Biomedical subjects

H Hosomi

Publications and source records attributed to H Hosomi.

At least 91 records · Page 5Linked to original sources

PubMed1988

Responsiveness of the ANP providing system to volume load in conscious dogs.

We examined in detail changes in arterial plasma ANP concentration in response to volume load in conscious dogs. In a 5-min volume load experiment, 18 ml/kg of isosmotic and isooncotic 3% Dextran 40 in saline was infused over a period of 5 min. Mean left atrial pressure (MLAP) increased transiently by 7.6 +/- 0.9 mm Hg. Plasma ANP level (P-ANP) did not significantly increase. Assayed P-ANP levels were corrected for hemodilution. Corrected P-ANP (C-ANP) significantly increased from 206 +/- 17 to 348 +/- 34 pg/ml. However, the level of C-ANP did not reach a steady state. No significant linear correlation was found between increases in MLAP and normalized C-ANP. In a 45-min volume load experiment, the elevated level of MLAP caused by the 5-min volume load was maintained for 40 min by supplemental infusion. C-ANP significantly increased from 196 +/- 18 pg/ml to 435 +/- 73 ng/ml. The level of C-ANP reached a steady state. A close linear correlation was observed between increases in MLAP and normalized C-ANP. However, the peak time of C-ANP lagged 10 min behind MLAP. These results indicate that it takes 10 min for P-ANP to reach a steady state in fully responding to a volume load, and that the long-term volume load is a prerequisite to the response of the ANP providing system.

Animals↗

PubMed1988

Depressed baroreflex control of renal nerve activity in conscious WHHL rabbits.

The baroreflex control of heart rate and renal nerve activity were examined in conscious Watanabe heritable hyperlipidaemic (WHHL) rabbits. Normal Japanese white rabbits were used as controls. The concentrations of serum cholesterol and triglyceride in WHHL rabbits were ten times higher than those in normal rabbits. The basal values of mean arterial pressure, pulse pressure and heart rate in WHHL rabbits were significantly higher than those in normal rabbits. Baroreceptors were stimulated or unloaded by raising or lowering arterial pressure with injections of phenylephrine or glyceryl trinitrate respectively. The peak changes in heart rate and renal nerve activity were plotted against the peak changes in mean arterial pressure, and a logistic function curve was fitted to the relationships between mean arterial pressure and heart rate, or mean arterial pressure and renal nerve activity. The slopes of both heart rate and renal nerve activity declined in WHHL rabbits. The response of renal nerve activity to acute volume expansion (10 ml.kg-1) with isotonic iso-oncotic dextran was further examined. In the normal rabbit, volume expansion caused renal nerve activity to decrease by 60 +/- 5%, while mean arterial pressure did not change. In the WHHL rabbit the decrease in renal nerve activity caused by volume expansion was significantly attenuated (42 +/- 3%). These results indicate that both sino-aortic and cardiopulmonary baroreceptor mediated changes in renal nerve activity were impaired in the WHHL rabbit.

Animals↗

PubMed1988

Effect of rapid sodium load on circulating atrial natriuretic polypeptide.

The hypothesis that an increase in plasma sodium concentration (PNa) causes an increase in circulating atrial natriuretic polypeptide (ANP) was examined in conscious dogs. NaCl solution in small volume (0.3 ml/kg body wt) and at high concentration (20%) was injected intravenously within 2 s to rapidly increase PNa. PNa rapidly increased to 5.1 +/- 0.3 meq/l. Urinary excretion of sodium and water increased to 4.1 and 2.5 times the control levels, respectively. Plasma vasopressin level increased to 3.7 times the control level. Plasma ANP level (PANP) did not change significantly. PANP corrected for sodium-induced hemodilution did not change either. On a different day, a double amount of sodium (0.6 ml/kg body wt of 20% NaCl solution) was intravenously injected into the dogs. PNa increased by 7.3 +/- 0.4 meq/l, which was significantly more than the increase after the 0.3 ml/kg injection. PANP with or without correction for hemodilution again did not change. These results indicate that a rapid increase in PNa within the physiological range does not cause elevation of circulating ANP. This suggests that ANP does not contribute to the regulation of plasma sodium concentration.

