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H Hosomi

Publications and source records attributed to H Hosomi.

At least 73 records · Page 4Linked to original sources

Neural control of urinary sodium excretion during hypertonic NaCl load in conscious rabbits: role of renal and hepatic nerves and baroreceptors.

We examined responses of renal nerve activity, urine flow, and urinary Na+ excretion to a hypertonic NaCl infusion in chronically instrumented conscious rabbits with unilateral renal denervation. The intravenous infusion of 20% NaCl, at 0.2 ml/min for 30 min, increased plasma osmolality by 27 +/- 5 mOsm/kg, and plasma Na+ by 16 +/- 3 mEq/l, and decreased hematocrit by 5 +/- 1%. These changes were accompanied by a marked decrease in renal nerve activity by 82 + 7%. Urine flow and urinary Na+ excretion increased gradually and peaked at the end of infusion. The innervated kidney excreted 23.3 +/- 3.3 ml urine and 5.5 +/- 0.7 mEq Na+ for the subsequent 60 min. However, the contralateral denervated kidney excreted only 9.5 +/- 2.0 ml urine and 2.2 +/- 0.6 mEq Na+; these values were significantly less than those of the innervated kidney. To examine the role of the sinoaortic and cardiopulmonary baroreceptors and the hepatic nerves in the response of renal nerve activity to the hypertonic NaCl infusion, renal nerve activity was examined in conscious rabbits with sinoaortic baroreceptor denervation (SAD) plus vagotomy and/or section of the anterior and posterior hepatic nerves (SAPH). In rabbits with SAD plus vagotomy or SAPH, the NaCl infusion also decreased renal nerve activity. After combining SAPH and SAD plus vagotomy, the decrease in renal nerve activity was completely blocked. These results indicate that hypertonic NaCl infusion elicits a marked decrease in renal nerve activity which is mediated predominantly by sinoaortic and cardiopulmonary baroreflexes and the hepatic nerves, and that the decrease in renal nerve activity plays an important role in the augmentation of renal function.

Afferent Pathways↗

Effects of hepatic NaCl receptor stimulation on renal nerve activity in conscious rabbits.

The effects of intrahepatic NaCl or osmo-receptor stimulation on renal nerve activity were examined in chronically instrumented conscious rabbits. Combined infusions of 9% NaCl via the portal vein and distilled water via the inferior vena cava did not alter plasma osmolality or plasma Na concentration of the systemic circulation but decreased renal nerve activity. Combined infusion of 6.5% LiCl and distilled water did not have any effects on renal nerve activity. The decrease in renal nerve activity induced by portal 9% NaCl infusions was completely abolished after section of the anterior and posterior hepatic nerves. These results indicate that stimulation of the intrahepatic NaCl receptors, not of the osmoreceptors, elicits a reflex decrease in renal nerve activity, which is mainly mediated by the anterior and posterior hepatic nerves.

Animals↗

Conservative treatment of Bell's palsy with steroids and dextran-pentoxiphylline combined therapy.

In 1980, Stennert proposed for the treatment of Bell's palsy an infusion therapy consisting of initially high dosages of steroids in combination with low-molecular dextran and pentoxiphylline. Excellent results were reported as a consequence of administering this treatment scheme. This "steroid-dextran" medication was modified (SD therapy) and administered in 172 cases of Bell's palsy. The results were compared with those of a group of 59 patients who had been treated with orally administered low-dose steroids in combination with vasodilators, adenosine triphosphate and vitamins. All patients with incomplete palsies recovered completely, regardless of the mode of treatment. In cases of complete palsy, 87% of patients recovered completely when treated with SD therapy. In contrast, 68% of the patients treated with orally administered steroids recovered completely.

Dextrans↗

Reflex control of renal nerve activity originating from the osmoreceptors in the hepato-portal region.

