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R C Prielipp

Publications and source records attributed to R C Prielipp.

67 records · Page 4Linked to original sources
PubMed1991

Normal parathyroid hormone responses to hypocalcemia during cardiopulmonary bypass.

To determine whether the calcium-magnesium-parathyroid hormone-calcitriol (vitamin D) axis responds appropriately to the hypocalcemia that routinely follows initiation of cardiopulmonary bypass (CPB), we measured blood ionized calcium (CaI), total calcium (CaT), total magnesium (MgT), ultrafilterable magnesium (MgI), total protein, intact parathyroid hormone (PTH), and calcitriol concentrations at eight defined time points in 28 patients undergoing elective cardiac surgery. With the onset of CPB, CaI decreased from 1.14 +/- 0.02 to 0.91 +/- 0.03 mM, P less than 0.05) (n = 17), and then gradually returned to a normal value by the time of separation from CPB (0.98 +/- 0.01 mM). CaT, MgI, MgT, and total protein concentrations declined significantly upon initiation of CPB and remained depressed thereafter. PTH initially decreased upon initiation of CPB (from 50 +/- 8 to 24 +/- 9 pg/ml, n = 9, P less than 0.05), remained inappropriately decreased during the early phases of CPB, and then gradually increased to maximal concentrations in response to hypocalcemia (103 +/- 15 pg/ml) before emergence. Calcitriol concentrations (n = 8) were unchanged during surgery. Based on these initial results, which suggested an association between hypomagnesemia and the slow PTH response to hypocalcemia, measurements were repeated in 10 additional patients, to whom magnesium (Mg) (1 g MgSO4 in two separate intravenous doses) was administered. Mg administration neither altered the PTH response to ionized hypocalcemia nor hastened the return of CaI to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcitriol↗
PubMed1991

Hemodynamic profiles of prostaglandin E1, isoproterenol, prostacyclin, and nifedipine in experimental porcine pulmonary hypertension.

BACKGROUND AND METHODS: We compared the hemodynamic effects of four vasodilators in experimental embolic pulmonary hypertension in a randomized controlled trial, using nine pigs weighing 16 to 23 kg. After anesthesia induction and cannulation with arterial, central venous, and thermodilution output pulmonary artery catheters, animals were repetitively embolized with glass beads (60 to 160 mu) in order to establish pulmonary hypertension (pulmonary artery pressure [PAP] doubled from baseline). Prostaglandin E1 (PGE1), isoproterenol, prostacyclin (PGI2), and nifedipine were compared at doses producing equivalent reduction in systemic BP. RESULTS: Only PGE1 and PGI2 decreased both PAP and pulmonary vascular resistance (PVR). PGE1 decreased PAP from 39 +/- 1 to 33 +/- 1 mm Hg; prostacyclin decreased PAP from 38 +/- 1 to 31 +/- 1 mm Hg and produced the largest increase in cardiac output (Qt). Isoproterenol did not change PAP, markedly increased heart rate (162 +/- 8 to 216 +/- 11 beats/min), and resulted in significant arrhythmias. Nifedipine increased PVR from 1044 +/- 113 to 1125 +/- 100 dyne.sec.cm-5 and decreased Qt. CONCLUSIONS: Vasodilators demonstrate unique hemodynamic drug profiles. Isoproterenol infusion is characterized by tachycardia and arrhythmias. Both PGE1 and PGI2 effectively decrease PAP and PVR. Nifedipine depressed Qt significantly in this glass-bead embolization model of acute pulmonary hypertension.

Alprostadil↗
PubMed1991

Leukotriene synthesis inhibition and receptor blockade do not inhibit hypoxic pulmonary vasoconstriction in sheep.