Animals↗

PubMed1988

Opiate receptor-mediated decrease in renal nerve activity during hypotensive hemorrhage in conscious rabbits.

Effects of hemorrhage on renal nerve activity and of subsequent opiate receptor blockade with naloxone were studied in conscious rabbits. Mean arterial pressure remained constant at 77 +/- 2 mm Hg through 17 +/- 2 ml/kg hemorrhage, while renal nerve activity increased by 159 +/- 16%. After 25 +/- 1 ml/kg hemorrhage, mean arterial pressure fell by 42 +/- 3 mm Hg, and renal nerve activity decreased below the prehemorrhagic control level by 41 +/- 15%. Bolus injection of naloxone (3 mg/kg i.v.) increased mean arterial pressure to 79 +/- 2 mm Hg, not significantly different from the prehemorrhagic control level. Renal nerve activity increased by 171 +/- 28%, comparable to the peak increase during nonhypotensive hemorrhage. On a different day, hemorrhage was repeated, and phenylephrine was infused during the subsequent hypotension. Phenylephrine increased mean arterial pressure to the prehemorrhagic control level. With increasing mean arterial pressure, renal nerve activity increased from its level during hypotensive hemorrhage and recovered toward the prehemorrhagic control level (-26 +/- 11%), but it did not return to the peak value reached during nonhypotensive hemorrhage. To further examine the blocking effects of naloxone on changes in mean arterial pressure and renal nerve activity induced by exogenous opiate peptides, methionine-enkephalin was injected both in the control state and after treatment with naloxone. A bolus injection of methionine-enkephalin (10 micrograms/kg) decreased mean arterial pressure (-8.1 +/- 2.0 mm Hg) and renal nerve activity (-95 +/- 1%). Pretreatment with naloxone (0.5 mg/kg) effectively blocked this depressor effect and reduction in renal nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Physiological factors of atrial natriuretic polypeptide release and its neural regulation in conscious dogs.

We have examined physiological factors in atrial natriuretic polypeptide (ANP) release and whether or not the cardiac nerves control release of ANP. Two possible factors were tested, an increase in plasma sodium level (PNa) and an increase in atrial pressure. Injection of 1.0 or 2.0 mEq/kg of sodium ions elevated PNa by 5.3 +/- 0.3 or 7.3 +/- 0.4 mEq/L, respectively, but plasma ANP level (PANP) did not change. Infusion of 18 ml/kg of 3% Dextran-40 over 5 min increased mean left atrial pressure (MLAP) by 7.6 +/- 0.9 mmHg. PANP increased from 206 +/- 17 pg/ml to 260 +/- 25 pg/ml, which was not significant. PANP, corrected for hemodilution, significantly increased to 348 +/- 34 pg/ml. These results suggest that PNa increase does not promote ANP release, but that an atrial pressure increase does. This transient volume load did not induce full response of the ANP releasing system. A prolonged volume load for 45 min increased corrected PANP to 435 +/- 73 pg/ml. A close linear correlation was found between the increases in MLAP and PANP. These facts indicate that prolonged volume expansion is necessary to induce full response of the ANP releasing system. Complete cardiac denervation did not affect the tonic level of plasma ANP, volume expansion-induced increase in PANP, or the sensitivity of the ANP releasing system. Thus we conclude that the cardiac nerves do not control ANP release caused by volume expansion.

Animals↗

PubMed1988

Medical treatment of Bell's palsy. Oral vs. intravenous administration.