The reflex effects of hepatic osmoreceptors on the renal sympathetic nerve activity (RNA) were studied in 30 pentobarbital anesthetized, vagotomized and sino-aortic baroreceptor denervated (SAD + VD) rabbits. The changes in mean arterial pressure (MAP), heart rate (HR), and RNA were examined when 9% NaCl, 6.5% LiCl or 50% glucose solution was infused into the hepatic portal vein at a rate of 0.15 ml/kg/min for 10 min. Infusion of 9% NaCl solution into the hepatic portal vein increased the plasma osmolality by 10.8 +/- 1.0 mOsmol/kg from the control level in the blood of the hepatic portal vein and by 2.8 +/- 2.0 mOsmol/kg from the control level in the systemic blood. MAP was significantly elevated by 10.2 +/- 5.0 mmHg but HR did not change with hepatic portal infusion of 9% NaCl solution. Intraportal infusion of 9% NaCl solution significantly decreased the RNA by 28.6-34.2% from the control level, 6.5% LiCl solution by 28.6 +/- 4.7%, and 50% glucose solution by 26.2 +/- 3.0%. Femoral arterial infusion of hypertonic NaCl solution, however, did not evoke any significant change in RNA in SAD + VD rabbits. These findings suggest that increases in osmolality and NaCl concentration in the systemic circulation do not result in a decrease of RNA. Furthermore, after section of the anterior and posterior plexus of the hepatic nerve, hepatic portal infusion of hypertonic NaCl solution elicited no change in RNA. The present data indicate that an increase in osmolality in the hepatic portal venous blood results in a reflex decrease of RNA. This reflex may be important for restoration of a postprandial increase in osmolality.

Animals↗

Effects of atrial natriuretic peptide on water and NaCl absorption across the intestine.

Previous studies have demonstrated that atrial natriuretic peptide (ANP) causes natriuresis and diuresis. However, it is not established whether ANP also alters fluid and electrolyte balance via actions on intestinal absorption of water and sodium chloride. Therefore, the purpose of the present study was to investigate the effects of ANP on water and NaCl absorption across the intestine. First, we determined that ANP was taken up from the intestinal circulation in conscious dogs. During the intravenous infusion of ANP (0.3 microgram.kg-1.min-1), 27.4% of the ANP delivered to the intestinal vascular bed were removed from the circulation at that vascular bed, whereas only 1% of the ANP delivered to the hepatic circulation was removed at the hepatic vascular bed. Second, we determined the effects of the ANP infusion on splanchnic circulation in conscious dogs. ANP decreased hepatic arterial blood flow by 14%, portal venous blood flow by 16%, total hepatic blood flow by 15%, and cardiac output by 14%. Finally, we studied the effects of ANP on intestinal absorption of water and NaCl. ANP suppressed net absorption of water by 61%, Na+ by 43%, and Cl- by 42% across the jejunum but not the ileum. These results suggest that ANP modulates water and NaCl homeostasis across the jejunum but not across the ileum.

Animals↗

Atrial natriuretic peptide attenuates an increase in pulmonary vascular incremental resistance due to high pulmonary venous pressure.

The aim of this study was to determine whether an elevation of pulmonary venous pressure (PVP) and atrial natriuretic peptide (ANP) affects pulmonary vascular resistance (PVR) and pulmonary vascular incremental resistance (iPVR). We vascularly isolated the left lower lobe of the lung and perfused it with blood using a pulsatile pump. Blood flow (PBF) to the isolated lobe was decreased in 6 to 7 steps from about 8 to 1 ml/(kg.min). PVR was calculated from measurements of PBF and the pressure difference between pulmonary arterial pressure and PVP at four different levels of fixed PVP. iPVR was estimated from a slope of the pressure-flow relationships between effective pulmonary driving pressure and PBF at four different levels of fixed PVP. iPVR was 2.2 +/- 0.2, 2.2 +/- 0.1, 2.4 +/- 0.1, and 2.6 +/- 0.2 mmHg.min.kg/ml, when PVP was 0, 5, 10, and 15 mmHg, respectively. To test whether or not the response of the pulmonary vascular bed to the elevated PVP is modulated by ANP, iPVR was estimated before and after an administration of ANP in the perfusion circuit. Increased iPVR from 2.1 +/- 0.2 to 2.5 +/- 0.2 mmHg.min.kg/ml in response to the elevation of PVP from 0 to 15 mmHg decreased to the control level after the administration of ANP. ANP, however, did not change the control iPVR. PVR decreased with increasing PVP. ANP decreased PVR when PVP was 0 mmHg, but did not change it when PVP was 15 mmHg. These results suggest that ANP decreases PVR and restores the decreased pulmonary vascular compliance.

Animals↗

Effect of exercise on fractional extraction of catecholamines by the denervated heart in conscious dogs.

To examine the applicability of Halter's assumption to the denervated heart during exercise, we measured the concentrations of norepinephrine (NE) and epinephrine (E) in arterial and coronary sinus plasma in cardiac denervated dogs. As the level of exercise was increased from 0 (at rest) to 3, 6, and 12 km/h, fractional extraction (FE) of NE significantly decreased from 51 +/- 7 to 39 +/- 5, 34 +/- 6, and 30 +/- 5%, respectively. FE of E did not decrease at exercise (at rest, 57 +/- 10; 3 km/h, 60 +/- 9; 6 km/h, 60 +/- 5; and 12 km/h, 66 +/- 6%). There was no significant difference between FE of NE and E at rest and at 3 km/h, but FE of NE was significantly less than that of E with 6 and 12 km/h exercise. We conclude that FE of NE by the denervated heart decreases during exercise, and that FE of NE and E are approximately equal at rest and at mild exercise, but not at strenuous exercise.

