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I Ninomiya

Publications and source records attributed to I Ninomiya.

At least 145 records · Page 8Linked to original sources
PubMed1985

[Difference of arterial pressure regulatory mechanism between awake and anesthetized human subjects].

This experiment was conducted to clarify difference of arterial pressure regulatory mechanism between awake and anesthetized human subjects. In 18 subjects who were scheduled for surgical operations, passive tilting test was performed both in awake and anesthetized conditions. Arterial pressure and heart rate were measured during four types of tilting test, i.e., 1. supine-10 degrees head down tilt 2. 10 degrees head down tilt-supine 3. supine-10 degrees head up tilt 4. 10 degrees head up tilt-supine. Relative changes in arterial pressure and heart rate in response to these four tilting tests were compared. After postural changes, all anesthetized subjects showed significant arterial pressure changes followed by restoration of arterial pressure towards control level with opposite changes of heart rate. This initial arterial pressure changes were mainly induced by shift of blood due to gravity and subsequent arterial pressure and heart rate changes were mainly by baro-receptor reflex. On the other hand, awake subjects showed transient increase of heart rate immediately after tilting followed by arterial pressure rise 2 to 3 seconds later in all four tilting tests. However, arterial pressure did not change so remarkably as in anesthetized condition and remained almost constant during tilting test. In awake subjects, their arterial pressure was regulated rapidly and reflex control of arterial pressure was masked. This rapid regulation of arterial pressure may be induced directly by higher central nervous system.

Adult↗
PubMed1984

Identification of 19-nor-deoxycorticosterone in normal rat serum by enzyme immunoassay and gas chromatography-mass spectrometry.

Recent reports on the isolation and identification of 19-nor-deoxycorticosterone from the urine of rats with adrenal regeneration hypertension give rise to the possibility of a role of this steroid in the pathogenesis of low renin essential hypertension. The present study was undertaken to investigate the presence of 19-nor-deoxycorticosterone in normal rat serum both by a sensitive enzyme immunoassay and by gas chromatography-mass spectrometry (GC/MS). 19-Nor-deoxycorticosterone in rat serum was separated from other steroids prior to enzyme immunoassay by using high performance liquid chromatography (HPLC). The average concentration of 19-nor-deoxycorticosterone in normal rat serum was 137 +/- 62 ng/dl (mean +/- SD, n = 32). Pooled normal rat serum (50 ml) was purified by HPLC and the purified sample was acetylated with acetic anhydride for GC/MS measurement. The retention time and m/z ions (358, 285, and 257) on the resulting mass fragmentogram coincided in position with those of authentic 21-acetoxy-19-nor-deoxycorticosterone and acetylated normal rat serum extract. The combined characteristics of HPLC elution, antigen-antibody reaction, GC retention and selected ion responses provided strongly evidence supporting the presence of 19-nor-deoxycorticosterone in normal rat serum.

Alkaline Phosphatase↗
PubMed1983

Heart rate-independent energetics and systolic pressure-volume area in dog heart.

Left ventricular (LV) systolic pressure-volume area (PVA), a new measure of total mechanical energy for the contraction, linearly correlates with its oxygen consumption per beat (VO2) regardless of contraction mode in a canine heart with stable chronotropism and inotropism. PVA is the area in the pressure-volume (PV) diagram circumscribed by the end-systolic and end-diastolic PV relation curves and the systolic segment of the PV loop and has dimensions of energy. We investigated whether primary changes in heart rate would affect the VO2-PVA relation. In the excised cross-circulated canine heart with left ventricular load controlled with a servo pump, we changed heart rate by pacing to compare the VO2-PVA relations at low [124 +/- 17 (SD) min-1] and high (193 +/- 23) heart rates. In 15 left ventricles, VO2 (ml O2 X beat-1 X 100 g LV-1) was (1.75 +/- 0.57) X 10(-5) PVA (mmHg X ml X beat-1 X 100 g LV-1) + 0.031 +/- 0.011 (ml O2 X beat-1 X 100 g LV-1). The VO2-PVA relation was virtually independent of heart rate in individual hearts. We conclude that the load-independent VO2-PVA relationship is not affected by chronotropism in a given canine left ventricle.

Animals↗
PubMed1983

Different cardiac and renal inhibitory and excitatory areas in rabbit hypothalamus.