Infusion therapy using low-molecular dextran in combination with high-dose cortisone was modified from Stennert's original protocol and indicated in 50 cases of Bell's palsy. The effects of infusion were compared with the outcome in 36 cases treated by orally-administered steroids and vasodilators. In the case of incomplete palsy, the recovery rate was excellent regardless of the mode of treatment. If the palsy is not progressive, it is not necessary for patients with this condition to have infusion therapy. In the case of complete palsy, 95% of those with normal nerve excitability (NE) experienced complete recovery when treated by infusion. However, only 71% of this group experienced complete recovery when treated with oral administration. In the group with diminished or absent NE, complete recovery was obtained in 58% of the patients treated with infusion, whereas only 18% recovered completely when given oral administration. Thus, the recovery rate increased sharply in the case of infusion therapy. Therefore, the above-mentioned method of infusion therapy is indicated in cases of complete or progressively incomplete Bell's palsy except in those cases where its use is contra-indicated for some other reason.

Adenosine Triphosphate↗

PubMed1988

Effects of chronic bile-duct ligation on the baroreceptor reflex in dogs.

The purpose of the present experiments was to examine the effects of chronic bile-duct ligation (CBDL) on the baroreceptor reflex system. The open-loop gain (G) of the baroreceptor reflex system and pressor response to noradrenaline were measured in seven dogs with CBDL for 4 to 6 weeks, and the data were compared with those of seven control dogs. The liver function of the CBDL-dogs was significantly impaired. G was assessed as (delta API/delta APS)-1, where delta API and delta APS represent the immediate and steady-state decreases in arterial pressure at the aortic arch following a fast step-wise reduction in blood volume. The value of G was 8.8 +/- 0.9 (mean +/- SE) in the control-group and 5.3 +/- 2.1 in the CBDL-group (p less than 0.05). The maximum increase in arterial pressure in response to a bolus injection of noradrenaline (0.5 micrograms/kg i.v.) was 29.3 +/- 4.4 mm Hg in the control-group and 19.7 +/- 1.6 mm Hg in the CBDL-group (p less than 0.05). These findings suggest that CBDL leads to a decrease in responsiveness of the vascular smooth muscle to noradrenaline which in turn results in a decrease in open-loop gain of the baroreceptor reflex system.

Animals↗

PubMed1987

Effect of pentobarbital anesthesia on renal sympathetic nerve activity in the rabbit.

The effects of pentobarbital (PB) anesthesia on arterial pressure, heart rate, and renal nerve activity (RNA) were studied in chronically instrumented intact rabbits and rabbits with sinoaortic baroreceptor denervation (SAD). In intact rabbits, PB caused an initial decrease in mean arterial pressure from 82 +/- 2 to 42 +/- 5 mm Hg, which then returned to the control level within 5 min. RNA increased by 144 +/- 19% in response to hypotension induced by PB then also returned to the control level within 5 min. Heart rate increased by 56 +/- 10 from 244 +/- 11 beats/min and remained elevated for 60 min. Sensitivities of baroreflex control of heart rate and RNA were markedly impaired by PB anesthesia. In SAD rabbits, PB caused hypotension (-46 +/- 5 mm Hg), which lasted for 15 min. RNA decreased initially by 80 +/- 5%, then gradually returned toward the control level. However, at 45 min after injection of PB, RNA was still depressed significantly. Tachycardia induced by PB was abolished by SAD, i.e. heart rate actually decreased by 53 +/- 10 beats/min. These results suggest that in intact rabbits steady-state effects of PB were: no change in mean arterial pressure or RNA, and tachycardia, all due to baroreflex compensation. However, in the absence of baroreflex compensation, PB elicited hypotension, bradycardia, and a decrease in RNA.

Anesthesia↗

PubMed1987

Lack of neural control of atrial natriuretic peptide release in conscious dogs.

