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Biomedical subjects

M Omata

Publications and source records attributed to M Omata.

At least 397 records · Page 22Linked to original sources
PubMed1994

Prospective assessment of incidence of fulminant hepatitis in post-transfusion hepatitis: a study of 504 cases.

The incidence of posttransfusion hepatitis and "fulminant" hepatitis was investigated by a plan devised at our hospital in December 1982. Of 2959 blood recipients between January 1982 and December 1988, 504 (22.5%) developed posttransfusion hepatitis, with a mean transfusion volume of 10.2 units. Of the 504 cases of posttransfusion hepatitis, "icteric" (T-Bil > 2.0 mg/dl) and "overt icteric" hepatitis (T-Bil > 5.0 mg-dl) developed in 111 cases (22.0%) and 28 cases (5.6%), respectively. Of the 28 overt icteric hepatitis cases, 13 (2.8%) were thought to be true overt icteric posttransfusion hepatitis because the icterus was caused by other reasons in the other 15 cases (seven neonatal jaundice, four hemolytic anemia, one radiation hepatitis, one halothane-induced hepatitis; two other cases were excluded because chronic liver disease was diagnosed by imaging procedures despite serum ALTs in the normal range before transfusion). The anti-HCV serostatus was investigated in five of the 13 true overt icteric posttransfusion hepatitis patients using blood specimens taken 180 days or more following the onset of posttransfusion hepatitis. Anti-HCV seroconversion occurred in three of the five cases (60%). HCV seroconversions were not seen in the cases in which the icterus was due to other reasons.

Alanine Transaminase↗
PubMed1994

Effects of interferon beta on non-A, non-B acute hepatitis: a prospective, randomized, controlled-dose study. Japan Acute Hepatitis Cooperative Study Group.

BACKGROUND/AIMS: Non-A, non-B acute hepatitis progresses to a higher incidence of chronicity and hepatocellular carcinoma. To avoid the development of chronic liver disease, resolution of acute hepatitis C might be most effective. The aim was to establish the effect of interferon in disturbing progression to chronicity and to determine the most appropriate treatment protocol. METHODS: Ninety-seven acute non-A, non-B hepatitis cases were randomly assigned to six different protocols and treated with 8.4-336 MU of interferon; 90 cases were finally completely analyzed. Titers of hepatitis C virus (HCV) RNA and HCV genotypes were determined. RESULTS: Seventy-four cases were positive for second-generation anti-HCV. Of these, 65 (89%) were positive for HCV RNA. In these 65 cases, the resolution rate was 32%, and this rate was dependent on the total treatment dosage. Only the group treated with 336 MU showed a high (83%; 10/12) resolution rate; the other five groups had 0%-38% resolution. CONCLUSIONS: Interferon treatment for acute hepatitis C could be regarded as a "vaccinelike" therapy by preventing the development of the virus carrier state.

Adult↗
PubMed1994

Molecular mechanism of cibenzoline-induced anticholinergic action in single atrial myocytes: comparison with effect of disopyramide.

The anticholinergic effects of cibenzoline were examined and compared with those of disopyramide in atrial myocytes isolated from guinea pig heart. The tight-seal whole-cell voltage clamp technique was performed with a patch pipette filled with guanosine-5'-triphosphate (GTP) or guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S). In GTP-loaded cells, both acetylcholine (ACh) and adenosine (Ado) induced a specific K channel current through GTP-binding proteins by binding to the muscarinic and Ado receptors, respectively. Both cibenzoline and disopyramide suppressed the ACh-induced K current effectively in a concentration-dependent manner. The concentrations for half-maximal inhibition of the current (EC50) caused by cibenzoline and disopyramide were 8 and 3 microM, respectively. In GTP gamma S-loaded cells, the K current was irreversibly activated because GTP binding proteins were directly elicited by GTP gamma S. Cibenzoline effectively caused a decrease in the GTP gamma S-induced K current, whereas the extent of disopyramide action on the GTP gamma S-induced K current was much less. Cibenzoline also caused significant inhibition of Ado-induced K current in GTP-loaded cells. However, the action of disopyramide was less effective in inhibiting Ado-induced K current. These results indicate that cibenzoline has less potent anticholinergic effects than disopyramide in atrial myocytes. In addition, cibenzoline effectively inhibits the muscarinic K channel itself and/or GTP-binding proteins coupled to the channel, whereas the effect of disopyramide is attributed mainly to blockade of muscarinic receptors. These findings provide novel understanding of the molecular mechanism of anticholinergic action of cibenzoline.

