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Biomedical subjects

S Y Chou

Publications and source records attributed to S Y Chou.

At least 55 records · Page 3Linked to original sources
PubMed1990

Growth hormone inhibits activation of phosphatidylinositol phospholipase C by insulin in ob/ob mouse adipose tissue.

The cellular mechanism(s) by which GH produces insulin resistance in peripheral tissues is poorly understood. Recent evidence suggests that insulin exerts certain of its intracellular actions by rapidly activating phosphatidylinositol-specific phospholipase C(s) (PI-PLC) in the plasma membranes of target cells. Therefore, the present study was conducted to determine whether insulin can activate PI-PLC in adipose tissue of the genetically obese (ob/ob) mouse, an animal that responds markedly to GH with enhanced peripheral insulin resistance. Also, experiments were performed to determine whether the activation of PI-PLC by insulin could be blocked by S-carboxymethylated human GH (RCM-hGH), a GH derivative possessing mainly diabetogenic activity. Isolated adipose segments were incubated for various periods with insulin (10 mU/ml), homogenized and centrifuged to obtain a 150,000 x g pellet, and the latter was assayed for the ability to produce [3H]inositol phosphate from phosphatidyl[3H]inositol. PI-PLC activity was significantly stimulated 5 min after exposure of the segments to insulin. By 10 min, the insulin effect was no longer apparent, and after 30 min, insulin reduced the activity of the enzyme. One hour after exposure to insulin, PI-PLC activity returned to the control level. When adipose segments of RCM-hGH-treated mice (200 micrograms/day for 3 days sc) were incubated for 5 min with insulin, the ability of insulin to activate PI-PLC was abolished. However, RCM-hGH did not alter basal PI-PLC, indicating that its action involves the mechanism by which the enzyme is activated by insulin. Also, studies utilizing acute RCM-hGH treatment showed that its inhibitory effect on insulin activation of PI-PLC occurs within the same time frame as the onset of enhanced insulin resistance in the adipose tissue. Thus, the ability of GH to inhibit the activation of PI-PLC by insulin in adipocytes may account, at least in part, for its ability to induce insulin resistance in these cells.

Adipose Tissue↗
PubMed1990

The biosynthesis of cholesterol side-chain cleavage cytochrome P-450 in the rabbit corpus luteum depends upon estrogen.

To gain a better understanding of the luteotropic action of estrogen, we have investigated the effect of estrogen on the synthesis of the enzyme, cholesterol side-chain cleavage cytochrome P-450 (P-450scc) in the rabbit corpus luteum. Using an established protocol, rabbits were treated with estradiol, and the estradiol was then withdrawn on day 9 of pseudopregnancy, which caused an 88% fall in serum progesterone within 48 h. In other rabbits, estradiol was replaced at 48 h which stimulated a 6.6-fold increase in serum progesterone concentration within the next 24 h. Luteal tissues were incubated with [35S]methionine and homogenized, and a mitochondrial fraction lysate was obtained. Equal trichloroacetic acid-precipitable radioactivity was taken for immunoprecipitation using a well-characterized polyclonal antiserum against bovine adrenal P-450scc. The immunoisolated proteins were resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and radioactivity was visualized by autofluorography. The results indicate that the rate of synthesis of P-450scc in 48 h-estradiol withdrawn animals was markedly reduced, and by 72 h of withdrawal was barely detectable. When estradiol was reintroduced, the synthesis of P-450scc was increased. Despite the prominent changes in P-450scc synthesis, immunoblotting revealed only a minimal (approximately 30%) decrease in relative P-450scc content by 72 h after estradiol withdrawal. Analyses of DNA and protein contents of luteal tissues revealed an increase in DNA per mg luteal tissue, a decline in total tissue protein/DNA ratio, but no change in mitochondrial fraction protein/DNA ratio after estrogen withdrawal. The results indicate that de novo synthesis of P-450scc in the corpus luteum is sensitive to estrogen; however, the estrogen-sensitive rate-limiting step(s) for steroidogenesis are at other sites in the steroid biosynthetic pathway.

Animals↗
PubMed1989

Acute non-Q wave cocaine-related myocardial infarction.

