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L J Drop

Publications and source records attributed to L J Drop.

At least 37 records · Page 2Linked to original sources
PubMed1985

Myocardial recovery after hypothermic arrest: a comparison of oxygenated crystalloid to blood cardioplegia. The role of calcium.

We compared multidose crystalloid hyperkalemic cardioplegic solutions with and without added red cells in 24 canine hearts subjected to 5 hr of arrest at 10 degrees C. All cardioplegic solutions were fully oxygenated at 4 degrees C before delivery. Since blood cardioplegia contained Ca++ carried over with the red cells, Ca++ was added to the crystalloid solution in one group. The table below shows the hematocrit (HCT) and ionized Ca++ concentrations of the cardioplegic solutions, and coronary arteriovenous oxygen difference during infusion of cardioplegic solution (AVO2) (ml O2/100 ml). Recovery during reperfusion is shown as percent of prearrest left ventricular function (LVF) and prearrest myocardial ATP concentration.

Adenosine Triphosphate↗
PubMed1984

Reduction of postischemic myocardial dysfunction by substrate repletion during reperfusion.

We studied the effect of selected metabolic substrates on recovery of myocardial function and ATP concentration when added to the reperfusate after normothermic ischemia. The hearts of 30 anesthetized, open-chest mongrel dogs were subjected to 45 min of global ischemia at 37 degrees C followed by 90 min of reperfusion. Left ventricular function curves were generated on right heart bypass before and at 30 min intervals after the ischemic period. ATP concentration was measured before, at the end of, and 90 min after the ischemic period. Experiments were randomized into five groups distinguished by the content of the myocardial reperfusate during the first 10 min of the reperfusion period. Hearts received either unmodified oxygenated pump blood (control; group I), normothermic oxygenated 28 mmol/liter potassium-blood cardioplegic solution (KBC; group II), 25 mmol/liter glutamate in KBC (group III), 250 mumol/liter adenosine with 1 mg erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (EHNA) and glutamate in KBC (group IV), or 2 mmol/liter ribose and glutamate (group V) in KBC. Hearts reperfused with KBC showed improvement early (group II vs group I; p less than .02) but not late recovery of left ventricular function over control. Glutamate, which replenishes Krebs cycle intermediates lost during ischemia, increased functional recovery (group III vs group II; p less than .002). Ribose, which is important in purine salvage and resynthesis, added to glutamate-KBC further improved functional recovery (group V vs group III; p less than .01). Adenosine, a precursor of ATP, with EHNA, an inhibitor of rapid adenosine catabolism, added to glutamate-KBC depressed early recovery (group IV vs group III; p less than .01); however, recovery improved with time. Both glutamate and ribose with glutamate in KBC improved ATP recovery (groups III and V vs group II; p less than .002). Thus selective substrate repletion during initial reperfusion after severe normothermic ischemia can improve recovery of myocardial function and ATP concentration.

Adenosine↗
PubMed1983

Global and regional function in the regionally ischaemic left ventricle related to plasma ionised calcium.

To study the response of function in the regionally ischaemic left ventricle to increased and decreased concentrations of plasma ionised calcium, twenty-two anaesthetised dogs were placed on right heart bypass with constant mean aortic pressure and heart rate. Regional (sonomicrometry) and global left ventricular function were assessed before coronary artery ligation. Then, following ligation, function after 45 min stable ionised hypercalcaemia [( Ca2+] = 1.68 +/- 0.01 mmol x litre-1) and hypocalcaemia [( Ca2+] = 0.73 +/- 0.02 mmol x litre-1) were each compared to function during an immediately preceding normocalcaemic period. Control of cardiac output enabled paired comparisons to be made at matched preloads: systolic shortening from common end-diastolic chord lengths (n = 10), and stroke work at common left ventricular end-diastolic pressures (n = 22). With hypercalcaemia, systolic shortening in the ischaemic region (2.11 +/- 0.39 mm preligation) increased from -0.62 +/- 0.17 to -0.04 +/- 0.20 mm (P less than 0.01), whereas in the control region systolic shortening increased from 1.47 +/- 0.12 to 2.00 +/- 0.15 mm (P less than 0.01) reaching its preligation value (1.67 +/- 0.13 mm). Stroke work at a left ventricular end-diastolic pressure of 1.37 kPa increased (0.248 +/- 0.019 to 0.299 +/- 0.021 joules x beat-1, P less than 0.001) but not to preligation levels (0.364 +/- 0.016 joules x beat-1). Hypercalcaemia also increased myocardial oxygen consumption (by 1.0 +/- 0.3 cm3 x min-1 x 100 g-1, P less than 0.005) but not coronary blood flow. With hypocalcaemia, systolic shortening decreased in ischaemic and control regions, global function curves were markedly depressed, and myocardial oxygen consumption did not change but coronary blood flow increased. Thus hypercalcaemia improved function in ischaemic and control regions but improvement in the ischaemic region was small compared with the depression associated with ischaemia itself. Hypercalcaemia also improved global function, but not to preischaemic levels, at an increased oxygen cost.

