Search PubMed⌕ Search

Biomedical subjects

S Ikema

Publications and source records attributed to S Ikema.

9 recordsLinked to original sources

Growth and metabolic disturbances in a patient with total parenteral nutrition: a case of hypercalciuric hypercalcemia.

Hypercalciuria is a common side effect during total parenteral nutrition (TPN). We report a patient with long-term TPN, who demonstrated hypercalciuria, hypercalcemia and growth retardation. The patient is a six-year-old Japanese girl with Hirschsprung disease (jejunal agangliosis). Jejunostomy was performed at one-month old and since then her nutrition has depended mostly on TPN. When she was 3 years old, continuous TPN was switched to cyclic TPN (on TPN for 11 hrs and off TPN for 13 hrs). The urinary calcium level has been elevated (Ca/Cre ratio, 1.0) since 3 months of age, whereas serum calcium levels stayed within normal range for a while. The serum calcium levels started to elevate to 12 to approximately 13 mg/dl when she was 3 years and 8 months old. She showed growth retardation (height SD score was -4.2SD when she was 5 years and 8 months old) and deteriorated renal tubular function with renal glycosuria, elevated beta 2-microglobulin (beta2-MG) and N-acetyl-beta-D-glucosaminidase. She was referred to our division for the investigation and treatment of growth disturbance and Ca metabolism. Her bone age was delayed (BA/CA 0.62) and serum IGF-I level was decreased but her GH response to provocation test was normal. Bilateral nephrocalcinosis was revealed by renal echogram and CT scan. By reducing calcium content in TPN solution, the serum and urinary calcium levels could be maintained within normal range and her renal function and growth velocity was improved.

Calcium↗

A 75-kD autoantigen recognized by sera from patients with X-linked autoimmune enteropathy associated with nephropathy.

Autoimmune enteropathy (AIE) is a rare disorder characterized by intractable diarrhoea and antienterocyte autoantibody. In this study, we detected a 75-kD autoantigen which distributed through the whole intestine and the kidney, as assessed by Western blot analysis using sera from two unrelated cases of AIE associated with nephropathy. Our results suggest that the detection of the autoantibody against the 75-kD antigen has a diagnostic value in AIE and that the autoimmune reaction against the 75-kD antigen may be implicated in the development of intestinal and renal tissue damage in this rare disorder.

Antigens↗

[Sexual precocity].

Sexual precocity results from both GnRH-dependent and GnRH-independent mechanisms. The GnRH-dependent forms of precocious puberty can be treated effectively with long-acting agonist analogues of GnRH. However, for some children who have a poor growth rate during the analogue therapy, an additional growth hormone therapy should be considered to get them near to their normal final height. The analogue treatment could be continued until a bone age of 13 or more. The GnRH-independent forms of precocious puberty have unique mechanisms and unknown pathophysiology. For instance, even though it is known that testotoxicosis and McCune Albright syndrome are caused by the molecular mechanism disorders, further elucidation of their etiologic basis of sexual precocity is needed. Thus being, in treating the GnRH-independent forms they should be assessed for each particular disorder.

Child↗

Correlation of contractile dysfunction and abnormal tissue energy metabolism during hypoperfusion with norepinephrine in isolated rat hearts: differences between normal and diabetic hearts.

The relationship of myocardial high-energy phosphate depletion and lactate accumulation with contractile dysfunctions was investigated in streptozotocin-diabetic (DM) and normal rat hearts. The isolated hearts were perfused with 10(-6) M norepinephrine (NE) at various low-flow rates (0.4-6 ml/min/g heart wt) for 1 h. Left ventricular pressure (LVP) and contractile force (CF) were monitored, through a water-filled balloon in LV and through a hook attached to the apex, respectively. In DM hearts resting CF (diastolic tension) increased, when the perfusion flow rate was reduced below 6 ml and reached a maximum at a flow rate of less than 3 ml. The large increase in LV stiffness correlated with an elevation in diastolic LVP. In normal hearts these parameters were elevated at a flow rate below 1 ml. A flow-dependent decrease in developed CF was more prominent in DM than in normal hearts, while developed LVP and perfusion pressure were slightly higher in DM hearts with a marked increase in the LV stiffness. A flow-dependent decrease in high-energy phosphates and increases in inorganic phosphate and lactate were more prominent in the inner than in the outer layer of LV free wall in both groups. The change of ATP in the inner layer was greater, while increases of lactate in both layers were smaller in DM hearts. Changes in mechanical parameters correlated well with the ATP decrease and lactate increase in the inner layer in both groups. The correlation curves, however, were not coincidental: at the same low ATP and high lactate level, the LV stiffness was higher in DM hearts. Results indicate that DM hearts are more susceptible to flow-reduction with NE and depletion of total ATP in their tissue, and easily suffer from increased LV stiffness. This cannot be explained by the rate of decrease in total ATP and lactate accumulation alone.

Adenosine Triphosphate↗

Effects of norepinephrine on hypoperfusion-reperfusion injuries in hearts isolated from normal and diabetic rats.

