We observed recently three cases of ureteral polyps including a case of multiple polyps. The first patient was a 33-year-old man with multiple polyps at the left upper ureter. The second patient was a 51-year-old man and the third 49-year-old man, and both cases were complicated with ureteral stones. We divided 88 ureteral polyps reported in Japan from 1970 to 1990 into polyps in children and those in adults. We further divided the individual polyps into single and multiple polyps and examined them clinically. Characteristic findings were obtained in polyps in children; namely, multiple polyps were dominant, almost all of them occurred at the left upper ureter and no cases were complicated with ureteral stones. Furthermore, many of the multiple polyps in adults occurred at the left upper ureter and few were complicated with stones as in the children. In conclusion, the ureteral polyps in children and multiple ureteral polyps in adults were similar in character and we presumed that some congenital factors might be involved in their occurrence.

Adult↗

PubMed1993

Effects of aspirin DL-lysine on thrombin generation in unstable angina pectoris.

To evaluate the effects of aspirin on thrombin generation in patients with unstable angina, plasma levels of thrombin-antithrombin III complex (TAT) as a new marker of thrombin generation and of 11-dehydro-thromboxane B2 (11-dehydro-TXB2) as an indicator of platelet activation were measured in 18 patients with unstable angina, including 8 patients with prolonged rest angina (> 15 minutes). Aspirin DL-lysine (900 mg) was administered intravenously to 9 of the 18 patients (aspirin group); the other 9 were not given aspirin during the first 24 hours of hospitalization (non-aspirin group). Clinical characteristics, angiographic features and medications other than aspirin were similar between the 2 groups. Levels of plasma TAT and 11-dehydro-TXB2 were significantly higher (p < 0.05) in patients with prolonged rest angina than in those without the condition (n = 10). In 5 patients with prolonged rest angina who received aspirin, plasma TAT levels (ng/ml) were significantly decreased (4.52 +/- 1.18 at baseline, 2.50 +/- 0.65 at 1 hour and 2.16 +/- 0.42 at 24 hours after aspirin administration, p < 0.01) with a significant decrease in plasma 11-dehydro-TXB2 levels. However, the reduction in TAT after aspirin administration was slight in patients without prolonged rest angina (n = 4). In contrast, levels of plasma TAT and 11-dehydro-TXB2 in the non-aspirin group remained unchanged during the study period. These results suggest that aspirin rapidly reduces thrombin generation through inhibition of platelet activity in patients with unstable angina with prolonged rest angina.

Aged↗

PubMed1993

Organ-specific unresponsiveness induced by intrathymic injection of donor bone marrow cells and a short course of immunosuppression in the rat heart transplantation model.

Donor- and organ-specific unresponsiveness to Brown Norway (BN) heart allografts was achieved in Lewis (LEW) rats by giving intrathymic donor bone marrow cells (ITBMC) and immunosuppression at the time of transplantation. Antilymphocyte serum (ALS) (1 ml, days 0, 2, 4) extended graft survival to a median survival time (MST) of 29.5 days (n = 6), while ALS + ITBMC extended survival to over 120 days (n = 6). FK506 (1 mg/kg, days 0, 2, 4, 6, 8) too prolonged survival in the FK + ITBMC (n = 6; MST > 140 days) and FK (n = 5; MST > 140 days) groups. BN skin grafting provoked the rejection of long-surviving BN heart grafts in the FK group (n = 5; MST = 14 days), but did not do so in either the ALS + ITBMC (n = 2; MST > 100 days) or the FK + ITBMC (n = 4; MST > 93 days) groups. In the FK + ITBMC group, two of the rats which rejected BN skin grafts received a second BN heart, resulting in the graft being accepted indefinitely (> 100 days) without causing the rejection of the first BN heart grafts. These facts suggest that ITBMC and concurrent T cell depletion are decisive for induction of unresponsiveness by this protocol. BN and WF (Wistar Furth) skin grafts were eventually rejected in the LEW rats which accepted BN heart grafts. Persistent allogeneic chimerism was demonstrated in the graft and recipient spleen, suggesting that chimerism may be one of the possible mechanisms of unresponsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Acute effects of alcohol ingestion on blood pressure and erythrocyte sodium concentration.

