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J C Preiser

Publications and source records attributed to J C Preiser.

16 recordsLinked to original sources
PubMed1996

Effects of nitric oxide donor SIN-1 on oxygen availability and regional blood flow during endotoxic shock.

BACKGROUND: An excessive release of nitric oxide (NO) has been incriminated in the circulatory disturbances of septic shock. OBJECTIVE: To study the effects of an NO donor, 3-morpholinosydnonimine (SIN-1), an oxygen availability and regional blood flow during endotoxic shock to see if a beneficial effect of NO synthase inhibitors in septic shock could be conclusively demonstrated. MATERIALS AND METHODS: In 14 anesthetized and mechanically ventilated dogs, global invasive hemodynamic monitoring was completed and ultrasonic flow probes were placed around the superior mesenteric, left renal, and left femoral arteries for simultaneous measurements of regional blood flow. All dogs received Escherichia coli endotoxin, 2 mg/kg. A control group (n = 7) was administered saline at 20 mL/kg per hour, and a SIN-1 group (n = 7) was given a combination of saline with SIN-1 at successive doses of 1, 2, and 4 micrograms/kg per minute. RESULTS: Neither systemic nor pulmonary arterial pressures were influenced by SIN-1. Cardiac index, stroke index, and left ventricular stroke work index did increase at low to moderate doses of SIN-1 but tended to decrease at the highest dose. Systemic and pulmonary vascular resistances decreased. Fractional blood flow increased in the mesenteric bed at all doses used, was not influenced in the renal bed, but decreased in the femoral bed at the highest dose. Oxygen-derived variables were similar in the 2 groups. Blood lactate and plasma concentrations of tumor necrosis factor were not significantly influenced. At the end of the SIN-1 infusion, the administration of 5 mg/kg of methylene blue increased arterial pressure, pulmonary arterial pressure, and systemic and pulmonary vascular resistances but decreased cardiac index and regional blood flow. CONCLUSIONS: The administration of low to moderate doses of the NO donor SIN-1 can significantly increase cardiac index and superior mesenteric blood flow without deleterious effects on arterial pressure in this model of endotoxic shock. These findings support the hypothesis that NO is essential to maintain organ blood flow even during endotoxic shock.

Animals↗
PubMed1996

Nitric oxide production is increased in patients after burn injury.

OBJECTIVE: Human burn injury is associated with an inflammatory response and related hyperdynamic cardiovascular profile. Increased production of nitric oxide (NO), a potent endogenous vasodilator, has been reported in patients with inflammatory states, including sepsis, but not after trauma other than burns. We studied whether plasma levels of the stable byproducts of NO, nitrite (NO2-) and nitrate (NO3-), are increased in burn patients. DESIGN: Prospective controlled study. PATIENTS AND METHODS: In consecutive patients admitted to the intensive care unit of the burn center at the Queen Astrid Military Hospital in Brussels, plasma was drawn daily from day 1 to day 5 postadmission for determination of NO2-/NO3- levels (Griess' reaction). In a control group of nonseptic inpatients from the department of neurology in Erasme University Hospital who were matched for nutrition (30 to 40 kcal/kg/day of a standard enteral solution), plasma was drawn once for NO2-/NO3- determination. MEASUREMENTS AND MAIN RESULTS: The burn group included 16 patients (age 35 +/- 18 years, total burn surface area (TBSA) 37 +/- 19%) and the control group included six patients (age 64 +/- 18 years). For each comparison between the groups, NO2-/NO3- plasma levels were higher in those patients with burns than in the control group. In the burn group, there was no correlation between NO2-/NO3- plasma levels and TBSA, age, TBSA x age, blood pressure or time. However, in a subgroup of five burned patients who became septic during the study period, NO2-/NO3- plasma levels were slightly higher than in the non-infected patients (177 +/- 131 vs. 83 +/- 48 micromoles/L, NS). CONCLUSION: Human burn injury is associated with an increase in NO production. In this small-size study, NO production was not proportional to burn area, and seemed to be further enhanced in septic patients.

Adolescent↗
PubMed1996

Hypoglycemia associated with phenytoin intoxication.

