively. 4. Cardiac-related grouped discharges of renal sympathetic nerve activity, which were observed at rest, increased during eating. 5. When arterial blood pressure was elevated by noradrenaline (2-5 micrograms/kg I.V.), renal sympathetic nerve activity during resting was almost completely inhibited and the increase in renal sympathetic nerve activity during eating was not induced. 6. We conclude that renal sympathetic nerve activity increases in association with eating behaviour but not as firmly with the food presentation, and that the increase in renal sympathetic nerve activity is initiated by descending input from the higher central nervous system rather than either by the viscero-autonomic reflex due to food intake or by the baroreflex due to a decrease in arterial blood pressure.

Action Potentials↗
PubMed1987

Cardiac sympathetic nerve activity and catecholamine kinetics in cat hearts.

To understand the catecholamine kinetics in the heart during hypotension, we simultaneously measured cardiac sympathetic nerve activity (CSNA), concentrations of norepinephrine (NE) and epinephrine (Epi) in arterial and coronary sinus blood, and coronary sinus plasma flow in 11 cats. With hypotension, NE and Epi concentrations in arterial blood increased more than those in coronary sinus blood. The arteriovenous difference between NE and Epi concentrations increased, whereas coronary sinus plasma flow decreased. The net cardiac uptake of NE from coronary arterial blood was not significant (0.826 +/- 0.506 ng/min) under the control condition. With hypotension, it increased significantly to 9.658 +/- 3.182 ng/min (P less than 0.05) in spite of a CSNA increase to 302.0 +/- 30.3% of that during the control condition. The net cardiac uptake of Epi was significant (1.574 +/- 0.542 ng/min) under the control condition, and, with hypotension, it increased significantly to 4.721 +/- 1.049 ng/min (P less than 0.01). We concluded that during hypotension NE was supplied to the heart from sympathetic nerve endings distributing to the heart and also from coronary arterial blood.

Animals↗
PubMed1987

Nonuniform effects of histamine on small pulmonary vessels in cats.

In in vivo cat lung, using an X-ray TV system, we analyzed responses in internal diameter (ID), flow velocity, and volume flow of arteries and veins (100-500 microns ID) to histamine (8-15 micrograms/kg iv) under three conditions. With histamine alone, three types of ID response (constriction, dilatation, and no change) occurred in parallel-arranged arteries. Relative frequency and magnitude of constriction were maximum in arteries of 300-400 micron ID, whereas those of dilatation were maximum in arteries of 100-200 micron ID. In veins, relatively uniform constriction occurred. Under H2-blockade, histamine caused greater constriction than that with histamine alone in arteries and veins of 300-500 micron ID. Under beta-blockade, with histamine, ID of all vessels decreased significantly below the ID sizes under the above two conditions, and no dilatation occurred. In two parallel arteries that showed opposite ID changes to histamine, flow velocity increased, but volume flow decreased in a constricted artery while it increased in a dilated one. Those data indicated that, with histamine, qualitatively and quantitatively nonuniform ID response was induced in both parallel- and series-arranged small pulmonary arteries and, in turn, produced heterogeneous flow distribution. Factors to cause the nonuniformity may be partly explained by difference in density of H2- and beta-receptors in vascular walls.

Adrenergic beta-Antagonists↗
PubMed1987

Effects of prostaglandin F2 alpha and prostacyclin on pulmonary microcirculation in the cat.

In pulmonary microcirculation, using a new X-ray television system, we measured the effects of prostaglandin F2 alpha (PGF2 alpha) and prostacyclin on the internal diameter (ID), flow velocity, volume flow, and transit times of a contrast medium in small arteries (Ta) and veins (Tv) in anesthetized cats. The ID of the arteries and veins ranged from 100 to 500 micron. PGF2 alpha, 0.3, 1, and 3 micrograms/kg, predominantly decreased ID on the arterial side in a dose-dependent manner but increased flow velocity 27-62%. Consequently, volume flow was kept relatively constant. With PGF2 alpha, Ta and Tv were decreased 18-41% and 4-15%, respectively. Prostacyclin, 2 and 4 micrograms/kg, uniformly dilated the ID of small arteries 9-16% but did not change small veins. With prostacyclin, flow velocity was unchanged or decreased, whereas volume flow was increased significantly, 27-32%. No significant changes of Ta and Tv were observed in response to prostacyclin. When both prostaglandins, PGF2 alpha and prostacyclin, were administered, they canceled each other with respect to the ID of small pulmonary arteries. Prostacyclin also prevented the PGF2 alpha-induced vasoconstriction of the pulmonary venous microcirculation.

Animals↗
PubMed1987

Vagally and acetylcholine-mediated constriction in small pulmonary vessels of rabbits.