Animals↗

Non invasive analysis of hemodynamic changes in dogs with acute pancreatitis.

To elucidate the hemodynamic changes in the course of acute pancreatitis in dogs, various parameters were monitored non-invasively and real-timely by the ultrasonic flow probes which had been placed in advance. The dogs were divided into two groups, i.e., control group (CG) and infusion group (IG). In the infusion group, lactated Ringer solution was infused intravenously for 12 hours in order to maintain LAP or CVP at the mean +/- 1 mmHg of its control value before inducing pancreatitis. In the control group, lactated Ringer solution was not infused. Cardiac output (CO) and LV dp/dt abruptly decreased in a few hours and remained low levels in a control group (CG), but not in an infusion group (IG). It shows that the decreased CO was caused by a decrease in preload but not by a depression of contractility. Gastroduodenal arterial flow (GDAF) and GDAF/CO decreased in a few hours and kept low level in CG, but not in IG. Therefore, a decrease in GDAF is mainly caused by an increase in vascular resistance due to an increase in Hematocrit. Superior pancreatico-duodenal venous flow (SPDVF) and SPDVF/CO decreased immediately in both groups, revealing that there is severely depressive outflow from pancreas because of hemorrhage and destruction of pancreatic parenchyma immediately after the onset of pancreatitis. In CG, Total hepatic flow (THF) and Portal vein flow (PVF) gradually decreased in a few hours and kept low levels, but Common hepatic arterial flow (CHAF) did not decrease. This suggests that decrease of THF is due to decrease of PVF. THF/CO increased in CG. PVF/CO decreased in CG, while CHAF/CO increased in both groups. The increased CHAF compensated for the decreased PVF, which may play an important role in protecting the liver.

Acute Disease↗

Effects of portal infusion of hypertonic solution on jejunal electrolyte transport in anesthetized dogs.

Jejunal electrolyte absorption was measured in the jejunal loops of anesthetized dogs during infusions of hypertonic solutions via the portal vein. The net Na absorption was not influenced by the 9% NaCl infusion into the inferior vena cava, although it was significantly attenuated by the portal 9% NaCl infusion. This effect may not be due to the osmotic stimulus, since the portal 50% glucose or 6.5% LiCl infusion had no significant influence on the net Na absorption. To determine the mechanism of the decrease in the net Na absorption during the portal hypertonic NaCl infusion, the net Na absorption was measured after the section of anterior and posterior hepatic nerves (SAPH) or intravenous atropine injection. Both SAPH and the intravenous atropine injection completely blocked the effect of the portal 9% NaCl infusion on the net Na absorption. These results indicate that 1) net Na absorption in dog jejunum is depressed by the hypertonic NaCl infusion via the portal vein; 2) the effect is NaCl specific and may not be due to the osmotic stimulus; and 3) the afferent limbs of this effect are the anterior and posterior hepatic nerves, and the efferent limb of this effect is the vagus nerve. Thus the hepatojejunal reflex may play an important role in the regulation of body fluid homeostasis.

Absorption↗

Arterial pressure and its variability in conscious rabbits at different ages.

Mean level and its variability of mean arterial pressure (MAP) were studied in 25 unanesthetized rabbits aged 6, 12, 18, 24 and 30 months. They were selected from the same large colony and bred with an ordinary rabbit food under a given environmental conditions. MAP in the aortic arch was continuously monitored with a catheter-transducer system for 3 hrs. Mean (M) and variance (V) of MAP for 3 hrs were not significantly altered with aging (p greater than 0.05, Kruskal-Wallis' multi-sample test). Intra-animal variations of the M and SD were small. Most of histograms of MAP for 3 hrs shows an exaggerated mode at any age. Distribution pattern of the histogram was not specific to age. These suggest that responsiveness of the baroreflex system should not be affected by aging from 6 to 30 months.

Aging↗

Effects of brain natriuretic peptide on hemodynamics and renal function in dogs.

