Biomedical subjects

A B Groeneveld

Publications and source records attributed to A B Groeneveld.

At least 73 records · Page 4Linked to original sources

PubMed1995

Relation between myocardial uptake of thallium-201 chloride and fluorine-18 fluorodeoxyglucose imaged with single-photon emission tomography in normal individuals.

Recently, we have demonstrated the feasibility of imaging myocardial uptake of fluorine-18 fluorodeoxyglucose (FDG) with single-photon emission tomography (SPET) using a specially designed collimator. Thallium-201 was used to determine distribution of perfusion for comparison with FDG uptake. However, regional 201Tl and FDG activities may be different, based on differences in tracer attenuation and the use of different collimators. To study the relation between tracer activities imaged with SPET, nine healthy individuals underwent resting 201Tl SPET and FDG SPET during a hyperinsulinaemic euglycaemic clamp. The SPET data were analysed semiquantitatively, using circumferential profiles. Mean profiles of midventricular short-axis slices showed no significant difference between 201Tl and FDG activity. Regional fluctuations were similar for FDG and 201Tl; the highest tracer activities were observed in the lateral wall and the lowest activities in the septum. Finally, pooled data (n = 1620 segmental activities) in nine individuals showed a linear correlation (P < 0.0001) between 201Tl and FDG activity: FDG = 0.76 201Tl + 0.23 (r = 0.70). These data demonstrate the absence of major differences between regional 201Tl and FDG activity in normal myocardium, suggesting that no separate 201Tl and FDG SPET reference values are needed for comparison with patient studies.

Adult↗

PubMed1995

Abdominal compressions increase vital organ perfusion during CPR in dogs: relation with efficacy of thoracic compressions.

STUDY OBJECTIVE: Abdominal compressions can be interposed between the thoracic compressions of standard CPR (SCPR). The resulting interposed abdominal compression CPR (IAC-CPR) may increase blood pressures and patient survival, particularly if applied as a primary technique after in-hospital cardiac arrest. We used a predominant cardiac compression canine model to study the effects of IAC-CPR on blood pressures and total and vital organ perfusion as a function of time after cardiac arrest and efficacy of SCPR. DESIGN: In a crossover design, we measured blood pressures and total and regional blood flow (radioactive microspheres) during 6-minute episodes of mechanical SCPR and IAC-CPR, both early (4 to 16 minutes) and late (18 to 30 minutes) after induction of ventricular fibrillation in eight dogs (weight, 25 to 33 kg) under neuroleptanalgesia/anesthesia. RESULTS: During IAC-CPR, the ascending aortic-right atrial pressure gradient increased (P < .05), and retrograde pressure pulses contributed to the rise of ascending aortic pressure. Within 2 minutes after the start of IAC-CPR, end-tidal CO2 fraction increased by 0.6 +/- 0.4 vol% (P < .05), suggesting enhanced venous return. IAC-CPR enhanced (P < .05) total forward blood flow (574 +/- 406 versus 394 +/- 266 mL/minute during SCPR for the early phase) and vital organ perfusion (including myocardium), in both early and late phases. The IAC-CPR-induced augmentation of blood flow was greater if perfusion was relatively high during SCPR. CONCLUSION: Compared with predominant cardiac compressions alone (SCPR), the addition of interposed abdominal compressions (IAC-CPR) improves total and vital organ oxygen delivery through enhanced venous return and perfusion pressures.

Abdomen↗

PubMed1995

Effects of human growth hormone in critically ill nonseptic patients: results from a prospective, randomized, placebo-controlled trial.