Several lines of evidence suggest that leukotrienes may be mediators of hypoxic pulmonary vasoconstriction (HPV). However, the effect of leukotriene inhibition on HPV remains controversial. The present study investigated the effect of leukotriene synthesis inhibition and receptor blockade on HPV in the halothane-anesthetized sheep. After initial baseline measurements, the pulmonary pressor response to 15 min of global hypoxia (FIO2 = 0.13) was measured. A second set of baseline measurements was obtained and the sheep then received the combined cyclooxygenase/lipoxygenase inhibitor BW755C, the selective lipoxygenase inhibitor U60257, or the leukotriene receptor antagonist LY171883. Hemodynamic measurements were obtained after drug administration and during a subsequent hypoxic challenge (FIO2 = 0.13). Initial hypoxic challenge increased pulmonary artery pressure 68% and increased pulmonary vascular resistance 104%. Pulmonary hemodynamics after recovery from hypoxia were similar to initial baseline values. Drug administration had no significant hemodynamic effect. Hypoxic challenge after drug administration resulted in a pulmonary pressor response identical to the initial hypoxic challenge. Because leukotriene synthesis inhibition and receptor blockade did not alter the response to hypoxia, we conclude that leukotrienes are not obligatory mediators of HPV. A critical review of the literature supports a modulatory rather than an obligatory role for leukotrienes in HPV.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1991

Effects of amrinone on cardiac index, venous oxygen saturation and venous admixture in patients recovering from cardiac surgery.

The hemodynamic and oxygen transport effects of low-dose (0.75 mg/kg loading dose + 10 micrograms/kg/min infusion, n = 12) and high-dose (2.25 mg/kg loading dose + 20 micrograms/kg/min infusion, n = 12) amrinone were evaluated in extubated patients 24 h after CABG. At both doses, amrinone significantly (p less than 0.05) increased HR, but decreased mean arterial, mean pulmonary artery, central venous and pulmonary artery occlusion pressures. High-dose amrinone significantly decreased systemic vascular resistance. Arterial oxygen saturation decreased significantly following both low- (97.8 +/- 0.4 to 95.6 +/- 0.9 percent) and high- (98.8 +/- 3.4 to 93.9 +/- 1.2 percent) dose amrinone. Pulmonary shunt increased significantly following low-dose amrinone and markedly increased Qs/Qt after high-dose amrinone. Although amrinone significantly increased cardiac index in a dose-dependent fashion (low:3.0 +/- 0.2 to 3.3 +/- 0.3 L/min/m2; high:2.7 +/- 0.2 to 3.4 +/- 0.2 L/min/m2), mixed venous oxygen saturation did not change. Thus, mixed venous oxygen saturation may not predict the hemodynamic response to amrinone infusion in postoperative surgical patients.

Amrinone↗
PubMed1990

Vasodilator therapy in microembolic porcine pulmonary hypertension.

The hemodynamic effects of prostaglandin E1, sodium nitroprusside (SNP), nitroglycerin, and hydralazine were studied in a porcine model of elevated pulmonary vascular resistance (PVR) due to glass bead microembolization (60-150-microns diameter). Each animal received all four drugs. Each drug was titrated to produce a 30% reduction in mean systemic arterial pressure. Although all four drugs decreased PVR, distinct differences in the hemodynamic profiles of the four drugs were evident. Prostaglandin E1 produced the largest reduction in mean pulmonary artery pressure (from 41 +/- 1 to 32 +/- 9 mm Hg, mean +/- SEM) and PVR (25 +/- 3 to 18 +/- 2 mm Hg.L-1.min-1), and did not affect the ratio of PVR to systemic vascular resistance (PVR/SVR). Sodium nitroprusside and nitroglycerin produced moderate decreases in PVR (nitroglycerin 21 +/- 2 to 18 +/- 2 mm Hg.L-1.min-1, SNP 22 +/- 2 to 19 +/- 2 mm Hg.L-1.min-1) and in mean pulmonary artery pressure (nitroglycerin 39 +/- 1 to 35 +/- 1; SNP 40 +/- 1 to 36 +/- 2 mm Hg). Both drugs significantly increased the PVR/SVR ratio. Hydralazine was the only drug that significantly increased cardiac output (1.6 +/- 0.2 to 1.9 +/- 0.3 L/min). Hydralazine had no significant effect on mean pulmonary artery pressure, reduced PVR to the smallest extent (11%), and resulted in the largest increase in the PVR/SVR ratio (from 0.52 +/- 0.04 to 0.80 +/- 0.08). In this model of increased pulmonary vasculature resistance prostaglandin E1 caused an equivalent amount of pulmonary and systemic vasodilation, as expressed by the PVR/SVR ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗
PubMed1989