Since our initial report in 1984 of six patients with AMI temporally related to cocaine use, we have observed 19 additional patients in whom ischemic chest pain syndromes occurred shortly after intranasal or IV use of cocaine or after smoking the drug. Seventeen patients (89 percent) developed non-Q wave infarction and two had Q-wave infarction. One patient manifested angina with striking ST-segment elevation. None of the patients had diabetes or hypertension, and all but one were cigarette smokers. The serum cholesterol level was 162 +/- 7 mg/dl. Four of the five patients who consented to coronary angiographic studies displayed normal coronary arteries, and one showed proximal stenosis of the right coronary artery. The cold pressor test was performed in seven patients; none had angina or ECG changes induced by cold stimulation. We conclude that T-wave infarction is a common form of an acute cardiac event related to cocaine abuse, and its pathogenesis may involve that of the cocaine-induced coronary vasospasm.

Adult↗
PubMed1989

Pancreatic vasoactive intestinal polypeptide-secreting tumor: report of a case.

A 58-year-old Taiwanese woman was admitted to Mackay Memorial Hospital for evaluation profuse watery diarrhea. She presented with watery diarrhea, hypokalemia, and hypochlorhydria, and had experienced these problems for 2 years prior to admission. A pancreatic tumor with liver metastasis was noted by the ultrasound, abdominal CT scanning, and angiography studies. Surgical exploration disclosed an ill-defined ovoid tumor in the body and tail of the pancreas measuring 8 x 3 x 3 cm. The immunohistochemistry study of the tumor for VIP-immunoreactivity (VIP: vasoactive intestinal polypeptide) was markedly positive, and also stained slightly positive for other peptides, including pancreatic polypeptide (PP), calcitonin, glucagon, and neuron-specific enolase (NSE). Postoperatively, the patient recovered immediately from her symptoms and there has been no evidence of recurrence during the past 8 months of follow-up.

Adenoma, Islet Cell↗
PubMed1989

[Mucocele of appendix-report of three cases].

Mucocele of appendix comprises 0.07%-0.3% of the resection of appendix. Three such cases were encountered over the past four years at MMH. Tumor mass could be palpated before operation in two of our cases. The third case was found incidentally during sigmoid cancer resection. Mucocele of the appendix should be differentiated from submucosal lesion such as leiomyoma, lipoma, lymphoma in the cecum or appendiceal abscess. Recent advances of ultrasound, CAT scan as well as angiography have made correct preoperative diagnosis possible, yet literature still shows diverse opinion about its etiology (neoplastic vs. obstructive). Although most authors favor simple appendectomy for the management of this disease, some surgeons still think it should be managed aggressively with colectomy. Rupture of mucocele might result in pseudomyxoma peritonei and possibly a fetal outcome. Avoidance of iatrogenic rupture of appendix is essential. Aggressive removal of accessible masses and implants was suggested in the literature.

Adult↗
PubMed1987

Regulation of papillary plasma flow by angiotensin II.

We examined in anesthetized dogs the effects of left (L) intrarenal artery infusion of angiotensin II (AII) on renal hemodynamics, urinary concentration and Na excretion, and papillary plasma flow (PPF) (measured by the albumin accumulation technique) in both kidneys. Following AII infusion (0.5 ng/kg/min) into the L renal artery, urinary Na excretion decreased and osmolality increased slightly ipsilaterally, whereas Na excretion did not change significantly and osmolality decreased in the right (R) kidney. PPF was significantly lower in the L compared to the R kidney. When saline loading was superimposed on L intrarenal AII infusion, there was a blunted natriuretic response ipsilaterally with a significantly smaller decrease in urine osmolality compared with the R kidney. PPF increased significantly in the R, but not in the L kidney. Finally, AII blockade with saralasin prior to AII infusion and saline loading prevented the differences between the two kidneys, including PPF. In all groups GFR and renal blood flow did not differ between the two kidneys before or after AII. These data suggest that AII regulates regional blood flow in the medulla, and that the exogenously administered AII induces papillary ischemia, which serves to preserve medullary hypertonicity, preventing an increase in PPF during saline loading, and possibly contributing to the diminished natriuretic response.