BACKGROUND: Diphenylhydantoin, a widely used antiepileptic agent, can alter carbohydrate tolerance, and acute intoxication with diphenylhydantoin can be associated with hyperglycemia. CASE REPORT: We describe a patient who experienced a prolonged episode of hypoglycemia secondary to an acute voluntary intoxication with diphenylhydantoin 20 g and zopiclone 225 mg. This hypoglycemic episode was presumptively attributed to diphenylhydantoin and might be due either to an escape from the inhibitory effects of diphenylhydantoin on insulin secretion or an increased sensitivity of the tissues to insulin. Zopiclone was considered less likely since zopiclone overdoses have been only exceptionally associated with hyperglycemia.

Adult↗
PubMed1995

Methylene blue administration in septic shock: a clinical trial.

OBJECTIVE: A release of nitric oxide has been incriminated in the cardiovascular alterations of septic shock. Since guanylate cyclase is the target enzyme in the endothelium-dependent relaxation mediated by nitric oxide, we studied the acute effects of methylene blue, a potent inhibitor of guanylate cyclase in patients with septic shock. DESIGN: Prospective clinical trial. SETTING: Medical-surgical intensive care unit in a university hospital. PATIENTS: Fourteen patients with severe septic shock requiring adrenergic therapy. INTERVENTIONS: Short-term intravenous infusion of methylene blue. MEASUREMENTS AND MAIN RESULTS: Hemodynamic measurements were obtained at baseline, and 30, 60, and 90 mins after the infusion of 2 mg/kg of methylene blue. Methylene blue administration was followed by a progressive increase in mean arterial pressure (from 61.1 +/- 7.6 to 71.7 +/- 12.0 mm Hg at 60 mins, p < .01). Pulmonary arterial pressure, cardiac filling pressures, cardiac output oxygen delivery, and oxygen consumption were not significantly affected. Left ventricular stroke work increased from 42.5 +/- 17.9 to 48.9 +/- 14.5 g.m after 60 mins (p < .05). Arterial lactate concentration decreased from 3.4 +/- 1.4 to 2.7 +/- 1.3 mmol/L (p < .05). Since these effects were transient, a second dose of methylene blue was administered 90 mins later to six patients and was followed by a similar response. No adverse effect was observed. CONCLUSIONS: In septic shock patients, the administration of methylene blue results in a transient and reproducible increase in arterial pressure, associated with an improvement in cardiac function, but does not increase cellular oxygen availability. The significant reduction in blood lactate concentration is probably related to the reductor effect of methylene blue, rather than to an improvement in tissue oxygenation.

Adult↗
PubMed1995

Effects of methylene blue on oxygen availability and regional blood flow during endotoxic shock.

OBJECTIVE: We hypothesized that methylene blue, by inhibiting the activation of soluble guanylate cyclase mediated by nitric oxide, may reverse systemic hypotension, enhance myocardial function, and improve peripheral distribution of blood flow during endotoxic shock. DESIGN: Randomized, controlled, acute intervention study. SETTING: University intensive care laboratory. SUBJECTS: Twenty-one healthy, anesthetized, mongrel dogs, weighing 26 +/- 4 kg. INTERVENTIONS: Groups 1 (n = 7) and 2 (n = 7) received endotoxin (2 mg/kg iv) alone combined with increasing doses of 2.5, 5, 10, and 20 mg/kg iv of methylene blue. Each dose was administrated for 30 mins with a free interval of 30 mins. Group 3 (n = 7) served as a control group, receiving the same doses of methylene blue in the absence of endotoxin. All animals were given normal saline to keep cardiac filling pressures constant. Blood flow probes were placed around the superior mesenteric, renal, and femoral arteries to measure regional blood flow by ultrasonic technique. Data were collected every 30 mins during the study. MEASUREMENTS AND MAIN RESULTS: After endotoxemia, methylene blue increased systemic and pulmonary arterial pressure and vascular resistances in a dose-dependent manner up to 10 mg/kg, but had no effect on cardiac index. At the highest dose, methylene blue decreased arterial pressure and systemic vascular resistance. At doses of methylene blue of < or = 10 mg/kg, mesenteric and femoral blood artery flow increased. At the highest dose of 20 mg/kg, femoral artery blood flow further increased, but mesenteric blood flow decreased. Renal artery blood flow was unaffected by methylene blue. In the absence of endotoxin, methylene blue at doses of 2.5 or 5 mg/kg did not alter mean arterial pressure, but reduced cardiac index, indicating an increase in systemic vascular resistance. In contrast, the higher doses of 10 or 20 mg/kg of methylene blue decreased mean arterial pressure and systemic vascular resistance. However, pulmonary arterial pressure and pulmonary vascular resistance increased in a dose-dependent manner. Mesenteric and renal artery blood flow decreased but femoral blood flow increased. As in the presence of endotoxin, methylene blue induced dose-related increases in oxygen uptake and oxygen extraction ratio, but did not alter oxygen delivery. Methylene blue largely attenuated the endotoxin-induced increase in plasma nitrite concentrations. CONCLUSIONS: Low and moderate doses of methylene blue can significantly increase arterial blood pressure but not cardiac index during endotoxic shock. Methylene blue infusion may selectively increase mesenteric blood flow. High doses of methylene blue can worsen systemic hypotension, myocardial depression, and pulmonary hypertension after endotoxemia.