Animals↗
PubMed1982

Comparative evaluation of two calcium ion-selective electrode systems, and their utility for monitoring steady-state changes in [Ca2+].

We compared ionized calcium concentrations ([Ca2+]) as measured with two ionized-calcium analyzers: the NOVA 2 and the Orion SS-20. Samples were obtained from 43 human volunteers, 213 patients, and five dogs (106 samples). In the [Ca2+] range of 0.85 to 1.8 mmol/L, [Ca2+] measurements in whole blood with the NOVA 2 consistently exceeded those measured with the Orion SS-20. However, in the normal range, this difference appeared to be smaller when we compared values for plasma or serum, and was absent over the entire range when we compared aqueous solutions. The normal human [Ca2+] in whole blood as measured with the NOVA 2 is 1.22 +/- 0.01 mmol/L (mean +/- SEM) and that with the Orion SS-20 is 1.12 +/- 0.01 mmol/L (p less than 0.0001 by paired t-test); the 95% confidence intervals were from 1.14 to 1.30 and from 1.02 to 1.22 mmol/L, respectively. Using dogs, we also tested the usefulness of the ionized-calcium electrode for monitoring [Ca2+] during infusion of either citrate or calcium chloride solutions, to produce steady-state alterations in [Ca2+] equilibrium. Frequent successive [Ca2+] measurements were essential to appropriately adjust the infusion rates of these solutions to achieve steady-state [Ca2+].

Animals↗
PubMed1981

Relation between ionized calcium concentration and ventricular pump performance in the dog under hemodynamically controlled conditions.

The effect of plasma ionized calcium concentration on left ventricular function was studied in the canine heart on right heart bypass. Stroke volume, mean arterial pressure and heart rate were controlled. Plasma ionized calcium was lowered to 0.58 +/- 0.01 mM by citrate infusion and raised to 1.70 +/- 0.01 mM by calcium chloride infusion in random order in each dog. Left ventricular function at each of these ionized calcium levels was compared with that in an immediately preceding normocalcemic period. At a constant stroke work (16.9 +/- 0.2 g-m), sustained hypercalcemia was associated with a small decrease in left ventricular end-diastolic pressure (1.7 +/- 0.7 cm H2O, p less than 0.05) despite a marked increase in peak left ventricular dP/dt (first derivative of ventricular pressure) averaging 34 percent (p less than 0.001). Coronary blood flow, tension-time index and myocardial oxygen consumption were not significantly altered. Stroke work determined at a left ventricular end-diastolic pressure of 14 cm H2O, by interpolation in left ventricular function curves, was 11 +/- 4.4 percent above that at control normocalcemia (p less than 0.05). At a constant stroke work (16.9 +/- 0.2 g-m), sustained hypocalcemia was associated with a marked depression of left ventricular function as demonstrated by a substantial increase (from 4.9 +/- 0.3 to 12.7 +/- 1.1 cm H2O, p less than 0.0001) in left ventricular end-diastolic pressure (p less than 0.0001), decreased mean systolic ejection rate (p less than 0.01) and decreased peak left ventricular dP/dt (p less than 0.0001). Coronary blood flow increased (p less than 0.05) whereas myocardial oxygen consumption did not change significantly. A marked displacement of left ventricular function curves to the right (compared with curves obtained during normocalcemia) was observed, and stroke work determined at a left ventricular end-diastolic pressure of 14 cm H2O was 52 +/- 5.4 percent below control level (p less than 0.001). It appears that hypercalcemia, when initiated from a normal control level, provides only a small enhancement of ventricular pump performance (as indexed by the stroke work-left ventricular end-diastolic pressure relation) despite a marked increase in peak left ventricular dP/dt, whereas marked improvement of left ventricular performance may be expected when calcium infusion is initiated from an ionized calcium level that is below normal.