Angiotensin II↗
PubMed1987

Inner medullary hemodynamics in dogs with aortocaval fistula.

To investigate the role of medullary hemodynamics and vasoactive hormones in sodium retention in dogs with aortocaval fistula, we examined papillary plasma flow (PPF), solute content, and renal output of renin, norepinephrine, and prostaglandin E2 (PGE2) in anesthetized normal and fistula dogs. During hydropenia, cardiac output was elevated and systemic vascular resistance reduced in fistula dogs, accompanied by markedly increased renal output of renin, norepinephrine, and PGE2. In fistula dogs the blunted diuretic and natriuretic response to saline loading was not due to impaired myocardial contractility. During hydropenia and after saline loading, glomerular filtration rate (GFR) and renal blood flow were similar in normal and in fistula dogs; however, PPF was significantly lower in fistula dogs, accompanied by significantly greater papillary tissue osmolality and sodium content. These findings indicate that in fistula dogs enhanced medullary sodium reabsorption is associated with decreased PPF and stimulation of the renin-angiotensin and adrenergic nervous system. Furthermore, the reduced PPF obviates medullary solute washout during saline loading, and may contribute to the blunted diuretic and natriuretic response.

Animals↗
PubMed1986

Contribution of angiotensin to the control of medullary hemodynamics.

The unique architecture and organization of medullary vasculature permit regional regulation of medullary hemodynamics by vasoactive hormones and are conducive to the operation of the countercurrent multiplication system. Recent studies suggest that an increase in inner medullary blood flow causes medullary solute washout, which in turn decreases passive sodium transport in the thin ascending limb of Henle's loop. In canine models of chronic sodium retention accompanied by activation of the renin-angiotensin system, glomerular filtration rate (GFR), renal blood flow (RBF), and intracortical blood flow distribution were similar to those in normal dogs; however, papillary plasma flow (PPF) was markedly reduced and papillary tissue solute content was increased significantly both during hydropenia and after saline loading. During euvolemic diuresis with loop diuretics, there was an increased renin release associated with a marked reduction in PPF, despite an increase in total RBF. Direct intrarenal infusion of angiotensin II (AngII) (at a dose not affecting GFR and RBF) induced ipsilateral sodium retention, conservation of urinary concentration, and papillary ischemia. These studies provide evidence for regional regulation of medullary hemodynamics by AngII, possibly contributing to sodium retention in chronic salt-retaining states.

Angiotensin II↗
PubMed1985

Effects of chlorpromazine on ischemic rat kidney: a functional and ultrastructural study.

The effects of chlorpromazine, an agent with inhibitory effects of calcium influx, phospholipase activation, and Na-K-ATPase, on preserving renal function and proximal tubular ultrastructure were evaluated in renal ischemia. After right nephrectomy chlorpromazine (0.025 mg) or 1 ml of 0.9 per cent saline was selectively administered to the rat kidney immediately prior to a sixty-minute occlusion of the remaining renal artery. Pretreatment with chlorpromazine resulted in a significant attenuation in the rise in postischemic serum creatinine. Hypothermia of the kidney during ischemia provided an additional protective effect. Electron microscopic study of the proximal convoluted tubule demonstrated that the structural damage was less severe in chlorpromazine-treated rats and virtually complete preservation of a normal ultrastructure was observed when hypothermia was added.

Animals↗
PubMed1984

Inner medullary hemodynamics in chronic salt-depleted dogs.

The effects of chronic salt depletion on medullary hemodynamics remain unknown. In the present study, sodium excretion, renal hemodynamics including papillary plasma flow, measured by the albumin-accumulation technique, and papillary tissue solute content were determined during hydropenia in 13 anesthetized sodium-replete and 10 sodium-depleted dogs. Salt depletion induced a significant rise in plasma renin activity and aldosterone without potassium depletion. Mean arterial pressure, GFR, and renal blood flow were similar in sodium-depleted and sodium-replete dogs. Despite a similar distribution of cortical blood flow (measured by the microsphere method) in the two groups, papillary plasma flow was markedly reduced in sodium-depleted dogs (8.8 +/- 1.7 vs. 22.8 +/- 1.9 ml X min-1 X 100 g-1 in sodium-replete dogs), associated with a significant decrease in renal sodium excretion. Furthermore, papillary osmolality and sodium concentration were significantly greater in sodium-depleted dogs. Ultrastructure examination revealed smooth muscle cells surrounding the efferent arterioles and pericytes with contractile potential encircling descending vasa recta. These results suggest that included in the complex hemodynamic adjustment to chronic sodium depletion is a significant reduction in inner medullary blood flow that may be important in maintaining enhanced papillary solute concentration. In addition, the anatomy of the medullary vasculature is compatible with regional regulation of medullary blood flow.

