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Biomedical subjects

L J Drop

Publications and source records attributed to L J Drop.

8 recordsLinked to original sources
PubMed1979

Haemodynamic consequences of citrate infusion in the anaesthetized dog: comparison between two citrate solutions and the influence of beta blockade.

We have compared the effects of a solution of acid--citrate--dextrose (ACD) with those of a solution of citrate--phosphate--dextrose (CPD), infused at equal rates, on blood calcium ion concentration and different indices of haemodynamic performance in 17 dogs. The influence of beta adrenergic blockade on these changes was examined. The effects of ACD and CPD were studied in five dogs and were similar. Peripheral vascular changes were the principal cause of arterial hypotension. In six dogs, propranolol 0.5 mg kg-1 intensified the hypocalcaemia-induced left ventricular dysfunction.

Animals↗
PubMed1979

Ventricular pump performance during hypocalcemia: clinical and experimental studies.

We have compared indices of ventricular function during rapid transfusion of citrated (1.5 ml/kg/min) or heparinized (1.5 ml/kg/min) autologous blood in six patients following discontinuation of cardiopulmonary bypass. Infusion of citrated blood was associated with a lowering of plasma ionized calcium concentration ([Ca++], from 0.90 +/- 0.04 to 0.71 +/- 0.4 mM, p less than 0.001) and an increase in pulmonary artery balloon-occluded pressure (PA0, from 9.4 +/- 2.6 to 15.5 +/- 1.7 mm Hg, p less than 0.u1), without a change in left ventricular stroke work index, stroke index, or cardiac index. Transfusion of heparinized blood caused no change in plasma [Ca++]. A rise in PA0, which was similar in magnitude to that observed during citrated blood transfusion, was associated with increased left ventricular stroke work index, stroke index, cardiac index, and mean arterial pressure. Although data obtained during citrated blood transfusion suggest the presence of transient left ventricular dysfunction, its magnitude is not readily expressed in terms of ventricular function curves when accompanied by a simultaneous change in [Cized closed-chest dog by volume loading during hypocalcemia, when mean arterial pressure, heart rate, and [Ca++] were in a steady state, both prior to and following beta blockade with propranolol. Function curves obtained during severe hypocalcemia ([Ca++] = 0.43 +/- 0.02 mM) were shifted significantly to the right and downward, when compared to those obtained during normocalcemia ([Ca++] = 1.06 +/- 0.03 mM). Hypocalcemia combined with beta blockade resulted in severe left ventricular failure, as demonstrated by a flat ventricular function curve.

Aged↗
PubMed1978

Determination of blood ionized calcium in a large segment of the normal adult population.

In two different laboratories ionized calcium was determined by use of a calcium selective electrode system of recent design in specimens of whole blood drawn from a total of 100 volunteers. Identical mean values were obtained in each laboratory. A small standard deviation was found supporting the view that [Ca2+] is normally maintained within a narrow range. Ancillary factors in [Ca2+] determination were evaluated, including effects of in-vivo produced changes in pH, and effects of addition of small amounts of heparin to the whole blood sample. A veno-arterial difference in [Ca2+] was insignificant.

Adolescent↗
PubMed1975

Low plasma ionized calcium and response to calcium therapy in critically ill man.

Marked lowering of plasma ionized calcium concentrations [Ca++] occurred in eight patients (2 days to 54 years old) who required extensive pharmacologic support of the circulation. [Ca++]'s ranged from 0.21 to 0.53 mM. Only one patient survived. The hypocalcemia occurred in the absence of massive transfusion of citrated whole blood or well after such transfusions had been discontinued. These abnormally low concentrations of ionized calcium were not readily corrected by intravenous administration of calcium salts in doses generally recommended. The process responsible for inadequate hemodynamic function appeared to be associated with a severe disturbance in calcium metabolism. Contribution of the latter to the severity of hemodynamic deterioration is unclear, and little benefit from intravenous calcium therapy was found. In two patients, normal [Ca++] could not be restored by administration of CaCl2 alone, but [Ca++] rose to normal following continued calcium replacement therapy in conjunction with increased isoproterenol infusion. There was no predictable relationship between total and ionized plasma calcium concentrations. Thus, measurement of total calcium provided no indication of the level of the biologically active moiety. [Ca++] was low with both normal and low plasma pH values. The data suggest that a very high infusion rate of CaCl2 may required to restore [Ca++] to normal and that hypocalcemia occurring during low-flow states often cannot be corrected by calcium therapy alone. It is recommended that calcium replacement therapy be undertaken only with close monitoring of [Ca++].

Adolescent↗
PubMed1975

The hypocalcemia of acute pancreatitis.

Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.

Acute Disease↗