The hypothalamic area was stimulated in anesthetized rabbits at a large number of selected points, and the effects on the simultaneously recorded right cardiac sympathetic nerve activity (CSNA) and renal nerve activity (RNA) were analyzed quantitatively. Four characteristic patterns of CSNA and RNA responses could be observed. The most striking finding was the presence of opposite responses of CSNA and RNA at many hypothalamic stimulus points, in addition to the conventionally observed CSNA and RNA responses in the same direction. By a new method, we drew hypothalamic maps for CSNA and RNA response magnitudes. These maps show that the excitatory areas of CSNA and RNA are surrounded by respective inhibitory areas. Although the excitatory areas of CSNA and RNA correspond with each other on the right side, they are not identical on the left side. These data suggest that the heart and kidney are controlled by sympathetic nerve activities originating from different hypothalamic neural groups in the rabbit.

Animals↗
PubMed1983

Effects of ketamine on renal nerve activity, arterial pressure and heart rate in rats.

We recorded renal nerve activity (RNA) together with arterial pressure (AP) and heart rate (HR) in 24 Wister rats anesthetized with nitrous oxide to investigate the effects of ketamine on the sympathetic nerve activity and the cardiovascular dynamics. The magnitude and time course of the responses to four graded doses of ketamine (1, 5, 10, 25 mg/kg) were studied in 19 rats. RNA responded biphasically, initially decreasing dose-dependently to minimal values of 89 +/- 4.4, 77 +/- 8.2, 54 +/- 5.2, and 17 +/- 3.7% of control for 1, 5, 10, and 25 mg/kg, respectively, and then increasing above control dose-independently. AP showed a biphasic response. HR first decreased dose-dependently but then increased slightly. In the remaining five rats, we compared the effects of ketamine 5 mg/kg on RNA, AP, and HR before surgical baroceptor denervation with those after the denervation. The denervation abruptly increased RNA, AP, and HR. Ketamine decreased RNA, AP, and HR in the denervated state and returned them to pre-ketamine values without overshoot. The finding that in the nerve intact state ketamine produced the characteristically biphasic response of RNA could be explained by the following mechanisms: (1) ketamine depresses the vasomotor center causing the initial decrease in RNA; (2) ketamine depresses the inhibitory effects of baroreflex causing the successive increase in RNA. The biphasic change in AP could be partly attributed to biphasic responses of RNA to ketamine.

Animals↗
PubMed1983

Twenty-four-hour pattern of ventricular excitation rhythm in resting normal human subjects.

Using a biotelemetry system, the electrocardiogram (ECG) was continuously measured over 24 hr in a given environmental condition in 8 normal human subjects. The frequency of ventricular excitation rhythm (VER) was obtained from inverse of R-R interval of ECG. This study was undertaken to be informed of the variation of VER over 24 hr in resting normal subjects with different ages. The averaged frequency of VER per day (VERd) and its relative coefficient of variation (CV) ranged from 1.44 to 1.01 Hz (mean: 1.24 Hz) and 26 to 10% (mean: 20%) with age of 10 to 73 years (mean: 42 years). VERd and CV showed a tendency to decrease with age. The VERd histogram showed not a normal distribution but a multimodal distribution. Two or three large positive deviations, denoted as L, N, and H modal components, from the normal distribution curve were detected. The mode of L and H modal components was 1.01 and 1.37 Hz, respectively. The frequency distribution of L and H modal components changed with relation to a circadian rhythm and sleep-wakefulness cycles. An hourly histogram of ventricular excitation rhythm (VERh) frequently showed an unimodal distribution and the relative coefficient of variation of VERh ranged from 7.9 to 13.3% which was smaller than that of CV. The mode of VERh histogram changed in association with the circadian rhythm, the sleep-wakefulness cycles and a fluctuation period of 2 to 3 hr.

Adolescent↗
PubMed1982

Solid phase fluoroimmunoassay for 11-deoxycortisol in serum using 21-amino-17-hydroxyprogesterone.

Solid phase fluoroimmunoassay of serum 11-deoxycortisol (17,21-dihydroxy-4-pregnene-3,20-dione) was established using fluorescein isothiocyanate-labelled 11-deoxycortisol and anti-11-deoxycortisol antibody-conjugated polyacrylamide beads. 21-Amino-17-hydroxyprogesterone (21-amino-17-hydroxy-4-pregnene-3,20-dione) was synthesized as a useful derivative for preparing the fluorescent dye conjugate. Serum 11-deoxycortisol was measured with this assay system after extraction and purification by Sephadex LH-20 column chromatography. The minimal amount of 11-deoxycortisol detected was 40 pg/tube and the measurable range was from 0.04 to 5.0 microgram/dl. Intra- and inter-assay coefficients of variation were 8.3% (n=6) and 9.8% (n=5), respectively. 11-deoxycortisol values determined by the present assay correlated well with those determined by radioimmunoassay. The present assay is particularly suitable for estimating the conditions of the pituitary and adrenocortical functions.