Animals↗
PubMed1982

Retroperitoneal fibrosis presenting as spontaneously reversible renal failure.

Three patients are reported who presented with severe oliguric renal failure due to retroperitoneal fibrosis and obstructive uropathy in whom spontaneous diuresis and recovery of renal function took place, a course resembling acute tubular necrosis. There were, however, several clinical and laboratory findings that provided clues to the presence of obstructive uropathy. Two of the three patients had low back or abdominal pain. All three patients presented with anemia and significant hyperkalemic, hyperchloremic metabolic acidosis with only a small increase in anion gap and two of the patients had an inappropriately high urine pH. Neither tubular cell casts nor pigmented granular casts were identified in the urine in any of the patients. In all three patients the urine output increased from oliguric levels to 1400 - 2000 ml/day within 1 day associated with rapidly improving renal function. This report demonstrates and reinforces the need to rule out obstruction in all patients with renal failure of unknown etiology and adds retroperitoneal fibrosis to the list of diseases associated with renal failure and spontaneous recovery.

Acute Kidney Injury↗
PubMed1982

Effects of diuretics on inner medullary hemodynamics in the dog.

Although the hemodynamic effects of diuretics have been studied extensively, their effects on inner medullary blood flow remain unknown. In the present study, renal hemodynamics, including papillary plasma flow measured by the albumin accumulation technique, and associated alterations in papillary tissue solute content were determined in anesthetized, hydropenic dogs and during euvolemic diuresis induced by furosemide (3 mg/kg plus 2 mg/kg per hr, iv), ethacrynic acid (3 mg/kg plus 2 mg/kg per hr, iv) or chlorothiazide (10 mg/kg plus 10 mg/kg per hr, iv). Renal blood flow increased significantly after furosemide and ethacrynic acid and decreased significantly after chlorothiazide. Sixty minutes after diuretic administration, papillary plasma flow was 10.8 +/- 1.0 (mean +/- SE) in six furosemide- and 11.3 +/- 2.6 ml/min per 100 g in six ethacrynic acid-treated dogs, both significantly lower than in eight normal or eight chlorothiazide-treated dogs [26.4 +/- 2.6 and 26.7 +/- 2.7 ml/min per 100 g, respectively (P less than 0.01)]. A similarly low papillary plasma flow was also noted 10 minutes after diuretic administration in five furosemide and four ethacrynic acid dogs (13.6 +/- 2.3 and 13.4 +/- 1.8 ml/min per 100 g, respectively). In furosemide and ethacrynic acid dogs, papillary osmolality and sodium content were significantly lower than those in normal or chlorothiazide dogs. In normal and chlorothiazide dogs, papillary sodium content was similar, with a significantly reduced papillary osmolality in the latter. At the time papillary plasma flow was measured, extracellular fluid volume was similar among the four groups of dogs; however, plasma renin activity increased significantly in furosemide and ethacrynic acid dogs (P less than 0.01) and remained unchanged in normal and chlorothiazide dogs. Furthermore, papillary plasma flow was restored to normal (25.3 +/- 3.9 ml/min per 100 g) in five dogs in which furosemide was infused during angiotensin II blockage with saralasin, despite a similar diuresis and natriuresis as the other furosemide group. These data demonstrate that after administration of furosemide, ethacrynic acid and chlorothiazide, regulation of papillary plasma flow is independent of renal blood flow, and suggest that angiotensin II may play a role in the reduced papillary plasma flow in furosemide and ethacrynic acid dogs.

Animals↗