Animals↗
PubMed1994

Shock-induced refractory period extension and pharmacologic modulation of defibrillation threshold.

Shock-induced refractory period extension (RPE) has been suggested as a mechanism of electrical defibrillation. We measured RPE caused by localized field stimulation measured before and during infusion of disopyramide (n = 5), flecainide (n = 5), or E-4031 (n = 5) in anesthetized dogs and determined the effect of the drugs on the internal defibrillation threshold (DFT). In the baseline state (n = 15), 16 V/cm S2 field stimulation prolonged the effective RP by 36 +/- 15 ms (22 +/- 12% of RP without S2), whereas 4 and 8 V/cm S2 stimuli did not cause marked RPE. The RPE normalized by the RP without S2 was not significantly influenced by any drug (16 V/cm: disopyramide 30 +/- 11 vs. 27 +/- 11, flecainide 25 +/- 5 vs. 19 +/- 12, and E-4031 18 +/- 13 vs. 22 +/- 14%). Disopyramide did not alter the defibrillation threshold (4.2 +/- 0.6-4.4 +/- 0.6 J). In 2 dogs given flecainide, ventricular fibrillation became refractory to defibrillation. In contrast, E-4031 lowered the threshold from 4.5 +/- 2.4 to 2.2 +/- 1.2 J (p < 0.01). The results suggest that flecainide and E-4031 do not modulate defibrillation efficiency through their effects on RPE.

Animals↗
PubMed1994

Vasoconstrictors and renal protection induced by beta 1-selective adrenoceptor antagonist bisoprolol.

We investigated the role of the vasoconstrictors endothelin-1 (ET-1) and thromboxane in renal protection by the beta 1-selective adrenoceptor antagonist, bisoprolol, in Dahl salt-sensitive rats (Dahl S) and salt-resistant rats (Dahl R). Six-week bisoprolol treatment (20 mg/kg chow) reduced systolic blood pressure (SBP) by 14% in Dahl S rats fed a high-salt (4% NaCl) diet. This BP reduction was accompanied by a decrease in aortic wall thickness. ET-1 and thromboxane released from renal cortex was significantly decreased by 17 and 30% with bisoprolol, respectively. Other prostaglandin synthesis was unaffected. Renal function such as proteinuria, N-acetyl-beta-D-glucosaminidase (NAG) excretion, and glomerular filtration rate (GFR) was not influenced by bisoprolol. Morphologic investigation showed that bisoprolol significantly improved glomerular sclerosis by 29% and attenuated arterial damage by 71%, although tubular injury was not affected. The more severe the glomerulosclerotic lesions, the greater the generation of thromboxane and ET. The arterial lesions were positively correlated to thromboxane generation. These data indicate that long-term bisoprolol treatment reduces vasoconstrictive ET-1 and thromboxane generation and that these alterations may be partly responsible for the amelioration of glomerular and arterial injury in Dahl S rats.

Adrenergic beta-1 Receptor Antagonists↗
PubMed1994

New dihydropyridine calcium channel antagonist, pranidipine, attenuates hypertensive renal injury in Dahl salt-sensitive rats.

Interest in the cardiovascular protective effects of calcium channel antagonists has increased in the past decade. We investigated prevention of vascular wall remodeling by the long-acting calcium channel antagonist pranidipine in 12-week-old Dahl salt-sensitive (SS) rats with high-salt-induced (4% NaCl) hypertension. Six-week pranidipine treatment (60 mg/kg chow) decreased systolic blood pressure (SBP) by 22% in SS rats. This BP reduction was associated with decreases in cardiac mass and weight of the aortic wall. Glomerular filtration rate (GFR) was increased by 33%, but this did not lead to a decrease in urinary protein or NAG excretion. Morphologic investigation demonstrated striking resolution of arterial injury (medial necrosis and/or hyperplasia, inflammatory cell infiltration, and thrombus formation) by 87% after pranidipine treatment. Glomerular sclerosis was also attenuated by 61%, whereas tubular injury was improved by only 28%. These morphologic changes were reflected in the findings that the capacity of kidney homogenate for generating lipid peroxides was significantly decreased and that collagen levels and pattern type became similar to those of normotensive salt-resistant (SR) rats. Pranidipine also attenuated hypertensive vasculopathy in small arteries of the middle cerebral arteries. Thus, the calcium channel antagonist pranidipine can attenuate the vascular injury that occurs in salt-induced hypertension, a promising property that implicates its clinical usage, particularly in essential hypertension with cardiovascular complications.