OBJECTIVE: To examine the acute effects of alcohol on blood pressure and erythrocyte cation concentrations in patients with essential hypertension. DESIGN: An alcoholic drink or an isocaloric control drink was given during supper in random order on different days, and blood pressure and erythrocyte cation concentrations were measured before and 2 h after the meal. METHODS: The subjects were 21 men with essential hypertension who habitually drank alcohol. Blood pressure was measured with a semi-automated sphygmomanometer, and erythrocyte cation concentrations were measured by flame photometry after haemolysis with distilled water. RESULTS: Blood pressure decreased after both drinks, but the decrease was significantly larger after the alcoholic drink than after the control drink. There was a significant difference between the changes in erythrocyte sodium caused by the alcoholic and the control drink. Furthermore, there were significant positive correlations between the fall in blood pressures and the decrease in erythrocyte sodium concentration. CONCLUSION: The predominant acute effect of alcohol ingestion in patients with hypertension is blood pressure reduction, and it may be associated with a decrease in intracellular sodium.

Adult↗

PubMed1993

[The effect of nicardipine on internal carotid artery blood flow velocity, local cerebral blood flow and carbon dioxide reactivity].

To study the effect of nicardipine on the blood flow velocity of the internal carotid artery, on local cerebral blood flow (LCBF), and on carbon dioxide reactivity, an initial dose of 0.5 microgram/kg/min of nicardipine was administered in patients for scheduled craniotomy for cerebral aneurysm clipping under isoflurane anesthesia. This agent was administered until the mean arterial blood pressure decreased and could be maintained at about 75% of the initial value until the completion of aneurysm clipping. The measurements of hemodynamics and LCBF were performed after the exposure of the internal carotid artery (T0), and 10 min, 30 min after the starting of nicardipine (n = 13), (T1, T2 respectively), before aneurysm clipping (T3) and 30 min after its discontinuation (T4). Local cerebral blood flow was measured by the thermal gradient blood flow meter. The blood flow velocity of the internal carotid artery was measured at T0 and T3 by a 20MHz pulsed ultrasound Doppler Flow-meter under surgical microscope. Carbon dioxide reactivity was evaluated with % delta LCBF/delta PaCO2 (%/mmHg) at T0, T3 and T4. Mean arterial blood pressure decreased after nicardipine infusion. Local cerebral blood flow did not change during nicardipine infusion, but blood velocity increased significantly after nicardipine infusion from 43 +/-12 to 55 +/- 12 cm/sec (p = 0.024). Carbon dioxide reactivity did not change after nicardipine infusion but had a close correlation with LCBF before (rs = 0.64, p < 0.05), during (rs = 0.84, p < 0.01) and after hypotension (rs = 0.65, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Prolonged survival of rat cardiac allografts induced by intrathymic injection of donor bone marrow cells.

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Animals↗

PubMed1993

[Induction of prostaglandin E2 by interleukin 1 in human lens epithelial cells].

The authors proposed the hypothesis that pseudophakic inflammation, including the fibrin reaction, may be caused by interleukin (IL)-1, IL-6, other cytokines and/or prostaglandins (PGs), synthesized by residual lens epithelial cells (LEC). In testing our hypothesis, we have already detected IL-1 alpha, IL-6 and PGE2 in the culture media of human LEC obtained by capsulotomy during cataract surgery. In this paper, we studied the time course of PGE2-synthesis and interaction between IL-1 and PGE2. PGE2 concentration was measured by radioimmunoassay in the culture media to which rabbit antihuman IL-1 polyclonal antibody was added after culture for 6 h, 1 day, 1, 2, 3, 4, 5 and 6 weeks. There was no increase of PGE2, whereas in the untreated control culture media significant increase of PGE2 was confirmed. The results show that the antihuman IL-1 polyclonal antibody suppressed PGE2-synthesis. Thus, IL-1 induces PGE2 synthesis in human LEC culture.

Animals↗

PubMed1992

Angiotensin II does not increase renal prostaglandin E2 in response to pressure reduction.