To determine whether or not cardiac nerves control the release of atrial natriuretic polypeptide (ANP), we examined the effects of intrapericardial cardiac denervation on circulating ANP in conscious dogs. Base-line level of circulating ANP in six cardiac-denervated (CD) dogs (191 +/- 24 pg/ml) was not significantly different from that in seven intact (INT) dogs (196 +/- 18 pg/ml). Three percent dextran-40 in saline (18 ml/kg, 20% of estimated blood volume) was infused over 5 min, and the elevated left atrial pressure (LAP; approximately 8 mmHg) was maintained by supplemental infusion over 40 min. The increase in circulating ANP after infusion in the CD dogs (462 +/- 61 pg/ml) was not significantly different from that in the INT dogs (435 +/- 73 pg/ml). The regression line relating circulating ANP (normalized with regard to the control value) with the change in LAP in the INT dogs was not significantly different from that in the CD dogs. These results suggest that the cardiac nerves do not control the tonic release of ANP or the volume expansion-induced release of ANP.

Animals↗

PubMed1987

Flow-dependence of vasodilatory response in renal vascular bed to hemorrhage in dogs.

The vasodilatory response in the renal vascular bed was studied after quick mild hemorrhage under different levels of renal blood flow. In neuraxis intact dogs, the renal vascular resistance increased or decreased within 5 s after hemorrhage and reached a stable level close to the control within 10 s. The responses under neuraxis intact conditions may involve both responses of the renal vascular resistance to changes in renal sympathetic nerve activity caused by the baroreceptor reflex and responses to decrease in renal perfusion pressure after hemorrhage. In order to exclude baroreflex neural regulation of renal blood flow, we sectioned the carotid sinus and vagus nerves. The renal vascular resistance decreased within 5 s after hemorrhage, and was maintained at around this level for about 2 min. The decrease in renal vascular resistance and control (prehemorrhage) renal blood flow revealed a significant hyperbolic relationship. Since the systemic arterial pressure was not restored after hemorrhage and reflexogenic changes in sympathetic nerve activity were excluded after barodenervation, the vasodilatory response in the renal vascular bed after hemorrhage should reflect only hemodynamic changes. We conclude that the vasodilatory response to pressure fall in the renal vascular bed increases with a decrease in the control renal blood flow.

Animals↗

PubMed1986

Participation of baroreceptor reflexes in blood pressure and sympathetic nerve responses to a synthetic human atrial natriuretic peptide in anesthetized dogs.

The effects of a synthetic alpha human atrial natriuretic polypeptide (hANP) on systemic blood pressure and renal nerve activity were studied before and after sinoaortic denervation with vagotomy in anesthetized dogs. Intravenous injection of hANP (1 microgram/kg) in animals with the neuraxis intact produced a mild decrease in systemic blood pressure and a significant increase in renal sympathetic nerve activity. However, in animals with sinoaortic denervation and vagotomy, a profound fall in blood pressure occurred after administration of hANP. Renal nerve activity in these animals was reduced significantly, in parallel with decreases in systemic blood pressure. These results indicate that activation of peripheral baroreceptors minimizes the hypotension induced by intravenous injection of hANP, and may mask at least centrally mediated cardiovascular effects of hANP.

Animals↗

PubMed1986

Auditory brain stem responses in relation to the clinical symptoms of schizophrenia.

Auditory brain stem responses (ABSR) were examined systematically both in normal and schizophrenic subjects. All ABSR wave forms were evoked by click stimuli, which were delivered binaurally through headphones both to normal subjects and to a nondeteriorated group of schizophrenics. However, in the group of schizophrenics with marked deterioration of personality, not all wave forms were elicited, and the amplitudes were low. The characteristics of the ABSR wave forms correlated well with the clinical symptoms of the schizophrenic illness. The cause of these ABSR wave form changes in schizophrenics is discussed.

Adult↗

PubMed1986

Effect of atherosclerosis on the responsiveness of the rapidly acting arterial pressure control system in WHHL rabbits.