Animals↗
PubMed1994

Is endotoxin-induced hypotension related to nitric oxide formation?

Nitric oxide (NO), an endothelium-derived relaxing factor (EDRF), is released by different types of cells under the influence of endotoxin and various cytokines: a causative role of endothelium-derived NO in the endotoxin-induced hypotension has thus been suggested. To test the hypothesis that NO may be involved in the acute hypotension following endotoxin challenge, we administered a competitive inhibitor of NO synthase, L-N-monomethylarginine (L-NMMA) to anesthetized dogs in the presence and absence of endotoxin. Dogs were randomly allocated to three groups. Group 1 (n = 3) was given Escherichia coli endotoxin (3 mg/kg, i.v.), group 2 (n = 3) was given L-NMMA (5 mg/kg, i.v. bolus) 15 min after endotoxin and group 3 (n = 3) was given L-NMMA only. One additional dog was given L-arginine (100 mg/kg, i.v. bolus) after L-NMMA and endotoxin to reverse the inhibition of NO synthase. In each animal, saline was infused intravenously throughout the experiment to restore and maintain pulmonary artery occluded pressure at baseline level. After L-NMMA, the increases in mean arterial pressure were similar in group 2 (from 55 +/- 18 to 75 +/- 15 mm Hg, p < 0.01) and in group 3 (from 107 +/- 27 to 128 +/- 24 mm Hg, p < 0.01). Systemic vascular resistance increased from 2,994 +/- 72 to 3,658 +/- 673 dyn.s.cm-5 (p < 0.01) in group 3. Group 1 had lower plasma lactate levels than group 2 (3.5 +/- 2.3 +/- vs. 2.0 +/- 1.6 mEq/l, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1993

Inotropic agents.

When fluid administration is not sufficient to restore hemodynamic stability, inotropic agents may be given to restore the tissue perfusion pressure and to increase oxygen delivery (DO2) to the cells. Dopamine remains the drug of choice in the resuscitation of septic shock but norepinephrine can also have a place in the treatment of profound cardiovascular collapse or severe right ventricular failure. Dobutamine has become the inotropic agent of choice to increase DO2 to the tissues. Unfortunately, the beneficial effects of these agents on the extraction capabilities of the tissues are questionable. The potential of other adrenergic agents (such as dopexamine) or nonadrenergic agents (such as phosphodiesterase inhibitors) is also discussed in this article. Inotropic therapy should be guided not only by measurements of systemic BP but also by repeated assessments of the metabolic function of organs.

Animals↗
PubMed1993

[Should bicarbonates still be administered in lactic acidosis?].

Bicarbonate administration during lactic acidosis seems logical in view of the myocardial depression associated with the decrease in intracellular pH. This treatment has been recently challenged on the basis of observations showing an increase in the veno-arterial gradient for CO2 during acute circulatory failure. The partial transformation of bicarbonate in CO2 carries the risk of aggravating the phenomenon and thereby decreasing intracellular pH. Alternatives to sodium bicarbonate--carbicarb, THAM and dichloroacetate--are discussed.

Acidosis, Lactic↗
PubMed1992

Addition of alinidine, a specific bradycardic agent, to dobutamine in a canine model of endotoxic shock.