OBJECTIVES: To study the effects of growth hormone administration on insulin-like growth factor I concentration, nitrogen balance, and fuel utilization, and to study its safety in critically ill nonseptic patients. DESIGN: Prospective, randomized, placebo-controlled trial. SETTING: Medical intensive care unit of a university hospital. PATIENTS: Eighteen critically ill nonseptic patients were studied for 8 days after admission. INTERVENTIONS: Growth hormone (0.1 mg/kg/day) or placebo was administered as a continuous intravenous infusion on the second, third, and fourth days after admission. The study period was 8 days. MEASUREMENTS AND MAIN RESULTS: Plasma hormone concentrations were measured every 6 hrs and average daily values were calculated. The 24-hr urinary nitrogen and 3-methylhistidine excretion were measured. Indirect calorimetry was used to calculate fuel utilization. Insulin-like growth factor I concentrations increased in the treatment group from subnormal to normal values and remained increased despite discontinuation of growth hormone treatment (p = .02). Nitrogen balance differed between the groups upon admission: growth hormone group (3.9 +/- 4.1 g/day) vs. controls (13.8 +/- 5.4 g/day), but improved with growth hormone. This finding appeared independent of the imbalance between the groups. The 3-methylhistidine excretion was not different between the groups and did not change during growth hormone administration. Free fatty acids and glycerol concentrations increased during growth hormone treatment, but calculated fuel utilization did not change. During growth hormone treatment, insulin concentrations increased, due to the increased administration of insulin necessary for glycemic control. Side effects other than hyperglycemia were not observed. CONCLUSIONS: Growth hormone administration in a heterogeneous group of critically ill nonseptic patients resulted in normalization of insulin-like growth factor I levels, even after cessation of growth hormone treatment. Nitrogen balance improved, but this change was transient. Hence, growth hormone affects nitrogen balance, probably partly independent of insulin-like growth factor I.

Blood Glucose↗

PubMed1995

Methylene blue increases myocardial function in septic shock.

OBJECTIVE: To study whether the circulatory changes of human septic shock are mediated in part by nitric oxide. DESIGN: Open-label, nonrandomized clinical trial on the effects of methylene blue, an inhibitor of nitric oxide action. SETTING: Intensive care unit of a teaching hospital. PATIENTS: Nine consecutive patients with documented septic shock and a pulmonary artery catheter in place, after initial resuscitation with fluids, sympathomimetics, and mechanical ventilation. INTERVENTIONS: Hemodynamic and metabolic variables were measured before and then 15, 30, 60, and 120 mins after the start of a 20-min infusion of 2 mg/kg of methylene blue. MEASUREMENTS AND MAIN RESULTS: Patients had a hyperdynamic circulation, and methylene blue increased (p < .01) mean arterial pressure from 84 +/- 18 to 109 +/- 31 mm Hg and cardiac index from 4.7 +/- 0.9 to 5.6 +/- 1.2 L/min/m2, before and 30 mins after starting the methylene blue infusion, respectively. Cardiac filling pressures did not change. In the same time interval, the subnormal systemic vascular resistance index increased (p = .09) and arterial compliance decreased (p < .05). Oxygen delivery and oxygen uptake increased (p < .05) from 714 +/- 188 to 865 +/- 250 mL/min/m2 and from 160 +/- 39 to 186 +/- 44 mL/min/m2, respectively. Except for heart rate, which increased by 11 +/- 8 beats/min (p < .01), variables returned to baseline values at time = 120 mins. CONCLUSIONS: After initial resuscitation from human septic shock, a single dose of methylene blue transiently increases mean arterial pressure and oxygen uptake, associated with a decrease in arterial compliance and increases in myocardial function and oxygen delivery. Hence, nitric oxide may be a mediator of the circulatory changes of human septic shock.

Aged↗

PubMed1995

Transient increase in interleukin-8 and pulmonary microvascular permeability following aortic surgery.

Aortic surgery results in ischemia/reperfusion of the lower body. This may liberate inflammatory mediators that activate neutrophils, and may result in lung microvascular changes with increased permeability and respiratory failure. We studied circulating inflammatory mediators and the pulmonary leak index (PLI) of 67Ga, a measure of transvascular transferrin transport and permeability, in patients scheduled for elective aortic and peripheral vascular surgery, before and after surgery. Aortic surgery patients in Groups 1 (n = 10) and 2 (n = 7) were studied before and at a median of 2.5 and 21.0 h after surgery, respectively. A control Group 3 (n = 6) was studied before and at a median of 2.9 h after peripheral vascular surgery. The PLI (median) increased from a median of 9.1 (range, 6.6 to 14.7) before to a median of 23.4 (range, 18.7 to 86.4) x 10(-3)/min after surgery in Group 1 but not in the other groups (p < 0.001). The postoperative increase in circulating neutrophils and elastase-alpha 1-antitrypsin, a marker of neutrophil activation, was similar among the groups. Plasma levels of activated complement 3a and tumor necrosis factor (TNF-alpha) did not change in any of the groups. In contrast, plasma levels of interleukin-8 (IL-8) increased in Group 1 from < 3 (range, < 3 to 37) before to 324 (range, 36 to 868) pg/ml after surgery, but did not change in the other groups (p < 0.005). The decrease in plasma levels of angiotensin converting enzyme (ACE) was greater in Group 1 than in the other groups (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1995