Animals↗
PubMed1994

Antithrombin and thrombolytic effects of a new antithrombin agent: angioscopic and angiographic comparison with heparin or batroxobin.

The antithrombotic effect of three different types of antithrombotic agents (antithrombin:argatroban, heparin, defibrinogenating agent:batroxobin) were evaluated in canine coronary and iliac arteries. An occlusive thrombus was produced by balloon injury. One of the three agents was infused intravenously at 1 hour after thrombus formation (heparin 250 U/kg, argatroban 0.5 mg/kg, batroxobin 0.5 U/kg) and the effect of thrombus size reduction was evaluated. On the contralateral side of the iliac artery, the preventive effect of these agents on thrombus formation was evaluated after balloon injury. In the iliac artery, angioscopic percent area obstruction by the thrombus before and 60 minutes after treatment reduced from 69% to 32% in the argatroban group, and from 64% to 51% in the batroxobin group (P < 0.0001 and P < 0.05, respectively). No significant change was observed in the heparin group. Angiography demonstrated the same trend. The percent area stenosis with thrombus at 60 minutes following balloon injury was 0.75% in the argatroban group, 18.9% in the heparin group (P < 0.05 vs argatroban), and 12.9% in the batroxobin group. Thrombus size at the treated site was smaller than that at the control site in all three groups (P < 0.05 vs control). In the coronary artery, angioscopic percent area obstruction by the thrombus before and 60 minutes after treatment reduced from 84% to 53% in the argatroban group, and from 86% to 68% in the batroxobin group (P < 0.0001 and P < 0.05, respectively). No significant change was observed in the heparin group. Angiography also demonstrated the same trend. The activated partial thromboplastin time (APTT) was prolonged to 189% of the control value with argatroban and to 1253% of the value with heparin (P < 0.0001). Fibrinogen was markedly reduced with batroxobin. These results showed that both the antithrombin agent and the defibrinogenating agent have a preventive effect on thrombus formation and the effect on thrombus size reduction, without marked prolongation of the APTT.

Angiography↗
PubMed1994

Contraction-excitation feedback in atrial reentry: role of velocity of mechanical stretch.

To determine the effects of atrial stretch on atrial flutter, we analyzed variations in atrial flutter cycle length (CL) caused by ventricular contraction in five dogs with artificially induced atrioventricular block. In contrast to absence of variations in CL during sustained ventricular asystole, atrial stretch by ventricular contraction consistently produced phasic variations in CL. The variations were not confined to any specific atrial sites, but depended on the time of ventricular contraction relative to atrial activation phase. The phase-response curve of the variations was closely related to that of the velocity of changes in the atrial pressure with no time lags, but not to that of the atrial pressure itself. Pharmacological denervation did not abolish the variations. Conventional electrophysiological study revealed greater changes in intra-atrial activation time by atrial stretch at a short pacing cycle length than at a longer one, suggestive of changes in repolarization by mechanical stretch. In conclusion, atrial stretch caused by ventricular contraction produces phasic variations in CL, the extent of which depends on the velocity of the mechanical stretch of atrial muscles.

Animals↗
PubMed1994

Participation of ouabainlike compound in reduced renal mass-saline hypertension.

We examined the role of ouabainlike compound in reduced renal mass-saline hypertension using a population of rats immunized with ouabain. To develop ouabain-immunized rats, ouabain-bovine serum albumin conjugates were injected subcutaneously three times at 4-week intervals. Titer determinations were made 2 weeks after the third immunization, and rats with high titers were used in the study. Immunoglobulin G fractions from ouabain-immunized rats effectively inhibited the contractile response of guinea pig aorta to exogenous ouabain (150 nmol). Fourteen ouabain-immunized and seven nonimmunized control rats underwent subtotal nephrectomy. An additional eight ouabain-immunized and six nonimmunized rats served as sham-operated rats. Four groups of rats drank 1% NaCl solution for 3 weeks, and systolic blood pressure was measured weekly by the tail-cuff method. Two groups of sham-operated rats remained normotensive. In contrast, two groups of subtotally nephrectomized rats developed hypertension. However, among these rats, systolic blood pressure was significantly lower in ouabain-immunized rats than in nonimmunized rats (161 +/- 5 versus 180 +/- 3 [+/- SEM) mm Hg, P < .01). The decrease in blood pressure was accompanied by a significant inhibition of aortic hypertrophy (P < .05). These results indicate that chronic blockade of circulating ouabainlike compound partly ameliorates reduced renal mass-saline hypertension and suggest that circulating ouabainlike compound may be involved in the pathophysiology in this model of hypertension.