Using a new X-ray TV system, we analyzed effects of vagal nerve stimulation (VNS; 1-30 Hz) and intravenous injection of acetylcholine (Ach; 0.3-0.9 microgram) on the internal diameter (ID; 100-1,500 microns) of small pulmonary arteries and veins in anesthetized rabbits. In selective segments of the arteries, ID decreased abruptly and maximally by 50-70% in a specific stimulus frequency to the vagal nerve and a dose of ACh. The vasoconstrictor sites were distributed near the branching points of the arteries, particularly those downstream, and their numbers increased with an increase in the stimulus frequencies and ACh doses. The relative frequencies of occurrences were 15.3% with VNS (30 Hz) and 5.3% with ACh (0.9 microgram). In nonselective segments with VNS, ID decreased frequency dependently by 0, 4, 12, and 26% at 1, 4, 15, and 30 Hz, respectively, and with ACh, decreased dose dependently by 21 and 35% with 0.3 and 0.9 microgram, respectively. The vasoconstriction in response to VNS and ACh was attenuated by atropine, enhanced by eserine, and not affected by phentolamine. That vasoconstriction to VNS was abolished by hexamethonium. No selective constriction was found in veins and the ID was decreased uniformly by 1-2% with VNS and ACh.

Acetylcholine↗
PubMed1987

Effect of metabolic acidosis on pulmonary microcirculation in the cat.

Using a new X-ray TV system, we studied the effects of metabolic acidosis, produced by intravenous injection of lactic acid, on internal diameter (ID; 100-500 micron), flow velocity, and volume flow in pulmonary microcirculation of anesthetized cats. We found that metabolic acidosis decreased the ID of arteries by 21%, whereas it increased flow velocity by 28% but not volume flow.

Acidosis, Lactic↗
PubMed1986

Cardiac sympathetic nerve activity and heart rate during coronary occlusion in awake cats.

Responses in efferent cardiac sympathetic nerve activity (CSNA) and heart rate (HR) to a 100-s anterior descending coronary artery occlusion were measured in cats under awake, atropinized, anesthetized, or anesthetized and atropinized states. In the conscious state, at 20 and 90 s of occlusion, CSNA increased by 23% and then decreased by 7%, respectively, whereas HR decreased by 5 and 17%, respectively. With atropinization and/or anesthesia, the initial increase in CSNA was inhibited and the later decrease in CSNA was enhanced, whereas the bradycardia was diminished. HR changed in proportion to CSNA responses with high correlations, i.e., r = +0.89, +0.90, +0.96, and +0.91 for the four states, respectively. In the conscious state, the CSNA-HR relation line shifted toward bradycardia, but this shift was blocked by atropinization and anesthesia. This finding suggested that, in the conscious state, cardiac vagal nerve activity (CVNA) increased immediately and did not decrease during occlusion. At the early stage of occlusion, HR response (bradycardia or tachycardia) was determined by the relative contribution of enhanced CSNA and CVNA. At the later stage of occlusion, bradycardia was induced by a combination of decreased CSNA and enhanced CVNA. In anesthesia and/or atropinization it was induced mainly by the decreased CSNA.

Anesthesia↗
PubMed1986

Effects of regional alveolar hypoxia and hypercapnia on small pulmonary vessels in cats.

Using an X-ray TV system, we analyzed responses in the internal diameter (ID), flow velocity, and volume flow in small pulmonary vessels (100-600 microns ID) during unilobar hypoxia and hypercapnia in cats. In the hypoxic and hypercapnic lobes, the ID reduced in proportion to the degree of hypoxia and hypercapnia, respectively. The ID reduction was larger in the arteries than in the veins for a given stimulus. In the arteries, the ID reduced nonuniformly in the series-arranged vessels in response to both stimuli. The percentage ID reduction was maximal in the arteries of 200-300 microns ID, in which it was 21, 26, 28, and 36% with 5% O2, 0% O2, 5% CO2, and 10% CO2 inhalations, respectively. On the other hand, in the veins, uniform ID reduction occurred for a given stimulus. In the contralateral normoxic lobe, the ID did not change significantly. In both hypoxic and hypercapnic lobes, the flow velocity and volume flow of the small arteries decreased, with 5% O2, by 18 and 40%, respectively, and, with 5% CO2, by 23 and 50%, respectively. In contrast, in the normoxic lobe, they increased significantly during 5% O2 and 5% CO2 inhalations. We concluded that regional alveolar hypoxia and hypercapnia induced a local vasoconstriction particularly in the small arteries of 200-300 microns ID and decreased the flow velocity and volume flow in the same lung region.

Angiography↗
PubMed1985

X-ray TV system for measuring microcirculation in small pulmonary vessels.