Feasibility of planar fluorine-18-FDG imaging after recent myocardial infarction to assess myocardial viability.

UNLABELLED: The aim of this study was to define the clinical feasibility of planar myocardial 18F-fluorodeoxyglucose (FDG) imaging and to assess the relation between 201Tl, FDG and left ventricular function early after myocardial infarction. METHODS: Fifty-one patients were studied 5 +/- 2 days after infarction. Scintigraphic images were visually and quantitatively analyzed using a circumferential profiles technique. FDG uptake was normalized to the area with maximal 201Tl uptake. Scintigraphic data were compared with left ventricular wall motion as assessed by ventriculography in 22 patients. Relative regional 201Tl uptake was categorized as normal (> or = 75% of peak activity), moderately reduced (50%-75%) or severely reduced (< 50%). These tracer defects were considered viable if FDG uptake exceeded 201Tl uptake by > or = 20% and/or if FDG uptake was normal (> or = 75%). All regions with FDG uptake 20% less than 201Tl uptake were considered nonviable. RESULTS: Four hundred forty-one myocardial regions were analyzed; 200 showed normal 201Tl uptake, 241 had reduced uptake, 191 had moderately reduced 201Tl uptake and 50 regions had severely reduced uptake. Viability for moderately and severely reduced regions was observed in 62% and 48%, respectively. A concordance between flow and metabolism was observed in 38% and 52%, respectively. CONCLUSION: Myocardial FDG imaging is feasible with standard gamma camera systems and enables the identification of regions with preserved glucose metabolism in patients shortly after infarction.

Coronary Angiography↗

PubMed1994

Local mitochondrial enzyme activity correlates with myocardial blood flow at basal workloads.

To study whether heterogeneous myocardial blood flow relates to the local oxidative capacity of cardiac muscle, local blood flow at resting cardiac workloads and the activity of the mitochondrial enzyme succinate dehydrogenase (SDH) were determined in small regions of the left ventricle of seven anaesthetized, mechanically ventilated, open-chest pigs (25-35 kg). Following injection of radioactive microspheres (15 microns phi) into the left atrium, the heart was rapidly excised and cut into five transverse slices, which were simultaneously freeze-clamped between two aluminum blocks precooled at -80 degrees C. The left ventricle was then subdivided into 84 samples of about 0.9 g. Myocardial blood flow was 0.88 +/- 0.34 ml/min/g wet weight (ww), and SDH activity 1.46 +/- 0.33 mumol/min/g ww (mean +/- S.D., n = 7). Local data were normalized to their respective mean values in each pig, and then pooled. Local blood flow ranged from 0.32 to 1.63 of the mean, and blood flow heterogeneity characterized by the coefficient of variation (CV = S.D./mean) was 18.4%. Normalized local SDH activity ranged from 0.16 to 1.94, with a CV of 21.8%, significantly exceeding measurement error (CV = 4.5%). Local blood flows and SDH activities did not vary among transmural sublayers of the left ventricle, but variation within each sublayer was considerable. In six of the seven pigs, local blood flow correlated (P < 0.05) with SDH activity, with correlation coefficients (r) ranging from 0.26 to 0.54 (for pooled data: r = 0.27, P < 0.0001). When expressed per gram dry weight, heterogeneity of SDH activity increased (P < 0.05), and here also local blood flow correlated with SDH activity in all pigs (for pooled data: r = 0.45, P < 0.0001). Hence, heterogeneity of mitochondrial capacity within cardiac muscle partly explains the heterogeneity of myocardial blood flow, even though myocardial perfusion at rest was studied in relation with a maximal enzyme rate. The low correlation coefficient clearly indicates that at resting workloads other factors also play a role.

