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Biomedical subjects

O S Better

Publications and source records attributed to O S Better.

At least 55 records · Page 3Linked to original sources
PubMed1989

Portal hypertension ameliorates arterial hypertension in spontaneously hypertensive rats.

Systemic hemodynamic effects of portal hypertension in arterial hypertension and their relationship to serum bile acid levels were investigated using spontaneously hypertensive rats 2 and 15 weeks after partial portal vein ligation (SHR-PVL) or sham operation (SHR-SH) and normotensive controls. Mean arterial pressure in SHR-PVL at 2 weeks was decreased to normal due to a decrease in peripheral resistance. Mean arterial pressure and peripheral resistance in SHR-PVL at 15 weeks did not differ from SHR-SH. Resolution of this arterial hypotensive effect and systemic hyperdynamic circulation was associated with decreased portal-systemic shunting. Bile acid levels were increased in both SHR-PVL groups. These results suggest that an endogenous circulating vasodilator(s) associated with portal hypertension ameliorates the systemic vasoconstriction in SHR. Bile acids, while not direct mediators of these hemodynamic events, may be prototypic of this vasodilator. This arterial hypertensive model may aid further investigation of the mechanisms contributing to the hyperdynamic state in portal hypertension.

Animals↗
PubMed1989

Traumatic rhabdomyolysis ("crush syndrome")--updated 1989.

In rescue operations for people trapped under fallen debris, i.v. replenishment of the massive internal fluid volume losses should be started as soon as physical contact has been established with the injured person. This should be followed by induced alkaline-mannitol diuresis. This regimen will stabilize the impaired hemodynamics, prevent myoglobinuric and hyperuricosuric renal failure, and correct the hyperkalemia and metabolic acidosis often seen in rhabdomyolysis. This treatment is effective even in individuals rescued after 28 h. Local treatment of the crushed limbs should be conservative. A closed injury should not be converted into an open one unless distal arterial perfusion has been compromised.

Animals↗
PubMed1989

End-stage renal disease replacement therapy in Israel: demographic and regional differences.

Incidence (by sex and ethnic group), prevalence and mortality rates (by age) of end-stage renal disease (ESRD) replacement therapy in Israel were calculated for the periods 1975-78 and 1979-82. Rates were higher for males (relative risk male/female 1.70 for the first period and 1.83 for the second). Incidence and prevalence rates increased with age among men; among women the maximal rates were attained by the 45-64 age-group. Incidence and prevalence rates were higher during the second period. Among the Jewish population, rates of treatment were higher in the Asian and African-born groups, and European-American and Israeli-born Jews showed the lowest rates. Mortality rates during treatment were lower among Arabs. Rates of therapy rose with age, were higher for males and had a well-defined ethnic pattern. In order to assess differences in ESRD replacement therapy between districts, rates of incidence, prevalence and mortality during treatment (for the Jewish population) were computed by district and adjusted by age and continent of birth for both periods. Significant differences in ESRD therapy coverage were detected only during the second period. Prevalence rates were considerably higher in the central, Tel Aviv and southern districts, and incidence rates were considerably elevated in the central and Tel Aviv districts and low in Jerusalem. Mortality during treatment was lowest in Haifa. It seems improbable that these findings are due to differences in accessibility to ESRD replacement therapy; however, early diagnosis and prevention of disabling kidney conditions at the primary care level may play an important role.

Adolescent↗
PubMed1988

Renin-angiotensin system in dogs following chronic bile-duct ligation. Relation to vascular reactivity.

The pressor response to angiotensin II, blood volume, angiotensin II in arterial blood, renin substrate, renin concentration, renin activity and aldosterone in venous blood, liver function tests, kidney function tests, glucose, sodium, potassium, plasma osmolality and complete blood count were examined before and 1, 2, 3 and 5 weeks after ligation of bile ducts in nine conscious trained dogs. The pressor response to angiotensin II was markedly suppressed after bile-duct ligation, especially at 1-3 weeks postoperation. A maximal decrease in plasma renin substrate, and maximal increases in plasma renin concentration, plasma renin activity and aldosterone were noted at 1 week postoperatively. Plasma angiotensin II levels were elevated at 1 and 5 weeks postoperatively but were near normal 2 weeks postoperatively despite suppression of the angiotensin II pressor response. Endogenous levels did not correlate with suppression of the pressor response to exogenous angiotensin II.