17-Hydroxycorticosteroids↗
PubMed1982

Mechanism of higher oxygen consumption rate: pressure-loaded vs. volume-loaded heart.

The greater cardiac oxygen consumption (VO2) under pressure than under volume load has been accounted for by the greater ventricular wall force under pressure load. We cannot fully agree with this because the wall force has not always been uniquely correlated with VO2. We attempted to account for the greater VO2 under pressure load by the ventricular systolic pressure-volume area (PVA), which we previously showed uniquely correlated with VO2. In isolated supported canine hearts, we produced servo-controlled ejecting contractions the stroke work (SW) of which was doubled from control by doubling ejection pressure (P) with comparable stroke volume (SV) and by doubling Sv with comparable P. Despite comparable increments in SW from 370 to 680 mmHg.ml under two different loads, VO2 and PVA increased significantly more under pressure load (from 0.033 ml O2/beat and 800 mmHg.ml to 0.0560 and 1,800, respectively) than under volume load (increasing to 0.038 and 1,200, respectively; P less than 0.01). These results suggested to us a new mechanism underlying the greater VO2 under pressure load.

Animals↗
PubMed1982

Pericoronary nerve mediates inhibitory sympathetic response to coronary occlusion.

We determined the effect of pharmacological blood of the pericoronary nerve either along the experimentally occluded left circumflex (CX) or the nonoccluded left anterior descending coronary artery (LAD) on the reflex inhibition of renal nerve activity (RNA) during a brief CX occlusion. In 15 pentobarbital-anesthetized dogs with carotid sinuses denervated, CX was occluded under four different conditions of the pericoronary nerves. With intact pericoronary nerves, CX occlusion resulted in a significant decrease [-44 +/- 6.4 (SE) %] in RNA. The decrease in RNA remained basically the same (-34 +/- 10.0%) after block of the pericoronary nerve along LAD with local infiltration of 2% lidocaine. However, the reduction of RNA was abolished after block of the pericoronary nerve along CX (-6 +/- 4.9%) and after block of the pericoronary nerves along both LAD and CX (3 +/- 2.6%). These results indicate that the afferent input transmitted via the pericoronary nerve along the experimentally occluded coronary artery plays a dominant role in mediating the reflex inhibition of RNA during the coronary occlusion.

Animals↗
PubMed1982

Digital on-line computation of a predictor of cardiac oxygen consumption. Left ventricular systolic pressure volume area.

Left ventricular systolic pressure volume area (PVA) has been proposed as a reliable predictor of cardiac oxygen consumption per beat (VO2). PVA is the area in the pressure-volume (P-V) diagram that is circumscribed by the end-systolic and end-diastolic P-V relation curves and the systolic segment of the P-V loop trajectory. It represents the total mechanical energy required for the ventricle to contract, to change its wall's elastic state from end diastole to end systole, and to eject blood against afterload. PVA has so far been measured manually with a planimeter applied to the P-V diagram. To measure PVA more accurately and on line during experiments, we devised a new method of computing PVA with a digital computer. The method consists of integrating during systole the infinitesimally narrow triangular pressure volume area swept by the straight line segment connecting Vd (ventricular volume at which peak isovolumic pressure is zero) and the instantaneously counterclockwise moving P-V data point in the P-V plane, and adding a small area between the end-diastolic P-V relation curve and the line connecting Vd and the end-diastolic P-V point. This method has proved useful in our study of the relation between VO2 and PVA to evaluate the PVA's ability to predict VO2.

Blood Pressure↗
PubMed1982

Different reflex responses in cardiac and renal sympathetic nerve activities during coronary occlusion in the dog.