Contractile and energy-metabolic functions were investigated in paced hearts isolated from normal (Normal) and streptozotocin-diabetic rats (DM) during hypoperfusion at 1 ml/min with or without 10(-6) M norepinephrine (NE) and during reperfusion at the pre-hypoperfusion flow. Left ventricular pressure (LVP) and contractile force (CF) were monitored, respectively, through a water-filled balloon in LV and through a hook attached to the apex. A 1-h hypoperfusion without NE caused significant elevations in resting LVP and resting CF only in DM hearts, smaller transmural lactate accumulations in DM hearts, and similar ATP decreases in both groups. Significant decreases in developed LVP and developed CF were observed in both groups. NE during hypoperfusion caused deterioration of these cardiac dysfunctions in both groups, particularly in DM hearts. A 1-h reperfusion caused elevations in resting LVP and resting CF with no recovery in developed CF in Normal hearts, while it caused partial recovery in resting and developed CF in DM hearts. Both groups showed similar partial recovery of ATP. NE during hypoperfusion improved the mechanical dysfunction during reperfusion in DM hearts, but there was a smaller recovery in ATP than in hearts without NE. In vivo insulin treatment in DM restored the cardiac functions to Normal levels. Thus, DM hearts were more vulnerable to hypoperfusion, while Normal hearts were more vulnerable to reperfusion injury.

Animals↗

Improvement of hypoperfusion with norepinephrine injury by ex vivo insulin in isolated diabetic rat hearts.

Effects of insulin on contractile and energy metabolic dysfunctions during hypoperfusion (2 ml/min/g heart wt., 60 min) with 10(-6) M norepinephrine were studied in paced hearts isolated from streptozotocin-diabetic rats. Insulin (2 mU/min/g heart wt.) was infused 20 min before and during hypoperfusion (pre-treated group) or 30 min after the onset of hypoperfusion (post-treated group). Hearts in the non-treated group were hypoperfused without insulin and other hearts in the control group were not hypoperfused. In the non-treated group, resting contractile force (CF) and resting left ventricular pressure (LVP) were significantly elevated to maximum levels within 30 min after hypoperfusion and these elevations were restored in the pre-treated group but not in the post-treated group. Developed CF was depressed in the non-treated group and improved significantly in the pretreated group but not in the post-treated group. Developed LVP was depressed in the non-treated group, and depression was slightly larger in the pre-treated group. In the non-treated group, ATP and creatine phosphate contents in the left ventricle significantly decreased. Decreases in ATP and creatine phosphate contents in the inner layer were partially restored in the pre-treated group but not in the post-treated group. Lactate significantly increased in the non-treated group and increased even further in the insulin treated groups. These results indicate that contractile dysfunction during hypoperfusion with norepinephrine is improved by pre-treated insulin, as is partial recovery of energy metabolism.

Adenosine Triphosphate↗

Investigation on the effect of dipyridamole and papaverine on regional blood flow and cardiac hemodynamics in anesthetized dogs.

Vasodilating effects of dipyridamole were compared with those of papaverine in anesthetized open-chest dogs. Dipyridamole i.v. produced a significant fall in aortic blood pressure and significant increases in aortic and coronary blood flows. Vertebral blood flow did not alter, but renal blood flow was transiently decreased. Left ventricular dP/dt, heart rate and left ventricular enddiastolic pressure were hardly affected by dipyridamole. Papaverine i.v. significantly increased aortic, vertebral and coronary blood flows, left ventricular dP/dt and heart rate and significantly decreased aortic blood pressure and left ventricular enddiastolic pressure. Renal blood flow was instantly decreased by papaverine. Percent change in each vascular resistance showed decreases in total peripheral, vertebral and coronary vascular resistances in response to both drugs, and the decrease in coronary vascular resistance was the most remarkable. Renal vascular resistance was increased by dipyridamole, while it was decreased by papaverine. Percent change in double product (heart rate x systolic arterial blood pressure) showed a monophasic decrease pattern with dipyridamole and a biphasic pattern with an initial, transient decrease followed by an increase with papaverine. The present results indicate that dipyridamole and papaverine produce marked coronary vasodilatation, and that papaverine is different from dipyridamole in cardiotonic properties.

Anesthesia↗

Cardiovascular effects of the new calcium antagonist isradipine and of diltiazem in anesthetized open-chest dogs.

Cardiovascular effects of the new calcium antagonist, isradipine (PN 200-110), were compared with those of diltiazem in anesthetized open-chest dogs. Isradipine 5 micrograms/kg i.v. produced significant decreases in systolic, diastolic and mean aortic blood pressure (AoP) concomitant with a decrease in mean renal blood flow (RBF) and increases in mean vertebral blood flow (VBF), mean coronary blood flow (CBF) and left ventricular dP/dt (LVdP/dt), but almost unchanged heart rate (HR) and left ventricular enddiastolic pressure (LVEDP). Diltiazem 300 micrograms/kg i.v. also produced decreases in AoP and RBF and increases in AoF, VBF and CBF. LVdP/dt and LVEDP were not significantly changed, but HR was decreased by this drug. Duration of increase in AoF, VBF and CBF was significantly longer in isradipine than in diltiazem. The decrease of coronary vascular resistance relative to total peripheral resistance was significantly greater than 1.0 for diltiazem, but not for isradipine. Results indicate that isradipine produces effects on AoP, AoF, VBF, CBF, RBF and LVEDP similar to diltiazem and the drug increases LVdP/dt without a decrease in HR in contrast to diltiazem, and that the effects of isradipine were long sustained when compared with those of diltiazem.

Anesthesia↗