BACKGROUND AND METHODS: Alinidine is a recently developed antiarrhythmic medication that acts directly on the cardiac pacemaker cells to reduce heart rate (HR). At effective doses, alinidine might have cardiodepressant actions that could be hazardous in the presence of hemodynamic instability. On the other hand, one limitation of the use of catecholamines is tachycardia, and alinidine could be beneficial in situations such as septic shock, where adrenergic agents are commonly required. The present study explored the hemodynamic and gasometric effects of alinidine during dobutamine administration in a canine model of septic shock induced by endotoxin administration. In ten pentobarbital-anesthetized, mechanically ventilated dogs (weight 28 +/- 4 kg), Escherichia coli endotoxin (3 mg/kg) injection was followed 30 mins later by saline infusion to restore and maintain pulmonary artery occlusion pressure at the baseline value. Sixty minutes after the endotoxin administration, a dobutamine infusion was started at a rate of 10 micrograms/kg/min. Thirty minutes later, alinidine was administered as a bolus dosage of 1 mg/kg in five dogs; the other five dogs served as a control group. RESULTS: Alinidine administration resulted in a decrease in HR from 157 +/- 20 to 138 +/- 27 beats/min (p less than .01) and a nonsignificant increase in cardiac output from 5.2 +/- 3.0 to 6.8 +/- 2.8 L/min, as a consequence of increases in stroke volume from 31.9 +/- 15.3 to 49.2 +/- 13.9 mL (p less than .01) and in left ventricular stroke work from 32.1 +/- 20.0 to 57.4 +/- 32.1 g.m (p less than .05). CONCLUSIONS: During experimental septic shock, alinidine administration can reverse dobutamine-induced tachycardia and simultaneously improve ventricular function.

Analysis of Variance↗
PubMed1991

Interleukin-6 administration has no acute hemodynamic or hematologic effect in the dog.

To investigate the possible hemodynamic effects of interleukin-6 (IL-6), a single dose of 15 mcg/kg of recombinant IL-6 isolated from Escherichia coli was injected intravenously in six pentobarbital-anesthetized dogs. After 30 min, saline infusion was performed to maintain the pulmonary artery balloon-occluded pressure at baseline level. The animals were observed for up to 5 hours. No other hemodynamic alteration was observed than a gradual decline in cardiac output attributed to anesthesia. Hematologic variables, blood glucose, and total serum proteins were also constant. IL-6 levels were markedly elevated in the blood, but no tumor necrosis factor activity was detected. Thus a primary role for IL-6 in the early cardiovascular alterations associated with septic shock seems unlikely.

Animals↗
PubMed1991

Administration of the calcium agonist BAY K 8644 in endotoxic shock.

Septic shock is characterized by a decreased vascular tone and a depressed myocardial function. An impairment in cellular calcium availability has been incriminated in both phenomenons. The effects of BAY K 8644, a dihydropyridine-derivative agent acting as a slow calcium-channel activator, were studied and compared to those of norepinephrine (NE) on an experimental endotoxin shock model in the dog. Thirty minutes after intravenous administration of E. coli endotoxin (3 mg/kg), fluid therapy with normal saline was initiated to restore and maintain pulmonary artery capillary wedge pressure at baseline level. In the first part of the study (8 dogs), the effects of increasing doses of 1, 2, 4, and 8 mcg/kg/min of BAY K 8644 were evaluated. BAY K 8644 administration resulted in an increase in mean arterial pressure (MAP) (65 +/- 16 to 116 +/- 24 mmHg, P less than 0.001), systemic vascular resistance (SVR) (1,451 +/- 526 to 2,632 +/- 804 dynes.sec.cm-5, P less than 0.01), and left ventricular stroke work (LVSW) (0.08 +/- 0.04 to 0.16 +/- 0.07 g.m/kg, P less than 0.05), without change in mean pulmonary artery pressure, cardiac output, O2 transport, or O2 consumption (VO2). In the second part of the study (10 dogs), BAY K 8644 and NE were administered in a randomized order at increasing doses to achieve an identical increase in MAP. For a 20 mmHg increase in MAP, BAY K 8644 increased more SVR than NE (1,284 +/- 299 to 1,717 +/- 551 vs. 1,415 +/- 312 to 1,470 +/- 603 dynes.sec.cm-5, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Dichloroacetate administration in the treatment of endotoxin shock.