Circulating calcium modulates adrenaline induced cyclic adenosine monophosphate production.

Inotropic support of the failing myocardium may combine calcium with adrenaline in an attempt to augment the haemodynamic actions of each drug. We have previously shown, however, that calcium blunts adrenaline induced increases in blood pressure and cardiac output in animals and man. The mechanisms by which calcium may interfere with the haemodynamic actions of adrenaline are not well understood. Adrenaline is known to stimulate adenylate cyclase and increase levels of cellular cyclic adenosine monophosphate (cAMP), a crucial second messenger in cell regulation. We evaluated the effect of increased circulating calcium levels on adrenaline stimulated cAMP production in laboratory animals. Calcium infusion in rats nearly doubled the circulating ionised calcium concentration, from 1.27 (SEM 0.03) mM to 2.3(0.18) mM. Adrenaline infusion significantly increased plasma cAMP in saline infused control animals, from 26(6) pmol.ml-1 to 98(22) pmol.ml-1, whereas there was no increase in cAMP plasma levels in the calcium infused rats. The apparent inhibition of adenylate cyclase by calcium may participate in a negative feedback system which helps protect cells from harmful intracellular calcium overload.

Animals↗
PubMed1989

The longitudinal distribution of pulmonary vascular resistance during unilateral hypoxia.

Pulmonary capillary hydrostatic pressure and the longitudinal distribution of pulmonary vascular resistance (arterial and venous components) can be determined by analysis of pressure decay curves following pulmonary artery occlusion. To validate this technique in intact animals, pulmonary artery occlusion pressure decay curves were obtained from both lungs in six anesthetized sheep during control conditions (100% O2) and during unilateral hypoxic ventilation (100% O2 versus 100% N2). Analysis of pulmonary artery occlusion pressure curves indicated the following: 1) in the hypoxic lung, unilateral hypoxia increased the precapillary portion of pulmonary vascular resistance from 72% of the total resistance to 89% of the total resistance in that lung; 2) in the nonhypoxic lung, unilateral hypoxia did not significantly affect the distribution of pulmonary vascular resistance; and 3) unilateral hypoxia produced no significant change in pulmonary capillary pressure in the hypoxic lung compared with control; however, pulmonary capillary pressure was significantly greater in the nonhypoxic lung. These results are consistent with other evidence that hypoxic pulmonary vasoconstriction acts locally and primarily affects resistance at the arteriolar level. Pulmonary artery occlusion pressure decay curve analysis appears to be a valid technique for the measurement of pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance in intact anesthetized animals. These measurements pertain only to the vasculature distal to the site of pulmonary artery occlusion with the catheter, and, thus, caution must be used when applying this technique in a setting of nonhomogenous lung injury.

Animals↗
PubMed1988

Vasodilator therapy in vasoconstrictor-induced pulmonary hypertension in sheep.