Adrenal Glands↗
PubMed1994

Role of brain ouabainlike compound in central nervous system-mediated natriuresis in rats.

Intracerebroventricular infusion of artificial sodium-rich cerebrospinal fluid induces increases in blood pressure and urinary sodium excretion. To examine the role of brain ouabainlike compound in these central nervous system-mediated responses, we evaluated the effects of prior intracerebroventricular injection of the Fab fragments of digoxin-specific antibody (Digibind, 10 mg/mL, 10 microL) on changes in blood pressure and urinary sodium excretion after intracerebroventricular infusion of high-sodium (323 mmol/L, 150 microL/kg per 15 minutes) cerebrospinal fluid in anesthetized rats. Antiouabain action of Digibind was revealed by the inhibition of a contractile response to ouabain in guinea pig aorta. Similar significant increases in blood pressure were found in rats that received preinjection of Digibind (n = 14) compared with control rats that received injection of saline (n = 5) or normal sheep IgG (n = 8). In rats pretreated with Digibind the natriuretic responses to central high sodium were significantly diminished by 68% (P < .05) or 82% (P < .05) compared with rats treated with saline or normal IgG, respectively. In contrast, Digibind did not affect either pressor or natriuretic responses to intracerebroventricular angiotensin II (600 ng/30 microL per 10 minutes). These data indicate that Digibind significantly inhibits increases in renal sodium excretion in response to high central sodium and suggest that brain ouabainlike compound may be involved in central nervous system-mediated natriuresis with nonpressor mechanisms.

Animals↗
PubMed1994

Long-term administration of L-arginine improves nitric oxide release from kidney in deoxycorticosterone acetate-salt hypertensive rats.

To examine the effects of L-arginine (L-Arg) on endothelial function, we administered 0.5 g/L L-Arg in drinking water to deoxycorticosterone acetate (DOCA)-salt rats for 8 weeks and then measured nitric oxide (NO) release from isolated kidneys using a newly developed real-time chemiluminescence method. Renal pathology was also analyzed. Acetylcholine caused much smaller declines in renal perfusion pressure (10(-7) mol/L acetylcholine: -24 +/- 2% [SEM] versus -50 +/- 2%, P < .001) and NO release in DOCA-salt rats (+3 +/- 1 versus +33 +/- 3 fmol/min per gram kidney weight, P < .001) compared with control rats. L-Arg did not influence the time course of systolic blood pressure elevation in DOCA-salt rats (211 +/- 5 versus 208 +/- 6 mmHg, DOCA versus L-Arg/DOCA, P = NS). However, oral administration of L-Arg improved acetylcholine-induced declines in renal perfusion pressure (10(-7) mol/L acetylcholine: L-Arg/DOCA, -39 +/- 3%, P < .01 versus DOCA). This change was associated with an increase in NO release by acetylcholine (10(-7) mol/L acetylcholine: L-Arg/DOCA, +10 +/- 1 fmol/min per gram kidney weight, P < .05 versus DOCA). However, morphological changes in renal vessels and glomeruli were similar between DOCA and L-Arg/DOCA rats. These results suggest that L-Arg administration partially reverses renal endothelial function with respect to vasorelaxation and NO release independent of blood pressure changes, indicating that hypertensive vessels seem to be depleted of L-Arg and/or have defects in the availability of L-Arg for NO synthesis.

Acetylcholine↗
PubMed1994

IgG+, CD5+ human chronic lymphocytic leukemia B cells. Production of IgG antibodies that exhibit diminished autoreactivity and IgG subclass skewing.