Dichloroacetate (DCA), an activator of the pyruvate dehydrogenase complex, has been shown to reduce blood lactate levels effectively in various conditions. DCA administration has also sometimes resulted in beneficial cardiovascular effects. To assess its potential value in the routine management of septic shock, we studied the effects of DCA on a canine endotoxic shock model associated with moderate lactic acidosis. Eighteen dogs were pentobarbitone anesthetized, intubated, and mechanically ventilated. Thirty minutes after the administration of 3 mg/kg of Escherichia coli endotoxin, 10 dogs received 100 mg/kg followed by 100 mg/kg/hr of DCA, and eight dogs served as control. In all animals, fluid administration was titrated according to the left-sided filling pressures. In the DCA-treated animals, lactate levels rapidly fell from 3.1 +/- 1.2 to 1.3 +/- 0.8 mEq/liter after 30 min. The bolus of DCA was usually followed by a very transient increase in arterial pressure, but no sustained hemodynamic change was noted. Oxygen consumption (measured from the exhaled gases) was not affected. Four dogs in the DCA group and one dog in the control group survived the next morning (difference not significant). The present study confirms that DCA can effectively reduce blood lactate levels in endotoxic shock and might therefore be useful in severe lactic acidosis related to septic shock. However, the routine use of DCA in septic shock to improve hemodynamic status is not supported by the present findings.

Acetates↗
PubMed1989

Transthoracic electrical bioimpedance versus thermodilution technique for cardiac output measurement during mechanical ventilation.

To study the possible influence of mechanical ventilation on the accuracy of thoracic electrical bioimpedance (TEI) in the measurement of cardiac output, we determined cardiac output concurrently by TEI using Kubicek's equation and by thermodilution in 8 acutely ill patients who were mechanically ventilated (assist/control mode) but who had no underlying respiratory failure. Cardiac outputs were lower with TEI than with thermodilution (3.97 +/- 0.80 vs 4.83 +/- 1.16 l/min p = 0.004) and there was poor correlation between the values (r = 0.41). Although there is a need to develop non-invasive techniques to measure cardiac output, the present study indicates that TEI is not reliable in mechanically ventilated patients.

Adult↗
PubMed1989

Terminal events in the intensive care unit: review of 258 fatal cases in one year.

The last events before death were analyzed in 258 patients who died in our ICU. Deepening coma (104 patients) and acute circulatory failure (90 patients) were the most common events preceding death. Catastrophic events accounted for only 12% of deaths. In 168 (65%) of 258 patients, death was considered inevitable and CPR was not performed. Furthermore, 22 (9%) patients were allowed to die after withdrawal of intensive care support. These observations indicate that most deaths are expected in the ICU and that "do-not-resuscitate" orders can be reasonably given in the majority of fatal cases. Moreover, complete withdrawal of intensive care support should be considered as a reasonable option in hopeless patients. Since circulatory shock was identified as the most common potentially reversible problem, better prevention and management of acute circulatory failure are needed to improve survival.

Cause of Death↗
PubMed1989

Hypertonic saline solution-hetastarch for fluid resuscitation in experimental septic shock.

Hypertonic colloid solutions have been found efficacious in the resuscitation from hemorrhagic/traumatic shock. The present study investigated the hemodynamic, gasometric, and metabolic effects of hypertonic colloids in endotoxic shock in the dog. Thirty minutes after administration of 3 mg/kg normal body weight of Escherichia coli endotoxin, dogs were randomly assigned to receive 10 mL/kg hydroxyethylstarch (HES) either in 0.9% NaCl (HES, 10 dogs) or in 7.5% NaCl (HT-HES, 10 dogs) in 30 min. Thereafter, 0.9% NaCl solution was administered in volumes adequate to maintain pulmonary artery balloon-occluded pressure at baseline levels. Total fluid administered averaged 64 +/- 30 mL/kg (mean +/- SD) in the HES group and 73 +/- 34 mL/kg in the HT-HES group. As these differences were not statistically significant, total sodium load was higher in the HT-HES group. The persistent volume effect was associated with persistently lower hematocrit and protein levels in the HT-HES group. Initial fluid resuscitation with HT-HES resulted in arterial pressure, cardiac filling pressures, cardiac output, stroke volume, and rates of oxygen delivery and oxygen consumption that were greater than those with HES. Vascular resistances were similar. Analysis of left ventricular function curves also indicated an improvement in cardiac performance. However, these effects almost completely vanished during the remainder of the study. In the HT-HES group, serum sodium and osmolality levels increased to 167 +/- 4 mEq/L and 344 +/- 4 mOsm/kg H2O, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