A new natriuretic peptide has been found in the porcine brain and termed brain natriuretic peptide (BNP). To examine the effects of BNP on the cardiovascular system and kidney as compared with alpha-hANP (ANP), BNP, and ANP (33, 167, 667 pmol/kg) were intravenously administered to anesthetized dogs. BNP dose-dependently decreased arterial pressure and left atrial pressure and dose-dependently increased heart rate, cardiac output, renal blood flow, urine volume, and sodium excretion. These effects were not significantly different from the effects of respective doses of ANP. To eliminate the possibility that these results were confounded by opposing actions of the baroreflex system, we performed additional experiments following sinoaortic denervation and vagotomy. These results also demonstrated no differences between the effects of BNP and ANP on the measured variables. Finally, we determined that the pharmacokinetics of exogenously injected BNP and ANP are indistinguishable. These findings lead to the possibility that BNP physiologically works in the body in the same manner as ANP.

Analysis of Variance↗

Incremental pulmonary vascular resistance increases with elevation of pulmonary venous pressure.

The aim of this study was to determine whether elevation of pulmonary venous pressure affects incremental pulmonary vascular resistance. We vascularly isolated the left lower lobe of the lung and perfused with blood using a pulsatile pump. Blood flow to the isolated lobe was decreased in 6 to 7 steps from about 8 to 1 ml/kg/min. Incremental pulmonary vascular resistance was estimated from the slope of the pressure-flow relationship between pulmonary arteriovenous pressure difference and pulmonary blood flow at different pulmonary venous pressures. Incremental pulmonary vascular resistance increased as pulmonary venous pressure was elevated. This result suggests that an increase in cardiac output, i.e., an increase in pulmonary blood flow, results in a larger increase of pulmonary arterial pressure in high pulmonary venous pressure than in low pulmonary venous pressure.

Animals↗

Long-term profiles of sleep-related hemodynamic changes in the postoperative chronic cat.

The long-term postoperative changes in mean arterial pressure (MAP) and heart rate (HR) during sleep in cats (n = 4) were observed. In the first or second week after surgery, MAP and HR in slow wave sleep (SS) just prior to paradoxical sleep (PS) were higher than those in PS as described in previous reports. In the fourth or fifth week after surgery, the above relationships of MAP and HR between SS and PS were inverted as demonstrated in the present study. The results show that getting true physiological control data is not so simple but a complex task.

Animals↗

Alpha-agonist modifies baroreflex vasoconstriction by a postjunctional mechanism in dogs.

1. We examined whether or not circulating alpha-agonist modified baroreflex vasoconstriction of the hindlimb, using anaesthetized dogs in which the limb was vascularly isolated and perfused with blood from a donor dog using a pulsatile pump. 2. The open-loop gain (G) of the baroreflex was estimated from changes in mean arterial pressure following mild quick haemorrhage from the aorta of the recipient dog. 3. The hindlimb perfusion pressure increased after haemorrhage due to neurogenic vasoconstriction. 4. An overall gain (Gh) of the baroreflex hindlimb vascular bed control system was estimated from the ratio of the increase in hindlimb perfusion pressure to the change in systemic arterial pressure of the recipient dog. 5. Administration of a relatively selective alpha 1-agonist with no prejunctional beta 2 stimulating action (phenylephrine) or a selective alpha 2-agonist (clonidine) to the donor dog increased its systemic arterial pressure and augmented Gh. 6. Since both drugs were administered to the donor dog and could not enter into the recipient dog, these drugs did not affect the recipient's sympathetic nervous system, including the central nervous system and afferent limb of the baroreflex system. Therefore, these drugs could modify baroreflex vasoconstriction of the hindlimb only at the junction of the efferent sympathetic nerve and the vascular smooth muscle. 7. It was concluded that postjunctional alpha-adrenoceptor stimulation augments neurogenic vasoconstriction.

Adrenergic alpha-Agonists↗

Effects of brain natriuretic peptide on renal nerve activity in conscious rabbits.

Responses of renal nerve activity (RNA) to intravenous infusion of brain natriuretic peptide (BNP) were examined in chronically instrumented conscious rabbits with all baroreflexes intact, sinoaortic baroreceptor denervation (SAD), and SAD plus vagotomy. In intact rabbits, an infusion of BNP at a rate of 0.3 microgram.kg-1.min-1 for 30 min decreased mean arterial pressure (MAP) by 8 +/- 1 mmHg and increased RNA by 48 +/- 4% but did not alter heart rate (HR). The decrease in MAP in SAD rabbits (20 +/- 3 mmHg) was greater than in intact rabbits, whereas RNA increased less (21 +/- 7%). After SAD plus vagotomy, BNP lowered MAP by 25 +/- 4 mmHg, whereas RNA was not altered significantly. To further examine the effects of BNP on baroreflex control of HR and RNA, the baroreceptors were stimulated or unloaded by raising or lowering MAP by injections of phenylephrine or glyceryl trinitrate, respectively. The maximum change in each HR or RNA response to phenylephrine or glyceryl trinitrate was plotted against the maximum change in each MAP response and a logistic function curve was fitted to the MAP-HR and MAP-RNA relationship. BNP did not alter the slope of either curve but shifted both curves to the left. These results indicate that 1) in intact rabbits, BNP increases RNA due to sinoaortic and cardiopulmonary baroreflexes and 2) BNP resets the baroreflex control of HR and RNA to a lower arterial pressure.