Aldosterone↗
PubMed1988

Sodium taurocholate increases hydraulic conductivity in rabbit collecting tubule.

Abnormalities in renal tubular function occur commonly in the setting of hyperbilirubinemia. In the present studies, the possibility that the bile salt sodium taurocholate exerts a direct effect on renal epithelial transport was investigated in vitro. We found that addition of sodium taurocholate to fluid bathing perfused rabbit cortical collecting tubules increases hydraulic conductivity (Lp) in a manner similar in time course and significantly less in magnitude to that observed with maximal concentrations of arginine vasopressin. Sodium taurocholate reversibly potentiates rabbit cortical collecting tubular Lp stimulated by maximal concentrations of arginine vasopressin and a nonhydrolyzable cyclic AMP analogue. We also found that sodium taurocholate induces a dose-dependent leak from tubular lumen to bathing fluid of a small molecular weight substance (125I-iothalamate). Our studies suggest that sodium taurocholate increases rabbit cortical collecting tubular Lp by a cyclic AMP independent mechanism.

Animals↗
PubMed1988

Adult hemolytic uremic syndrome associated with nonimmune deposit crescentic glomerulonephritis and alveolar hemorrhage.

An 18-year-old girl presented with anuric rapidly progressive glomerulonephritis associated with hypoxemic respiratory failure due to diffuse lung hemorrhage. The course of the kidney disease terminated in end-stage renal failure. The patient had been on permanent hemodialysis since her first admission; episodes of lung hemorrhage recurred five times over a follow-up period of 8 months. Two months after her first admission, the patient manifested features suggestive of the hemolytic uremic syndrome, namely, microangiopathic hemolytic anemia, thrombocytopenia, and excessive hypertension complicated by hypertensive encephalopathy. Based on the sequence of events in the course of this patient's disease, the authors believe that the hematological abnormalities were superimposed on the glomerular disease rather than being a primary disorder. Possible mechanisms for the association of the two disorders are discussed.

Adolescent↗
PubMed1988

Role of renal prostaglandins in bile-induced diuresis in the dog.

To clarify the possible role of renal prostaglandins (PGs) in the phenomenon of bile-induced diuresis in the dog, we studied the effect of in situ unilateral infusion of bile on kidney function and PGs excretion, before and after PG-synthetase inhibitor administration in anesthetized dogs. The contralateral intact kidney served as control. In the first group of 6 dogs, infusion of bile diluted 1:20 resulted in a significant increase in urinary flow (117%; p less than 0.05), sodium (61%; p less than 0.01), potassium (26%; p less than 0.05), PGE2 (240%; p less than 0.05) and PGF2 alpha (137%; p less than 0.05) excretion rates. Further significant increases in urinary flow, sodium and PGE2 excretion rates were noted with infusion of bile diluted 1:10. All parameters returned to basal levels upon cessation of bile infusion. Significant linear correlation coefficients (p less than 0.005) were found between PGE2 excretion rates and urinary flow (r = 0.72), sodium (r = 0.91) and potassium (r = 0.88) excretion rates. In a second group of 6 dogs, intravenous administration of PG-synthetase inhibitor abolished the increase in renal PGs excretion and the increments in the rates of urinary flow and solute excretion in response to bile infusion. These findings support the notion that the acute diuretic and natriuretic effect of bile, and presumably that of cholemia is mediated, in part, through stimulation of renal PGs synthesis.

Animals↗
PubMed1987

Effects of bile acids on ventricular muscle contraction and electrophysiological properties: studies in rat papillary muscle and isolated ventricular myocytes.

The effects of sodium salts of various bile acids on the contractile force and the electrophysiological properties of rat ventricular muscle were studied in vitro. Primary, conjugated, and secondary bile acids were studied in a concentration range of 10(-9)-10(-6) mol/l, which corresponds to concentrations found in the plasma of patients with cholestatic jaundice. In general, the bile acid induced a negative inotropic effect which was manifested as a reduction in active tension, maximum rate of tension activation, and maximum rate of tension relaxation. Twitch duration and time to peak tension were unaffected by the bile acids. The negative inotropism was associated with a reduction in ventricular action potential duration. Resting potential, action potential amplitude, and maximum upstroke velocity of phase 0 depolarization were unaffected. Voltage clamp experiments in rat ventricular myocytes demonstrated that sodium taurocholate decreased the slow inward current and slightly increased the outward potassium current. Hence, these effects on the membrane currents are probably responsible for the negative inotropic effect.

