Hemodynamic interactions when combining verapamil, acute changes in extracellular ionized calcium concentration and enflurane, halothane or isoflurane in chronically instrumented dogs

1992 ◽  
Vol 36 (8) ◽  
pp. 806-811 ◽  
Author(s):  
E. S. Hysing ◽  
J. E. Chelly ◽  
L. Jacobson ◽  
M. F. Doursout ◽  
R. G. Merin
2010 ◽  
Vol 226 (1) ◽  
pp. 46-57 ◽  
Author(s):  
Rajiv P. Shrestha ◽  
Christopher V. Hollot ◽  
Stuart R. Chipkin ◽  
Claus P. Schmitt ◽  
Yossi Chait

Author(s):  
Rajiv P. Shrestha ◽  
Yossi Chait ◽  
Christopher V. Hollot ◽  
Stuart Chipkin ◽  
Claus P. Schmitt

A complex bio-mechanism, referred to as calcium homeostasis, regulates plasma ionized calcium (Ca++) concentration in the human body to within a narrow physiologic range which is crucial for maintaining normal physiology and metabolism. In this paper we present a qualitative model of the calcium homeostatic system and then focus on a particular sub-system, termed Ca-PTH axis. We consider the dynamics of the axis involving the response of the parathyroid glands to acute changes in plasma Ca++ concentration. We use a two-pool, linear time-varying model to describe the Ca-PTH axis. We show that this model, parameterized using a guided iterative parametrization scheme and induced hypocalcemic clamp test data, successfully predicts dynamics observed in clinical tests of induced hypercalcemia in normal humans.


1985 ◽  
Vol 63 (12) ◽  
pp. 1577-1580 ◽  
Author(s):  
L. O. Derewlany ◽  
I. C. Radde

Transplacental 45Ca and 32P flux was measured across the in situ perfused guinea-pig placenta under conditions of acute maternal hypocalcaemia and hypercalcaemia. Maternal hypercalcaemia induced acutely by calcium gluconate infusion caused an increase in maternal-to-fetal 45Ca flux which was proportional to the increase in maternal plasma ionized calcium concentration. Acute maternal hypocalcaemia was induced by EGTA infusion and resulted in a decrease in maternal plasma ionized calcium concentration proportional to a corresponding decrease in transplacental 45Ca transfer. A bolus of calcium gluconate caused a transient decrease in 32P flux, whereas EGTA administration was without significant effect on transplacental 32P transfer. Calcium transport across the placenta is not saturated under conditions of maternal normocalcaemia and may be altered according to acute changes in maternal plasma calcium concentration. Thus, control of maternal-to-fetal calcium transfer does not appear to be at the placental level. This suggests that fetal calcium homeostasis may be regulated by the fetus itself.


1979 ◽  
Vol 83 (3) ◽  
pp. 521-528 ◽  
Author(s):  
JJ Morrissey ◽  
DV Cohn

The biosynthesis, processing, and secretion of parthormone and the effect of calcium on these processes were measured in dispersed porcine parthyroid cells incubated with [(35)S]methionine. Proparathormone was detected at 10 min, the earliest time measured, and was rapidly and apparently quantitatively converted to parathormone. The half-life of the prohomormone pool was 15 min. Secretion of parathormone was detected by 20 min. In pulse-chase experiments there was a period between 20 and 40 min during which the wave of newly-synthesized parathormone was secreted. After 40 min during little additional radioactive hormone was secreted, but dibutyryl cyclic AMP, an agent that can mobilize stored parathormone, when added to the incubation mixtures enhanced radioactive parathormone secretion but only after 60 min, although it increased net hormone secretion as determined by radioimmunoassay to the same extent at all times studied. When the ionized calcium concentration of the medium was lowered, more radioactive hormone was secreted at all times but the effect was greatest on that hormone that was synthesized less than 60 min previously ; however, net hormone secretion in contrast to radioactive hormone was enhanced equally at all intervals. These data could mean that the refractoriness to secretion of parathormone 40-60 min of age was related to maturation of secretory container preparatory to storage. Low calcium (0.5 mM) stimulated hormone secretion up to fivefold compared to high calcium (3.0 mM) but did not affect synthesis of parathormone or proparathormne or conversion of the latter to hormone. During processing at least 70 percent of the intracellular parathormone was lost, presumably through proteolysis and this degradation was greater at high calcium. These data have been interpreted in light of the concept that two secretable pools of parathormone exist within the parathyroid.