Animals↗

Renal nerve blunts natriuretic and diuretic response to atrial natriuretic peptide in conscious rabbits.

The contribution of the renal nerve to the natriuretic and diuretic responses to rat atrial natriuretic peptide (rAMP) was investigated in conscious rabbits with unilateral renal denervation. Renal nerve activity (RNA) was measured at the contralateral innervated kidney. Catheters were bilaterally implanted into the ureters. Urine samples were collected from each kidney by gravity drainage at 10-min clearance intervals. In rabbits with all baroreflexes intact, infusion of rANP at 0.3 micrograms/(kg.min) for 30 min decreased mean arterial pressure by 8 +/- 4 mmHg and increased RNA by 53 +/- 13%. After sinoaortic baroreceptor denervation (SAD), hypotensive response to infusion of rANP was greater than that in intact rabbits, while RNA did not change. After SAD plus vagotomy, infusion of rANP lowered mean arterial pressure by 21 +/- 4 mmHg and RNA by 19 +/- 6%. In the denervated kidney, infusion of rANP increased Na+ excretion by 16.1 +/- 4.5 from 3.5 +/- 1.0 muEq/min and water excretion by 0.17 +/- 0.05 from 0.08 +/- 0.02 ml/min. In the contralateral innervated kidney, infusion of rANP increased the amount of Na+ and water excretion by 4.5 +/- 3.2 muEq/min and 0.07 +/- 0.04 ml/min, which were significantly less than those in the denervated kidney. These results indicate that infusion of rANP increases RNA, due to baroreceptor reflexes, and that this increase in RNA blunts natriuretic and diuretic action of rANP.

Animals↗

[Conservative treatment of Bell's palsy--high dose steroid infusion with low-molecular dextran].

The etiology of Bell's palsy has not been as yet completely elucidated and the treatment is empirical and controversial. The two most common forms of treatment are steroid therapy and surgery. On the basis of the pathophysiology of Bell's palsy that edema as well as primary or secondary ischemia lead to both compression and hypoxia, Stennert employed high doses of cortisone for a strong antiphlogistic and anti-edematous effect, and dextran in combination with pentoxifylline to increase peripheral nerve perfusion and reported high recovery rate. Since the past 3 years, we have been treating patients with Bell's palsy with a high dose of steroid plus low-molecular dextran (SD therapy). Hydrocortisone was added directly to 500 ml of dextran solution with ATP and vitamins, starting with 500 mg and finally down with 100mg during 7 days. Before we had adopted this regimen, the patients with Bell's palsy were treated with orally-administrated steroid. A half dose of steroid was administrated in the latter regimen. SD therapy was employed in 120 cases of Bell's palsy, and its results were compared with those of 82 cases with orally-administrated steroid. In a total of 67 cases with incomplete palsy, all cases obtained complete recovery within one month after the onset regardless of the mode of treatment. Each patients with complete palsy was examined with a nerve excitability test (NET) at the first visit and one week later. According to the response of NET, the patients with complete palsy were divided into the following three groups; "good", "poor" and "absent". In "good" group, all cases with SD therapy had complete recovery, while the recovery rate of 31 cases with orally-administrated steroid therapy was 90%. This difference was statistically significant (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

The range of renal blood flow for renal autoregulatory adjustments in resistance.

The study was designed to determine the range of renal blood flow over which autoregulation occurred. Pressure-flow relationships were obtained in the left kidney over a wide range of perfusion blood flow. Renal vascular resistance showed sigmoidal changes with changing renal blood flow over the range of 0.3 to 6.3 ml/min.g kidney wet weight. This curve shows two definite points of inflection at renal blood flows of 2.3 and 3.7 ml/min.g. Once renal blood flow rises above the normal range, renal vascular resistance changes hyperbolically with decreases in renal blood flow. We conclude that (1) the range of blood flow for autoregulatory adjustments in resistance is between 2.3 and 3.7 ml/min.g, and (2) the autoregulatory mechanism can be easily impaired by increasing renal blood flow far above the upper limit of the range.

Animals↗