The open loop gain of the rapidly acting arterial pressure control system was estimated in 15 Watanabe heritable hyperlipidaemic (WHHL) rabbits aged 3-31 months. Twenty five normal Japanese white rabbits, aged 6-30 months, were used as controls. After being anaesthetised by an intravenous injection of pentobarbital sodium, the rabbits were bled by 2 ml X kg-1 body weight within 1-2 s through a catheter inserted into the aortic arch. The arterial pressure change after this rapid haemorrhage was recorded for more than 2 min by a catheter placed in the aortic arch. The open loop gain was calculated as (delta API/delta APS)-1, where delta API was the immediate fall and delta APS the steady state fall. The pulse pressure, delta API, and delta APS increased and the open loop gain decreased with age in the WHHL rabbits, but the mean arterial pressure did not change significantly with age. After aortic denervation the open loop gain also decreased with age in the WHHL rabbits. These results indicate that the progress of atherosclerosis with aging in the Watanabe heritable hyperlipidaemic rabbit decreases the vascular compliance and impairs the arterial pressure restoring function of the rapidly acting arterial pressure control system.

Animals↗

PubMed1986

Interactions among reflex compensatory systems for posthemorrhage hypotension.

The open-loop gains of the carotid sinus, aortic, and cardiopulmonary baroreflex systems defined as the ratio of posthemorrhage hypotension without a reflex to that with the reflex were estimated from experiments with a mild and quick hemorrhage (2 ml/kg body wt in 1-2 s) in 81 pentobarbital-anesthetized rabbits. The overall gain when all the nerves were intact was 7.4. After the carotid sinus nerves were sectioned the gain decreased to 3.0. After aortic nerve sectioning, the gain was 2.8, whereas vagotomy decreased it to 3.8. When both the carotid sinus and aortic nerves were cut, the gain was 0.9. When the aortic and vagus nerves were severed, it was 1.8. When the vagus and carotid sinus nerves were cut, it was 1.6. From these gain values the gain of the interacting component between the carotid sinus and aortic reflexes was calculated as 0.4; that between the aortic and cardiopulmonary reflexes was 0.5; and that between the cardiopulmonary and carotid sinus reflexes as 0.1. The gain of the interaction among all of these baroreflex systems was estimated to be 2.1. The results suggest that all these facilitatory interacting components play an important role in restoration of arterial pressure decrease caused by mild hemorrhage.

Animals↗

PubMed1986

Renal opiate receptor mediation of renin secretion to renal nerve stimulation in the dog.

The present study was designed to evaluate renal opiate receptor mediation of the renin secretion response to electrical stimulation of the renal nerves in the pentobarbital sodium-anesthetized dog by use of the opiate agonist leucine-enkephalin (Leu-enk) and the opiate antagonist naloxone. In all animals studied, left kidneys were pump perfused at a constant renal blood flow. Renal perfusion pressure (RPP) and glomerular filtration rate (GFR) were unaltered at a stimulation frequency of 1.0 Hz; however, renin secretion rate (RSR) increased significantly in the nontreated group. High-frequency renal nerve stimulation (10 Hz) increased RPP and decreased GFR. RSR at the high-frequency stimulation was significantly augmented in the nontreated group. Renal arterial infusion of either Leu-enk (25 micrograms X kg-1 X min-1) or naloxone (7 micrograms X kg-1 X min-1) did not alter base-line levels of renal hemodynamics and RSR and did not produce significant changes in these variables even when renal nerves were stimulated at the low frequency; however, Leu-enk inhibited RPP and RSR responses to the high-frequency stimulation, and naloxone augmented these responses. Phentolamine (13 micrograms X kg-1 X min-1) prevented renal hemodynamic responses to the renal nerve stimulation, whereas RSR responses to the stimulation were unaffected. Propranolol (8 micrograms X kg-1 X min-1) resulted in decreases in RSR at the renal nerve stimulation despite the presence of changes in renal hemodynamics similar to the other groups. The results indicate that intrarenal opiate receptors may participate in inhibiting renal secretion of renin mediated by the renal nerves when renal vasoconstriction and reduction of GFR occurred at the high-frequency stimulation.