PEDIATRICS ◽  
1985 ◽  
Vol 76 (4) ◽  
pp. 543-550
Author(s):  
Pankaja S. Venkataraman ◽  
Don A. Wilson ◽  
Roger E. Sheldon ◽  
Radhakrishna Rao ◽  
Michael K. Parker

Traditionally, in infants, a serum calcium value less than 7.0 mg/dL is considered to impair cardiac function. In very-low-birth-weight infants, we studied the hypotheses that decline in serum calcium to 6.0 mg/dL (1) would not impair cardiac function and (2) ionized calcium would remain greater than 3.0 mg/dL. We also evaluated the effect of calcium infusion on cardiac function. We studied 15 normokalemic and normonatremic infants whose birth weights were 822 to 1,450 g and were less than 32 weeks' gestation. When serum calcium declined to less than 6.0 mg/dL, 18 mg/kg of calcium as 5% calcium gluconate was infused for 10 minutes. Serum total calcium concentration, blood ionized calcium concentration, ECG, and M-mode echocardiogram were obtained on entry into the study, when the infants were hypocalcemic, immediately after treatment with calcium, and eight hours after treatment. Ionized calcium values were calculated based on serum total calcium and serum protein, and corrected calcium values were calculated based on serum total calcium, serum albumin, and blood pH. In all infants, serum calcium value declined to less than 7.0 and in eight infants to less than 6.0 mg/dL. Assessment of heart rate, systolic blood pressure, ejection fraction, left ventricular systolic time interval, right ventricular systolic time interval, fiber shortening index, and left ventricular mean velocity of circumferential fiber shortening showed no significant alteration from baseline during hypocalcemia or in association with intravenous slow bolus infusion of 18 mg/kg of calcium. In association with a decline in serum total calcium to as low as 6.0 mg/dL, whole blood ionized calcium was maintained at more than 3.0 mg/dL. Serum total calcium and calculated ionized calcium values correlated significantly with measured blood ionized calcium concentrations; however, these measures were not reliable predictors of blood ionized calcium. We speculate that the hypoproteinemia and hypoalbuminemia noted in these infants may result in relative protection of the blood ionized calcium in these infants. We suggest that in neonates with wide ranges in gestation, serum protein, and blood pH levels, total serum calcium and calculated ionized calcium values may be poor measures of derangement of calcium metabolism. Decline in total serum calcium concentration to 6.0 mg/dL was not associated with impaired cardiac function, and slow bolus calcium infusion in these hypocalcemic very-low-birth-weight infants neither improved nor impaired cardiac function.


1994 ◽  
Vol 267 (1) ◽  
pp. E77-E87 ◽  
Author(s):  
S. E. Szal ◽  
J. T. Repke ◽  
E. W. Seely ◽  
S. W. Graves ◽  
C. A. Parker ◽  
...  

The purpose of the present study was to determine the changes in intracellular ionized calcium concentration ([Ca2+]i) or [Ca2+]i sensitivity accompanying spontaneous and agonist-induced contraction of human myometrium at term pregnancy, as well as to quantify the response to three prototypical agonists: 1) oxytocin, 2) vasopressin, and 3) phenylephrine. Uterine biopsies were obtained at the time of cesarean section from patients who delivered at or near full-term gestation. These preparations were used to measure isometric force development and [Ca2+]i levels with the luminescent calcium indicator aequorin. Concentration-response relationships were determined with respect to isometric force development in the presence of the agonist. [Ca2+]i-force relationships were determined with respect to spontaneous phasic contractions, as well as agonist-induced phasic and tonic contractions. The results provide evidence that the phasic nature of term human myometrium is due to 1) the resting [Ca2+]i level being less than the calcium threshold for contractions and 2) the inability of the tissue to maintain high [Ca2+]i levels for prolonged periods of time. In addition, calcium-independent mechanisms of regulation were suggested by the relatively minor calcium sensitizing action of oxytocin and the observation that relaxation of tonic contractions preceded the fall in [Ca2+]i levels.


1976 ◽  
pp. 491-493 ◽  
Author(s):  
S. Pors Nielsen ◽  
J. Trap-Jensen ◽  
O. Hartling ◽  
T. Falck Christiansen

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