Mechanisms of myocardial depression after bolus injection of sodium bicarbonate.

PURPOSE: The classic model for the effects of NaHCO3 on myocardial function predicts transient myocardial depression after an intravenous bolus of sodium bicarbonate in association with myocardial acidosis. METHODS: Five anesthetized, paralyzed, and ventilated dogs underwent midline sternotomy. Myocardial global function was assessed by cardiac output, left ventricular (LV) dp/dt, LV end-systolic, and LV end-diastolic pressures. Regional myocardial function assessed by measuring the LV regional end-systolic, LV end-diastolic lengths, and LAD coronary blood flow. Coronary sinus, intramyocardial and arterial pH were measured as was free serum Ca++. Animals were made acidemia by infusion of 0.3 N HCl and then given a bolus of sodium bicarbonate. This produced transient depression followed by recovery of myocardial function. RESULTS: During the depression phase there was no significant decrease in interstitial pH or an increase in A-VCO2 difference as predicted by the current model. However, there was a significant decrease in the serum free Ca++ that coincided with myocardial depression. CONCLUSION: We could not confirm the predictions of the classic model and hypothesize that myocardial depression may be caused by decreased availability of free Ca++ of decreased Ca++ flux rather than intracellular acidosis.

Transmembrane oxalate exchange: its relationship to idiopathic calcium oxalate nephrolithiasis.

Red blood cell oxalate flux rates were measured in various populations of stone patients and controls. Idiopathic and normocalciuric stone patients and post-prostatectomy patients exhibited rates significantly greater than the nonstone controls. The fact that this abnormality was not limited to patients with calcium oxalate nephrolithiasis suggests that this cellular defect is not universal nor an important etiological factor for calcium oxalate nephrolithiasis.

Hypocalcemia and hypercalcitoninemia in critically ill children.

To study Ca metabolism in critically ill children, we measured ionized Ca (Ca2+), parathyroid hormone (PTH), calcitonin, 25 hydroxycholecalciferol (25[OH] D3), 1-25 dihydroxycholecalciferol (1-25[OH]2D3, and gastrin levels in critically ill children and in healthy controls. Patients were considered hypocalcemic if Ca2+ was less than 1.1 mmol/L. Six (14%) of 45 patients were hypocalcemic. Five hypocalcemic patients were studied and were found to have higher calcitonin levels than normocalcemic patients and healthy controls and higher PTH levels than healthy controls. 25(OH)D3 and 1-25(OH)2D3 were not significantly different in the three groups of patients. Gastrin levels were low in critically ill patients, whether or not they were hypocalcemic. We conclude that hypocalcemia occurs frequently in critically ill children. It is associated with raised levels of calcitonin and PTH. The mechanism for the increase in calcitonin is unknown.

Absence of persisting parenchymal damage after extracorporeal shock wave lithotripsy as judged by excretion of renal tubular enzymes.

Four renal tubular enzymes, N-acetyl-beta-glucosaminidase, beta-galactosidase, angiotensin-converting enzyme and gamma-glutamyltransferase, were measured in the urine before, and 24 hours and 1 week after extracorporeal shock wave lithotripsy in 20 consecutive patients. Extracorporeal shock wave lithotripsy was performed on the Sonolith 2000 device with the patient under intravenous narcotic sedation with fentanyl. Enzymatic activity per gram of urinary creatinine was consistently but not significantly higher before extracorporeal shock wave lithotripsy than in control subjects. All 4 enzymes were elevated 24 hours after extracorporeal shock wave lithotripsy, with the increases in beta-galactosidase and angiotensin-converting enzyme being statistically significant. However, by 7 days after the procedure the enzymes had decreased to pre-procedure concentrations or below. These data suggest that any renal tubular damage induced by extracorporeal shock wave lithotripsy is of limited magnitude and brief duration.

Impact of percutaneous renal stone removal on renal function: assessment by urinary lysozyme activity.

Lysozyme in the urine in concentrations greater than 3 micrograms per milligram of creatinine reflects renal tubular disease or dysfunction in patients without bowel disease or leukemia. We therefore used urine lysozyme assays to assess renal response to percutaneous nephrostomy and stone removal in 42 patients. Eight patients had striking increases (4.2-21.1 [mean 7.58] micrograms/mg creatinine) immediately after nephrostomy puncture in urine obtained directly from the punctured kidney. Lysozyme declined sharply thereafter and was within normal limits in all cases by postoperative day 3. This increase appeared to result from bleeding into the urine from the tract. Five other patients had lysozymuria on admission, only 1 of whom had a sharp increase after nephrostomy puncture. In the remaining patients, the lysozyme levels remained within normal limits throughout the hospital course. These data are further evidence of the absence of significant deleterious effects of nephrostomy puncture on the kidney.