Action Potentials↗
PubMed1987

The effect of sodium taurocholate on proximal tubular reabsorption in the rat kidney.

Microperfusion of tubules in situ was used to study the direct effect of sodium taurocholate on reabsorption of fluid by the proximal tubule of the rat. Sodium taurocholate (0.1 mmol/l) in the tubular perfusate reduced proximal tubular fluid reabsorption by approximately 30%. Thus, the proximal tubule appears to be a major site at which bile salts cause a natriuresis in the rat, and possibly in obstructive jaundice in man.

Absorption↗
PubMed1987

Ultrastructure of the myocardium in dogs with induced jaundice.

Morphological aspects of the myocardium in dogs with experimentally induced jaundice were assessed ultrastructurally. Obstructive jaundice was produced by chronic bile-duct ligation and by choledochocaval anastomosis. The left ventricular myocardium and the papillary muscle were used. Statistical analysis of sarcomere length and of mitochondrial density showed no significant differences between jaundiced and sham-operated dogs. Qualitative evaluation of the mitochondria, the intercalated disc and other sarcoplasmic constituents revealed no damage to the jaundiced dogs.

Animals↗
PubMed1986

Renal bilirubin excretion in canine models of jaundice.

Renal handling of bilirubin and its relationship to blood bilirubin level were investigated for up to 2 weeks in two models of jaundiced dogs, namely, chronic bile duct ligation (CBDL), which are mildly icteric, and choledococaval anastomosis (CDCA), which develop deep jaundice. The mean (+/- SD) urinary bilirubin excretion in CBDL plateaued at 30.3 +/- 9.3 mg/24 hr whereas in CDCA it continued to increase above the normal bilirubin production rate (56-84 mg/24 hr) up to 130-150 mg/24 hr. The renal clearance of bilirubin in both models was inversely proportional to serum bilirubin concentration. It was approximately twice as high in the CDCA model, which induced also a moderate diuresis. It is suggested that higher serum bilirubin levels in CDCA dogs is due to the increased production of bilirubin which is not compensated by the renal clearance of bilirubin.

Animals↗
PubMed1986

Extreme unilateral hydronephrosis with normal glomerular filtration rate: physiological studies in a case of obstructive uropathy.

A 30-year-old man presented with massive left hydronephrosis caused by congenital stricture of the ureteropelvic junction. Glomerular filtration rate of the post-released kidney (inulin clearance and creatinine clearance) was preserved completely. Simultaneous individual kidney function tests showed the following values expressed as the ratio of post-obstructed to normal kidney: inulin clearance 142 per cent, urine flow rate 475 per cent, sodium clearance 221 per cent and urinary excretion of prostaglandin E2 617 per cent. Urinary osmolality was 257 and 791 mOsm./kg. in the obstructed and normal kidneys, respectively. Administration of indomethacin, a cyclo-oxygenase inhibitor, caused decreased urinary excretion of prostaglandin E2 in both kidneys, with drastic antinatriuresis manifested predominantly in the normal kidney. We conclude that the glomerular filtration rate may be preserved despite huge hydronephrosis, which suggests that the human kidney is salvageable even after a prolonged period of unilateral ureteral obstruction, and the contralateral normal kidney mitigates the volume losses from the obstructed kidney.

Adult↗
PubMed1986

Impaired renal acidification following acute renal ischemia in the dog.