Whether angiotensin II (Ang II) stimulates renal secretion of prostaglandin E2 (PGE2) synthesized in response to pressure reduction was examined. PGE2 and Ang II in aortic and renal venous plasma were measured before and during renal arterial constriction in anesthetized dogs, with or without an intrarenal arterial infusion of an Ang II antagonist, losartan potassium (1 mg/min), or saralasin (3 micrograms/min). In other anesthetized dogs, two doses of Ang II (30 and then 300 ng/min) were infused into the renal artery, and plasma Ang II levels and renal PGE2 secretion were measured. When renal perfusion pressure was reduced to 75 and 45 mm Hg by constriction, the renal secretion of PGE2 increased seven- and fourfold, respectively. Ang II levels in the renal venous plasma increased from 6.6 +/- 1.8 to 21.7 +/- 7.4 and then 48.1 +/- 15.3 pg/ml (both P less than 0.05) as the pressure decreased. Neither losartan nor saralasin suppressed the response of renal PGE2 secretion to the pressure reduction. The intrarenal infusion of Ang II (30 ng/min) elevated the Ang II level in the renal venous plasma from 9.8 +/- 4.6 to 33.7 +/- 4.2 pg/ml (P less than 0.01), but did not increase PGE2 secretion. The higher dose (300 ng/min) of Ang II increased it, but the Ang II level in the renal venous plasma was 166 +/- 63 pg/ml. These results suggest that the greater part of the increased renal synthesis of PGE2 in response to pressure reduction is not mediated by Ang II.

Angiotensin II↗

PubMed1992

Sodium and noradrenaline in cerebrospinal fluid and blood in salt-sensitive and non-salt-sensitive essential hypertension.

1. The effects of dietary sodium on blood pressure and levels of sodium, other electrolytes and noradrenaline (NA) in the cerebrospinal fluid (CSF) and blood of 15 patients with essential hypertension were studied. The CSF and blood sampling was carried out after 7 days of a high salt intake (16-18 g/day) and after 7 days of a low salt intake (1-3 g/day). 2. Blood pressure and sodium concentrations in CSF and serum were significantly higher in the high salt period than the low salt period (CSF Na+ concentration: 147.7 +/- 0.4 mmol/L vs 145.3 +/- 0.5 mmol/L; P less than 0.001). Levels of CSF pressure and potassium or calcium concentrations were not different between the two periods. Plasma NA and plasma renin activity (PRA) were lower and CSF NA levels tended to be lower in the high salt period. 3. The levels and the changes in sodium and NA in CSF were not significantly different between the salt-sensitive (n = 8) and the non-salt-sensitive (n = 7) subjects, but the changes in plasma NA and PRA were smaller in the salt-sensitive subjects. 4. These results indicate that the sympathetic nervous system is less suppressed in salt-sensitive subjects during high salt intake. This may be due to altered neural responsiveness to sodium loading rather than being greater increases in sodium concentration in the central nervous system.

Adult↗

PubMed1992

Synthesis of interleukin-1 and prostaglandin E2 by lens epithelial cells of human cataracts.

To test our hypothesis that pseudophakic inflammation, including the fibrin reaction, may be caused by cytokines, prostaglandins (PG), or both, synthesised by residual lens epithelial cells (LECs), we measured interleukin-1 alpha (IL-1 alpha) and PGE2 in the incubation medium of cultures of human LECs obtained by capsulotomy during cataract surgery. After 1 week radioimmunoassay showed that there were 1.46 (0.62) ng of PGE2/10(6) cells (mean (SD) six cultures), and after 4 weeks, there were 5.50 (2.20) ng of PGE2/10(6) cells (seven cultures). During culture the cells proliferated and underwent fibroblast-like cell changes on exposure to the plastic of the wells. In the medium of control plates to which sodium diclofenac had been added PGE2 was not detected. Some IL-1 alpha was found in four of 10 samples, each of which contained media from 12 cultures; 207 pg/10(6) cells in one of the two pools of 2-week cultures, 120 pg/10(6) cells in one pool and 139 pg/10(6) cells in another of the three pools of 3-week cultures, and 111 pg/10(6) cells in the one pool of 4-week cultures. PGE2 and IL-1 alpha may therefore be produced in vivo by residual LECs after cataract surgery, and may be involved in postoperative inflammation, including the fibrin reaction.

Cataract↗

PubMed1992

Intracellular free magnesium of red blood cells in patients with renal disease.

While serum magnesium (Mg) level is increased in patients with end-stage renal disease (ESRD), it is decreased in renal transplant recipients (TR) receiving ciclosporin. This study was performed to examine the cation metabolism of red blood cells (RBC) in these patients. Intracellular free Mg was measured with 31P-nuclear magnetic resonance spectrometry, and ouabain-sensitive sodium (Na) efflux rate (Eos) was measured from the increase in RBC-Na concentration when RBC were incubated in the presence of ouabain. The ouabain-sensitive Na efflux rate constant (ERCos) was obtained by dividing Eos by RBC-Na concentration. RBC free Mg and ERCos were significantly higher in the TR group than in the ESRD group. There was a significant correlation between RBC free Mg and ERCos (r = 0.474, p less than 0.01). These results support the views that the regulation mechanism for intracellular free Mg is different from that for extracellular Mg in patients with renal disease, and intracellular free Mg modulates Na pump activity of RBC.