This study was undertaken to scrutinize the difference in the response of cardiac sympathetic nerve activity (CSNA) and renal nerve activity (RNA) to coronary artery occlusion. The magnitudes and time courses of per cent changes in CSNA and RNA, recorded simultaneously in 22 dogs, were compared with each other during a 1 min occlusion of the left circumflex coronary artery under four different conditions. With afferent nerve intact, changes in CSNA and RNA showed similar biphasic patterns comprising initial increases (CSNA, 9 +/- 3.1% (S.E.); RNA, 16 +/- 6.4%, at 20 sec of occlusion) and subsequent decreases (CSNA, -3 +/- 4.3%; RNA, -11 +/- 6.5%, at 60 sec), despite the progressive fall in arterial pressure (from 109 +/- 4 to 89 +/- 4 mmHg). After carotid sinus denervation, the initial increases in both nerve activities were reduced and the subsequent decreases became more evident. The decreases in RNA (-47 +/- 8.0%) were significantly greater than those in CSNA (-23 +/- 5.6%). After bilateral cervical vagotomy, changes in both CSNA and RNA showed in contrast similar monophasic increasing patterns (CSNA, 18 +/- 4.0%; RNA, 25 +/- 5.6%, at 60 sec), where RNA increased more than did CSNA. After carotid sinus and vagoaortic denervation, CSNA and RNA increased only slightly throughout the occlusion. These results conclusively indicate that the reflex responses in CSNA and RNA during coronary occlusion are quantitatively different, though qualitatively similar, and that RNA is inhibited significantly more than CSNA by the reflex mediated through the afferent vagal nerves.

Animals↗
PubMed1981

Equal oxygen consumption rates of isovolumic and ejecting contractions with equal systolic pressure-volume areas in canine left ventricle.

Left ventricle systolic pressure-volume area (PVA) has been found to be highly linearly correlated with cardiac oxygen consumption rate per beat (VO2) in a given canine heart with a stable inotropic background. PVA is a specific area in the pressure-volume (P-V) diagram that is bounded by the end-systolic and end-diastolic P-V relationship lines and the systolic segment of the P-V loop, consisting of the sum of external mechanical work and what is considered the end-systolic elastic potential energy in the ventricular wall. In this study, we compared VO2's of steady state entirely isovolumic and variously ejecting contractions that were made to have equal PVA's in the canine left ventricle. We found that VO2's of these isovolumic and ejecting contractions with equal PVA's (isovolumic vs. ejecting = 1008 +/- 64 (SE) vs. 1022 +/- 62 mm Hg ml/beat, n = 32 pairs in 10 hearts) were equal to each other (0.0375 +/- 0.0021 vs. 0.0368 +/- 0.0021 ml O2/beat) regardless of the marked differences in stroke volume (0 vs. 9.8 +/- 0.6 ml), end-diastolic volume (20.3 +/- 0.8 vs. 23.7 +/- 0.9 ml), end-systolic volume (20.3 +/- 0.8 vs. 13.9 +/- 0.7 ml), peak pressure (123 +/- 5 vs. 88 +/- 5 mm Hg), stroke work (0 vs. 636 +/- 36 mm Hg ml/beat), and calculated peak total wall force (1588 +/- 77 vs. 1077 +/- 72 g). Therefore, we conclude that PVA can serve as a reliable predictor of VO2 in a given canine left ventricle with a stable inotropic background whether the contraction mode is isovolumic or ejecting.

Animals↗
PubMed1980

Critical evaluation of left ventricular systolic pressure volume areas as predictor of oxygen consumption rate.

Left ventricular systolic pressure volume area (PVA) has been reported to be a reliable predictor of cardiac oxygen consumption rate per beat (VO2) in a given heart with a stable inotropic background. PVA has been defined as the specific area in the pressure-volume (P-V) plane that is bounded by the end-systolic and end-diastolic P-V relationship lines and the systolic segment of the P-V loop trajectory. In the present experimental study, we separated PVA into two parts: EW and PE. EW is the area surrounded by the P=V loop, corresponding to the external mechanical work. PE is the area surrounded by the end-systolic and end-diastolic P-V lines and the relaxation segment of the P-V loop, corresponding to what is considered the end-systolic elastic potential energy in terms of a time-varying elastance model of the ventricle. We attempted to find an optimal weighting coefficient K of PE for the best correlation between VO2 and PVAW = EW + K . PE, changing K from 0 to infinity. Results in 7 canine excised cross-circulated hearts showed that PVAW best correlated with VO2 at K = 1.03 +/- 0.03 (SE). Since PVAW at K = 1 is identical with the original PVA, we concluded that PVA could serve as a reliable predictor of VO2. PVA is concluded to be physiologically significant in the coupling between cardiac mechanics and energetics.

Animals↗