Several questions exist regarding CD5+ B cells. These include the ability of these cells, as compared to CD5- B cells, to undergo an Ig isotype class switch, the subclasses utilized, and the effects that switching may have on antigen binding. To address these issues, ten patients with chronic lymphocytic leukemia (CLL) whose CD5+ leukemic B cell clones produced IgG were studied. Monoclonal IgG was collected from PMA-stimulated CLL cells and from heterohybridomas constructed with these cells, and then analyzed for IgG subclass utilization, autoreactivity, and DNA idiotype expression. The monoclonal B cells from 80% of the CLL patients produced IgG1 and those from 20% produced IgG3. None produced IgG2. In contrast to the known autoreactivity of IgM-producing CD5+ CLL cells (> 50% autoreactive), none of these IgG antibodies reacted significantly with the autoantigens tested. However, three did react significantly with autoantigen after artificially increasing antibody valency by crosslinking. Whereas five of the IgG molecules expressed a cross reactive idiotypic (CRI) marker characteristic of non-mutated kappa anti-DNA antibodies, three expressed a CRI displayed primarily on mutated IgG anti-DNA antibodies. Thus, some CD5+ human B cells can undergo an isotype class switch that for these CLL cells is biased against IgG2 and in favor of the IgG1 and IgG3. In their native state the IgG molecules secreted by these isotype-switched CD5+ cells have diminished autoreactivity, as compared to IgM-producing CLL cells. Since some of the IgG antibodies could be made auto- and poly-reactive by increasing antigen-binding valency, while others expressed idiotypic markers of mutated antibodies, certain of these CD5+ B cells probably utilize non-mutated Ig V genes coding for polyreactive antibodies, whereas others may use genes that have undergone somatic mutation and that code for more restricted specificities. Therefore, both valency and VH gene mutation may account for the diminished autoreactivity of these CD5+ B cell-derived IgG antibodies.

Adult↗
PubMed1994

A multicenter randomized controlled dose study of ursodeoxycholic acid for chronic hepatitis C.

The effect of ursodeoxycholic acid on liver function tests and on bile acid metabolism was investigated in a multi-center randomized controlled dose study for chronic hepatitis C. Twenty, 18 and 19 patients were administered 150, 600 and 900 mg/day, respectively of ursodeoxycholic acid every day for 16 wk. Serum liver parameters and bile acid composition in the treatment groups were compared with 17 control patients. A similarly significant decrease of serum alanine aminotransferase and serum gamma-glutamyltransferase was observed in patients administered 600 and 900 mg of ursodeoxycholic acid. Serum bile acid composition was determined by high-performance liquid chromatography. At entry, the relative proportions of major bile acids were similar to those observed in normal individuals. Maximal concentrations of total ursodeoxycholic acid were 0.30 mumol/L, 5.59 mumol/L, 21.42 mumol/L and 14.73 mumol/L in the control, 150, 600 and 900 mg/day groups, respectively. The fraction of the total ursodeoxycholic acid increased in a dose-dependent manner, and it was significantly higher than in controls (p < 0.001). The hydrophobicity index of bile acids was calculated by the method of Heuman, and its correlation with serum parameter levels was analyzed. In the 600 and 900 mg/day dose groups, serum alanine aminotransferase decreased in the cases in which hydrophobicity index significantly decreased during treatment. The same correlation was observed between the hydrophobicity index and serum gamma = glutamyltransferase in these two groups. There was no correlation between these parameters in the control and 150-mg groups. There was no correlation between reduction rate of serum alanine aminotransferase and initial liver histology.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMed1994

[Histological assessment of the liver long after interferon treatment in patients with chronic type C hepatitis].

The effects of interferon on chronic hepatitis C long after the treatments were assessed biochemically, virologically and histologically. Among the 12 cases who showed normal alanine aminotransferase (ALT) levels and seroconversion of HCV RNA after treatment, histological improvements were observed in 8. In contrast, among the 11 cases who showed abnormal ALT levels and HCV viremia after treatment, histological improvements were observed in only 1. Histological improvement of the liver was thus, well correlated with normalization of ALT levels and seroconversion of HCV RNA. These data indicate that complete histological resolution of chronic hepatitis C is obtainable by elimination of the virus by interferon treatment.

Biomarkers↗
PubMed1994

Effects of a calcium antagonist and an angiotensin II receptor antagonist on rat renal arterioles.