Transient renal tubular acidosis may complicate acute renal failure (ARF). To clarify this phenomenon, the present study examined tubular H+ ion secretory capacity in an ischemic model of ARF. Clearance studies were performed in dogs subjected to 60 minutes, unilateral renal artery clamping. The contralateral kidney served as control. One hour after release of clamp, mean glomerular filtration rate (GFR) was reduced by 50 to 70 percent in the ischemic kidney. Bicarbonate reclamation (mEq/liter GFR) was comparable in both kidneys. However, ischemia resulted in impaired distal acidification as judged by three separate maneuvers: minimal urinary pH following sulphate infusion was higher in ischemic than in control kidney (6.61 +/- 0.39 vs. 5.39 +/- 0.26, P less than 0.01), mean urine to blood PCO2 difference (U-B PCO2) was significantly lower during phosphate infusion (ischemic: 13.8 +/- 4.1 mm Hg, control: 37.2 +/- 6.8 mm Hg, P less than 0.01) and was completely abolished during isotonic NaHCO3 infusion in the ischemic kidney (-1.9 +/- 3.4 mm Hg) compared to control (40.1 +/- 14.8 mm Hg, P less than 0.05). Urinary potassium excretion was intact following ischemia and was appropriately suppressed by amiloride. Administration of 0.7 M NaHCO3 solution at a rate sufficient to produce maximally alkaline urine resulted in a similar U-B PCO2/UHCO3 relationship in both kidneys in the face of impaired distal acidification in the ischemic kidney. This suggests either that the defect may be reversed by massive bicarbonate infusion or, alternatively, that U-B PCO2 difference may be related to other factors in addition to distal H+ secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1986

Renal alpha-1-adrenoreceptors in rats with obstructive jaundice.

Alpha 1-Adrenoreceptor affinity constants (KD) and receptor numbers (Bmax) were determined in the kidneys of 3-day-old bile-duct-ligated (BDL) jaundiced rats using 3H-prazosin. The results were compared to 3-day-old pair-fed and nonpair-fed sham-operated rats as well as nonoperated rats as controls. Abdominal surgery (sham and BDL) resulted in a tendency towards a decrease in KD in all three groups of rats compared to nonoperated controls. The Bmax was also increased in the sham-operated groups compared to the nonoperated controls. In contrast, the tendency for a rise in the Bmax in the BDL group was significantly smaller than the rise seen in the two sham-operated groups. In summary, obstructive jaundice suppresses the normal renal alpha 1-adrenoreceptor response to abdominal surgery in the rat.

Animals↗
PubMed1986

Enhanced in vitro platelet aggregation in hemodialysis patients.

Hemodialysis patients suffer from premature atherosclerosis and various thrombotic and thromboembolic phenomena. Despite enhanced in vivo platelet activity, it is unclear whether in vitro platelet aggregation is increased or reduced in this population. We studied platelet aggregation in response to adenosine diphosphate and to epinephrine in 20 chronic hemodialysis patients and 21 controls. In the patient group the in vitro platelet aggregation was significantly enhanced in response to both aggregating agents. Our study demonstrated that in vitro platelet aggregation is enhanced in patients with chronic renal failure undergoing hemodialysis.

Adenosine Diphosphate↗
PubMed1986

The "jaundiced heart": a possible explanation for postoperative shock in obstructive jaundice.

Patients with obstructive jaundice are susceptible to postoperative shock and kidney failure. The cause of these potentially fatal complications has not been fully clarified. The present study was designed to assess the role of myocardial dysfunction in the hemodynamic disturbance of obstructive jaundice. We studied the effect of isolated cholemia on left ventricular performance in five conscious dogs before and 2 weeks after choledochocaval anastomosis by using measurements of systolic time intervals (STIs) and maximal dp/dt. Mean left ventricular ejection tiem (LVET) decreased after cholemia from 159 +/- 2.8 msec to 139 +/- 2.6 msec (p less than 0.005), while mean preejection period (PEP) and mean PEP/LVET were increased from 41 +/- 8.5 msec to 87 +/- 14 msec (p less than 0.05) and from 0.39 +/- 0.06 to 0.62 +/- 0.1 (p less than 0.01), respectively. During cholemia, STIs were unchanged after intravenous administration of ouabain, whereas in the control period, there was shortening of mean PEP from 71 +/- 8.8 msec to 58 +/- 7.6 msec (p less than 0.05) and of Q-S2 from 257 +/- 12 msec to 235 +/- 14 msec (p less than 0.005) in response to ouabain. Maximal dp/dt decreased after choledochocaval anastomosis from 4543 +/- 593 mm Hg/sec to 3666 +/- 648 mm Hg/sec (p less than 0.025). We conclude that cholemia in the dog is clearly associated with impaired left ventricular performance. The present data also support a previously published in vitro study from our laboratory showing that cholemia blunts the myocardial contractile response to sympathomimetic agents. The cardiodepressor effect of cholemia may explain the increased tendency of patients with obstructive jaundice to postoperative shock and renal failure.

Animals↗