Animals↗

PubMed1986

Temporal and spatial interactions between the carotid sinus and vagally mediated baroreflexes in dogs.

We investigated the temporal and spatial interactions between the carotid sinus and aortic arch baroreflex control of arterial pressure in 25 dogs anesthetized with pentobarbital sodium. The carotid sinus baroreceptor region was vascularly isolated to control the intracarotid sinus pressure. A hemorrhage catheter was inserted into the aortic arch. The systemic arterial pressure change after quick mild hemorrhage (2 ml/kg body weight within 1-2 s) was monitored. The open-loop gain of the vagally mediated baroreflex system was estimated from the mean arterial pressure response to the hemorrhage. Three protocols were employed to analyze the interactions. In the first protocol, we determined the effect of different levels of intracarotid sinus pressure on the open-loop gain of the vagally mediated baroreflex system. There was no significant effect. In the second protocol, the open-loop gain of the carotid sinus baroreflex system was determined after vagotomy. In the third protocol, the vagally mediated baroreflex system was activated by the hemorrhage without (spatial interaction) or with (temporal interaction) a delay after changing the intracarotid sinus pressure. The spatial interaction was facilitatory. A temporal interaction was found between the carotid sinus and vagally mediated baroreflex systems, when the delay was less than 30 s.

Animals↗

PubMed1985

Comparative responsiveness of the rapidly acting arterial pressure control system to quick mild hemorrhage and infusion in conscious rabbits.

The responsiveness of the rapidly acting arterial pressure control system to hemorrhage and infusion was investigated. Two catheters, one for pressure measurement and the other for inducing hemorrhage and infusion, were chronically implanted in 19 rabbits. A few days after the operation, each animal was quickly bled and transfused (2 ml/kg body weight) at intervals of 5 min while it was conscious. The hemorrhage-infusion experiment was repeated 16 times in each animal. The 16 strings of data were pooled for each animal. The overall open-loop gains (G) of the rapidly acting arterial pressure control system were estimated from the individually pooled responses to hemorrhage and infusion. There was no significant difference between the G-values, i.e., 7.2 +/- 1.2 by hemorrhage and 7.1 +/- 1.2 by infusion (mean +/- SD), as evaluated by the paired t-test (p greater than 0.5). Thus, the responsiveness of the rapidly acting arterial pressure control system to quick mild hemorrhage and to infusion appears to be similar.

Animals↗

PubMed1985

Time-dependent effect of sectioning carotid sinus nerves on the vagally mediated baroreflex.

The purpose of the reported experiments was to examine whether the vagally mediated baroreflex system (V-system) increases its feedback gain with time after sectioning of the carotid sinus nerves (CSN). In 10 dogs anesthetized with Nembutal, we determined the overall open-loop gain (G) of the rapidly acting arterial pressure control system. G was assessed as (delta API/delta APs)-1, where delta API and delta APs represent the immediate and steady-state decreases in arterial pressure at the aortic arch following a fast step-wise reduction in blood volume. delta API, delta APs and GINTACT in the intact condition (30th min before sectioning of the CSN) were -1.8 +/- 0.1 kPa, -0.20 +/- 0.01 kPa and 8.4 +/- 0.3 (mean +/- SE), respectively. The mean values of delta API, delta APs and G after sectioning of the CSN (Gv), first averaged within individual dogs and then averaged for ten dogs, were -2.53 +/- 0.07 kPa, -1.1 +/- 0.05 kPa, and 1.5 +/- 0.1, respectively. Gv did not change with time over about 4 h after sectioning of the CSN. It is concluded that the V-system cannot augment its ability to restore arterial pressure in compensation for the lost function of the carotid sinus baroreflex system over 4 h after sectioning of the CSN in the anesthetized dog.

Animals↗