The objective of this study was to investigate the effects of a dihydropyridine calcium antagonist, manidipine HCl, and an angiotensin II receptor antagonist, CV-11974, on renal microvasculature in hypertensive rats. Hydronephrosis was induced by ligation of the left ureter in 8-week-old stroke-prone spontaneously hypertensive rats. Two months after the operation, the hydronephrotic kidney was split longitudinally and spread out as a thin sheet, and the renal microvasculature was observed directly under a light microscope. Administration of manidipine HCl (20 micrograms/kg) caused a gradual fall in blood pressure (-34 mmHg). The afferent arterioles were dilated, and maintained the same level of dilatation until 30 min (+20%). The efferent arterioles were also dilated (+8%). Glomerular blood flow was significantly increased (+38%). Administration of CV-11974 (100 micrograms/kg) caused a sharp fall in blood pressure at 2 min (-24 mmHg), with a continuous fall in blood pressure until 60 min (-46 mmHg). The afferent arterioles were gradually dilated (+15%). The efferent arteriole was also dilated until 60 min, but to a lesser extent than the afferent arteriole. Glomerular blood flow was immediately increased (+35%). We conclude that both manidipine HCl and CV-11974 dilated both the afferent and efferent arterioles and increased glomerular blood flow.

Angiotensin Receptor Antagonists↗
PubMed1994

Does endothelin work as an intrarenal mechanism to alter pressure natriuresis in spontaneously hypertensive rats?

OBJECTIVE: To study the possible involvement of intrarenal endothelial dysfunction in the modulation of the pressure-natriuresis curve in spontaneously hypertensive rats (SHR). METHODS: We examined the effect of endothelin on pressure natriuresis in isolated perfused kidneys from 16-week-old SHR and Wistar-Kyoto (WKY) rats. Plasma and urinary endothelin levels in intact rats and the rate of endothelin release from isolated kidneys were also determined. RESULTS: Urinary sodium excretion by SHR kidneys was 60% less than by WKY rat kidneys at a given perfusion pressure. Endothelin-1 increased the renal vascular resistance dose-dependently and the change was comparable in SHR and WKY rats. A high perfusate concentration of endothelin-1 markedly reduced urinary sodium excretion, resulting in a significant rightwards shift of the pressure-natriuresis curve. However, endothelin-1 at concentrations below 0.1 nmol/l did not decrease urinary sodium excretion, despite its renal vasoconstrictory activity. In a different in vivo study, plasma endothelin-like immunoreactivity was similar in the two groups, as was the urinary endothelin excretion. However, the rate of endothelin release from isolated SHR kidneys was slightly greater than from WKY rat kidneys. CONCLUSION: Since the difference in endothelin levels is not remarkable, it seems unlikely that increased intrarenal production of endothelin plays a role in the maintenance of hypertension in SHR by modulating the pressure-natriuresis curve.

Animals↗
PubMed1994

Cardiovascular effects of 20 days bed rest in healthy young subjects.

To evaluate the effects of inactivity on the cardiovascular system in normal subjects, left ventricular echocardiography and vascular ultrasound of the common carotid artery, abdominal aorta and femoral artery, and lower body negative pressure tests were performed in 14 healthy volunteers (mean age: 22 years) before and after 20 days of strict bed rest. Cardiac output was calculated from echocardiographic measurements and peripheral arterial flows by multiplying cross-sectional area of an artery by heart rate and time-velocity integral measured by pulsed Doppler ultrasound with angle correction. Systemic vascular resistance, lower body vascular resistance, leg vascular resistance and head vascular resistance were also calculated. After bed rest, heart rate increased (69 +/- 2 to 79 +/- 3 bpm), while left ventricular diastolic dimension (49 +/- 1 to 45 +/- 1 mm), systolic blood pressure (137 +/- 5 to 116 +/- 4 mmHg), cardiac output (6.2 +/- 0.3 to 5.4 +/- 0.3 1.min-1), abdominal aortic flow (4.1 +/- 0.4 to 3.1 +/- 0.3 1.min-1), femoral artery flow (0.66 +/- 0.07 to 0.33 +/- 0.04 1-min-1), and lower body negative pressure test tolerance time (750 +/- 71 to 582 +/- 48 s) decreased significantly (p < 0.05). However, common carotid artery flow (0.97 +/- 0.09 to 1.03 +/- 0.08 1.min-1) did not change. Although no significant changes in systemic vascular resistance, lower body vascular resistance or head vascular resistance were observed, leg vascular resistance increased significantly after 20 days of bed rest (6933 +/- 2905 to 13221 +/- 2606 dyn.s.cm-1) (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