Adenosine Triphosphate↗

PubMed1992

Acute depressor effect of alcohol in patients with essential hypertension.

To investigate the time course of the effects of alcohol on blood pressure, we studied the response of ambulatory blood pressure, neurohumoral variables, and hemodynamics to a single moderate dose of alcohol in hypertensive patients. Sixteen Japanese men (22-70 years old) with essential hypertension who were habitual drinkers were examined under standardized conditions. On the alcohol intake day, they ingested 1 ml/kg ethanol (vodka) at dinner, and on the control day they consumed a nonalcoholic beverage. The order of the two periods was randomized. Mean ambulatory blood pressure was lower in the alcohol intake period than in the control period (125 +/- 3/74 +/- 2 versus 132 +/- 4/78 +/- 2 mm Hg, p less than 0.05), and the significant depressor effect of alcohol lasted for up to 8 hours after drinking. Blood pressure on the next day did not differ with or without alcohol intake. The acute hypotensive effect of alcohol was associated with an increase in heart rate and cardiac output and with a decrease in systemic vascular resistance as determined by echocardiography. Plasma catecholamine levels and renin activity rose significantly at 2 hours after dinner, whereas vasopressin and potassium levels fell on the alcohol day. Blood glucose and serum insulin levels were comparable between the two periods. Three patients with marked alcohol-induced flush had greater hypotensive and tachycardiac responses than those who did not show an alcohol-induced flush. The change in mean blood pressure induced by alcohol was negatively correlated with age, the baseline blood pressure, and the change in plasma norepinephrine. These results indicate that the major effect of acute alcohol intake is to lower blood pressure through systemic vasodilatation in hypertensive subjects. Ambulatory blood pressure monitoring may be useful for assessing blood pressure in habitual drinkers.

Adult↗

PubMed1992

Critical degree of renal arterial stenosis that causes hypertension in dogs.

The minimum degree of renal arterial stenosis needed to cause hypertension was identified by renal arterial angiography of anesthetized dogs. The effects of renal nerves and prostanoids on the critical stenosis were also examined. The left renal artery was constricted concentrically by a radiolucent constrictor device, and the stenosis of the artery was evaluated by cineangiography with the kidney either innervated or denervated. At this time, renal blood flow, renal perfusion pressure, and systemic blood pressure were serially monitored. In another group of dogs, renal venous and aortic blood samples were taken as the stenosis increased; these were assayed for prostaglandin E2 and plasma renin activity. The same experiments were done again after treatment with a cyclooxygenase inhibitor, aspirin DL-lysine (54 mg/kg). With the kidney either innervated or denervated, systemic blood pressure began to increase when the stenosis was more than 70% of the diameter of the renal artery; the renal blood flow decreased when the stenosis was more than 75% of the diameter. Aspirin treatment attenuated the increase in blood pressure but did not affect the autoregulation of the renal blood flow when stenosis was 70% or less. Prostaglandin E2 production increased in the stenotic kidney when the stenosis was more than 70%; aspirin inhibited prostaglandin synthesis and suppressed the stimulation of renin release. These results suggest that whether there is innervation or not, the critical degree of renal arterial stenosis that causes hypertension is more than about 70% of the diameter in the presence of renal prostaglandins; in their absence, the critical point above which hypertension occurs is 75% or more.

Animals↗

PubMed1992

Vascular responsiveness to angiotensin II and phenylephrine, the tubular function and the prostaglandin, renin-angiotensin system in a patient with Bartter's syndrome.

In a 39-yr-old female patient with Bartter's syndrome, vascular responsiveness to angiotensin II and phenylephrine was studied. Pressor responses to angiotensin II and to phenylephrine were markedly decreased prior to treatment and were improved by administration of indomethacin, dextran, KCl, captopril, propranolol or pindolol. Moreover, the responses of total peripheral vascular resistance to angiotensin II and phenylephrine were markedly decreased before treatment and were improved by the treatment. A relatively low fractional distal chloride reabsorption was found, and that was not changed after the administration of KCl or indomethacin. The results of this patient were compatible with the primary cause of Bartter's syndrome, defective chloride reabsorption at the loop of Henle, but the possibility of an abnormality in the vascular wall could not be denied.

Adult↗