We developed a new system that consists of 1) a specially designed X-ray apparatus, 2) an X-ray-sensitive 1-in. Vidicon camera, and 3) a digital image-processing device. The picture element is approximately 20 micron in size, and the time required for one frame is 1/30 s. Using this system, we measured the internal diameter (ID), the cross-sectional area, flow velocity, volume flow, and transit time of small pulmonary vessels of approximately 100-500 micron at control and with serotonin in anesthetized cats. Flow velocity and volume flow from large [458 +/- 22 (SE) micron] to small (340 +/- 32 micron) arteries were 5.4 +/- 0.4 cm/s and 0.53 +/- 0.06 ml/min, respectively. Transit times of the contrast medium from large to small arteries (Ta) and to large veins (Tv) were 0.68 +/- 0.04 and 3.71 +/- 0.25 s, respectively. Serotonin injection (20-30 micrograms/kg iv) decreased ID, flow velocity, and volume flow of arteries by 8-48, 32, and 76%, respectively, whereas Ta and Tv increased by 91 and 69%, respectively. The system can provide useful information regarding the local circulation in the lung.

Animals↗
PubMed1985

Length dependent potentiation and inhibition of post-rest twitch tension development in adult cat and kitten papillary muscles.

If a rest interval is applied to a regularly stimulated cardiac muscle, the first contraction after this interval (post-rest contraction) has either a greater (post-rest potentiation) or a smaller (post-rest inhibition) developed tension than the regular contraction. Positive inotropic interventions will augment the post-rest potentiation and reduce the post-rest inhibition. We examined the effects of muscle stretching on the post-rest contraction in papillary muscles isolated from adult cats and from kittens and compared the effects with those of two typical inotropic interventions: high frequency stimulation and high calcium concentration. We found that muscle stretching augmented the post-rest potentiation and reduced the post-rest inhibition in a manner similar to the two inotropic interventions in the adult cat papillary muscle, and that these effects were consistently reversed in the kitten papillary muscle. The similarity of the effect of muscle stretching to those of the two typical inotropic interventions in either adult cat or kitten papillary muscle suggests that the effect of muscle stretching is due to an inotropic effect of muscle length change.

Animals↗
PubMed1985

Non-uniform effects of neurohumoral agents on the internal diameter in parallel and series arranged small arteries in rabbit hindlimb.

Using X-ray angiography, the internal diameter (ID) of 31 sites of arteries in the hindlimb, i.e., the iliac, main femoral, profundal femoral, circumflex femoral, saphenous, and popliteal arteries, was measured in anesthetized rabbits. ID under the control condition was 294-1,796 micrometers, but was changed to 376-1,828 micrometers, 127-1,914 micrometers, and 423-2,098 micrometers with administration of hexamethonium bromide, noradrenaline, and phentolamine, respectively. The constrictor effects of noradrenaline and plasma catecholamine were larger in the femoral artery than in the iliac artery. At the transition site from the iliac to the femoral artery, ID per unit length increased from 190 micrometers/10 mm in the control to 320 micrometers/10 mm with noradrenaline. The constrictor effects of sympathetic nerve activity (SNA) on the profundal femoral, circumflex femoral, saphenous, and popliteal arteries varied among 19 out of 20 sites. Plasma catecholamine constricted ID at 18 sites but dilated it at 2 sites. Noradrenaline constricted ID at all 20 sites, particularly in the popliteal and saphenous arteries. It was concluded that the effects of SNA and plasma catecholamine on ID on rabbit hindlimb arteries were qualitatively and quantitatively non-uniform among different arteries and at different sites of the given artery.

Angiography↗
PubMed1985

Transient responses of heart rate, arterial pressure, and head movement at the beginning of eating in awake cats.

Time courses of heart rate (HR), arterial pressure (AP), and head movement at the beginning of eating were analyzed in conscious cats. The cats were trained to eat when movements of their body trunks were restrained. Food was presented for 10 sec at intervals of 100 sec. With the abrupt presentation of food, a head-down movement occurred immediately and thereafter eating started with a mean latency of 1.6 sec. During eating HR increased by 22% from the preeating value and AP was elevated by 11%. To determine the time relation between the onset of eating and the change in each variable in response to eating, mean time courses of HR, AP, and head movement were obtained from 7-40 trials in each cat. The head-down movement preceded the onset of eating by 1.3 sec. The increase in HR preceded the onset of eating by 0.2 sec; the change in AP followed it by 3-4 sec. This indicated that the increase in HR was not induced reflexly either by food intake or by the change in AP. After administration of hexamethonium, the changes in HR and AP in response to eating were abolished, although eating was evoked by the food presentation. Additionally, the increase in HR was also reduced by propranolol and atropine. Thus, the acceleration of HR at the beginning of eating may be induced by central activation of the autonomic nervous system.

Animals↗