A stable preparation of pulmonary hypertension in sheep was developed using a continuous infusion of the vasoconstrictor U46619, a stable endoperoxide thromboxane A2-mimetic. Using this model, the pulmonary and systemic effects of nitroglycerin, sodium nitroprusside, hydralazine, and prostaglandin E1 were compared at doses producing equivalent reductions in systemic blood pressure. Although all four drugs decreased pulmonary artery pressure and resistance, different drug hemodynamic profiles were found. Prostaglandin E1 demonstrated the greatest pulmonary specificity and resulted in the largest decrease in pulmonary artery pressure (from 33 +/- 1 to 23 +/- 1 mmHg). Nitroglycerin and sodium nitroprusside demonstrated intermediate pulmonary specificity and did not affect cardiac output. Hydralazine demonstrated the least pulmonary specificity and resulted in a large decrease in systemic vascular resistance, with only a moderate decrease in pulmonary artery pressure and resistance. Rational selection of pulmonary vasodilators for clinical application will vary depending on baseline heart rate and rhythm, pulmonary artery pressure, systemic artery pressure, and cardiac output.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1988

Hemodynamic profiles of prostaglandin E1, isoproterenol, prostacyclin, and nifedipine in vasoconstrictor pulmonary hypertension in sheep.

Patients with pulmonary hypertension challenge the anesthesiologist with complex alterations of hemodynamic function. To study the effects of multiple therapeutic interventions, a stable model of pulmonary hypertension in sheep was developed using continuous infusion of the vasoconstrictor U46619, a thromboxane A2-mimetic. The pulmonary and systemic effects of four pulmonary vasodilators (prostaglandin E1, isoproterenol, prostacyclin, and nifedipine) were compared at doses producing equivalent reduction in systemic blood pressure. Although all four drugs decreased pulmonary artery pressure and resistance, distinct differences in drug hemodynamic profiles were found. Prostaglandin E1 and isoproterenol demonstrated the greatest pulmonary specificity, increased cardiac output significantly, and decreased pulmonary vascular resistance. Prostaglandin E1 produced the largest decrease in pulmonary artery pressure (from 31 +/- 1 to 22 +/- 2 mm Hg). Isoproterenol markedly increased heart rate (from 119 +/- 6 to 182 +/- 10 beats/min) and resulted in significant dysrhythmias that necessitated limiting infusion of this drug; isoproterenol did not affect stroke volume. Prostacyclin demonstrated intermediate pulmonary specificity and produced the largest increase in cardiac output (from 1.7 +/- 0.2 to 3.1 +/- 0.3 L/min). Nifedipine exhibited the least pulmonary specificity and was the least effective agent in decreasing pulmonary artery pressure. In this model different pulmonary vasodilators exerted different hemodynamic effects, suggesting that appropriate drug selection for treatment of pulmonary hypertension should depend on baseline heart rate and rhythm, pulmonary artery pressure, systemic artery pressure, arterial oxygenation, and cardiac output.

Alprostadil↗
PubMedDate not supplied

Effect of enteral diets on whole body and gut growth in unstressed rats.

The composition of enteral feeding formulas may have different effects on total body and gut growth. We studied the growth effects in rats of a complex solid fiber-based diet (Prolab Rodent Diet) with that of three isocaloric and isonitrogenous commercially available liquid feeding formulas which differ in their type of protein (Osmolite HN, an intact protein formula; Reabilan HN, a peptide formula; and Vivonex-TEN, an amino acid formula). Total body weight gain was greatest with the rodent diet (93 +/- 2 g/10 days), followed by the peptide diet (72 +/- 5 g/10 days) and intact protein diet (58 +/- 8 g/10 days). Weight gain was significantly lower on the amino acid diet (43 +/- 7 g/10 days). Proximal and mid gut mass was comparable with all four diets, but distal gut mass was significantly lower with the amino acid diet. Somatomedin C levels on the rodent diet (13.3 +/- 1.8 nM), and the peptide diet (14.0 +/- 3.3 nM) were significantly higher than somatomedin C levels on the amino acid diet (8.0 +/- 1.0 nM). Somatomedin C levels on the intact protein diet (9.6 +/- 1.4 nM) were intermediate between the rodent diet and amino acid diet. We conclude that growth effects vary with different enteral diets (unrelated to total calories and protein) and may result from differences in the generation of tissue growth factors.

Amino Acids↗