Animals↗
PubMed1981

Persistent ionized hypocalcemia in patients during resuscitation and recovery phases of body burns.

Despite important physiological functions, the fluctuations in plasma ionized calcium concentrations [Ca++] after major thermal injury have not been defined. Measurements of [Ca++] were undertaken in 25 patients of age ranging from 6-75 years, with body surface area burns of 25-85%. Plasma total calcium [Ca], inorganic phosphorus [Pi] and magnesium [Mg++] were also followed. Urinary excretion of the same ions was quantified in nine patients for the first 6 days postburn. The control group consisted of 12 patients who had sustained a similar injury at least 16 months earlier. Significantly low [Ca++] persisted throughout the observation period, despite an average replacement of 0.2 mM/kg.day of CaCl2. The initial hypophosphatemia and hypermagnesemia tended toward normal during the latter phase of the injury. Urinary excretion of the of the cations was not significantly elevated in the first 6 days postburn. The usual reciprocal relationship between [Ca] and [pi] was not evident, and there was no correlation between [Ca++] and the size of burn. The use of McLean-Hastings nomogram poorly predicted the [Ca++] from [Ca]. Our data indicate that marked alterations in [Ca++] homeostasis occur after thermal injury. The etiology of hypocalcemia remains to be elucidated; the physiological consequences in terms of hemodynamic function deserve further study.

Adolescent↗
PubMed1980

Role of the systemic vasculature in the hemodynamic response to changes in plasma ionized calcium.

Hemodynamic consequences of sustained (one hour) hypocalcemia and hypercalcemia (plasma ionized calcium concentration [Ca++] maintained approximately 60% below or above normal, encompassing the clinical range) were studied and the influence of beta blockade on these hemodynamic alterations examined in 16 anesthetized, closed-chest dogs. Alterations in [Ca++] were associated with directionally similar changes in mean arterial pressure, whereas on the average cardiac output remained unchanged. Thus, the peripheral vasculature played an important role in the hemodynamic response to alterations in [Ca++]. The state of beta adrenergic activity was an important determinant of the hemodynamic response to hypocalcemia. Prior to beta blockade, hypocalcemia was associated with decreased systemic vascular resistance, whereas after beta blockade with propranolol hydrochloride, systemic vascular resistance was not different from control except at the five-minute observation period, and cardiac output and stroke volume fell.

Adrenergic beta-Antagonists↗
PubMed1980

Comparative effects of calcium chloride and calcium gluceptate.

Calcium chloride and calcium gluceptate were compared in their ability to increase plasma ionized calcium concentrations ([Ca2+]). To correct a low ionized calcium concentration, each of 10 critically ml of a 10% solution, containing elemental calcium 27 mg ml-1) and calcium gluceptate (20 ml, containing elemental calcium 18 mg ml-1) over a 5-min period in randomized order approximately 6 h apart. [Ca2+] and haemodynamic variables (mean arterial pressure (MAP), mean right atrial pressure (RAP) and heart rate (HR)) were monitored for a 30-min period following completion of calcium infusion. Infusion of either calcium preparation was associated with similar increases in [Ca2+] (5 min after infusion of calcium chloride: 33 +/- 3.1%; calcium gluceptate: 32 +/- 4.3% (mean +/- SEM)) and the effects on MAP were similar for each solution (11.1 +/- 1.8% and 9.7 +/- 2.4%, respectively).

Adult↗
PubMed1980

Chronic hypercalcaemia secondary to hyperparathyroidism: a risk factor during anaesthesia?

Hypercalcaemia (increased plasma total calcium concentration, [Ca]) has been associated with serious ventricular arrhythmia and sudden cardiac arrest in patients with hyperparathyroidism. To support our impression that the occurrence of such complications during surgery is rare, we examined the records and e.c.g. of 193 patients with moderate hypercalcaemia ([Ca] = 2.89 +/- 0.02 mmol litre-1, mean +/- SEM) secondary to histologically demonstrable parathyroid hyperfunction, who were admitted to hospital between 1974 and 1978 We found that ventricular arrhythmia was not recorded for any patient, and A-V junctional rhythm was present at the beginning of operation in two. Before operation a statistically significant although minimal shortening of corrected values of Q-T interval occurred compared with a control group (n = 60). However, duration of the corrected Q-T interval was not diagnostic of increased [Ca] in a given patient with hyperparathyroidism.

Adolescent↗
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↗