Animals↗

PubMed1994

Acute effect of ibopamine and isosorbide mononitrate on blood volume distribution in congestive heart failure.

In order to compare ibopamine (IBO), a dopamine congener, with isosorbide mononitrate (ISMN) and to study their interaction in effects on the capacitance vasculature in congestive heart failure (CHF), a prospective, randomized, placebo-controlled, double-blind clinical trial was performed in 32 patients with New York Heart Association class II-IV CHF, randomly assigned to receive single oral doses of placebo, 200 mg IBO, 20 mg ISMN, or both IBO and ISMN. After labelling of red cells with 99mTc, changes in regional radioactivity, indicative of changes in blood volume, were recorded using a gamma-camera before and at 30, 60 and 120 min after drug administration. At 30 and 60 min, arterial systolic and pulse pressures were higher with IBO than with ISMN and placebo (for pulse pressure by mean 13.7 mmHg, 95% confidence interval 4.5-23.0 mmHg, at 30 min), probably reflecting an IBO-induced rise in stroke volume at unchanged heart rate and mean arterial pressure. IBO did not change regional radioactivity except for a transient increase of 4.4% (0.5-7.6%) in the thorax at 30 min. This was attenuated by concomitant ISMN treatment since, starting at 30 min, the drug increased radioactivity in the legs, compared with patients not receiving the drug, by 8.0% (95% confidence interval 0.2-15.8%), leading to a fall in thoracic and left ventricular radioactivity at 30 min of 3.4% (0.3-7.0%) and 6.4% (0.8-11.9%), respectively, and a fall of 5.5% (0.5-10.5%) in hepatic radioactivity at 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1994

Effects of human growth hormone on fuel utilization and mineral balance in critically ill patients on full intravenous nutritional support.

PURPOSE: The effects of recombinant human growth hormone (GH) on fuel utilization, mineral and fluid balance in critically ill patients were studied. METHODS: Twenty patients requiring mechanical ventilation and receiving standard parenteral nutrition were studied. GH 0.1 mg/kg/day (n = 10) or placebo (n = 10) was administered as continuous intravenous infusion for 3 days. Plasma mineral levels, urinary nitrogen, and mineral excretion were measured. Indirect calorimetry was used to calculate energy production rate and fuel utilization. RESULTS: Insulin-like growth factor I concentrations increased: day 4 GH, 18.9 +/- 7.0 ng/mL; controls 11.6 +/- 3.2 ng/mL (P < .05). During GH administration, the nitrogen balance became zero, whereas it remained negative in controls (P = .03). Fuel utilization did not differ between the groups. Neither did oxygen consumption, carbon dioxide production, or the respiratory quotient (RQ). Nonprotein RQ showed a tendency to decrease in the GH group, whereas an increase was present in controls. Mineral balance improved in both groups. Phosphate balance improved by 250% in the GH group (P = .054). CONCLUSIONS: GH administration in critically ill patients reduces nitrogen loss and improves phosphate retention but does not have an important effect on fuel utilization.

APACHE↗

PubMed1994

Splanchnic tonometry: a review of physiology, methodology, and clinical applications.

The objective of this article is to review splanchnic tonometry. The English literature, involving both animal and human studies, was used for review, with emphasis on papers on physiological and methodological principles and clinical applications. Tonometry involves the measurement of intraluminal PCO2 as a measure of mucosal PCO2 in the gastrointestinal tract via a catheter in, for instance, stomach or sigmoid colon, and the calculation, with help of the blood bicarbonate content and the Henderson-Hasselbalch equation, of the mucosal pH (pHi). The latter is considered as a relatively simple index of the adequacy of mucosal blood flow. Concerning methodology, it is still unclear whether acid secretion should be inhibited for proper assessment of PCO2 in the stomach. Buffering of bicarbonate by gastric acid may elevate the intraluminal PCO2 independently from mucosal PCO2, thereby confounding pHi as a measure of perfusion adequacy. This can be prevented by inhibition of acid secretion. Authors have raised doubts whether the composite variable pHi is of additive value to the acid-base status of arterial blood, so that it is unclear whether a subnormal pHi is a specific and sensitive indicator of mucosal ischemia, as suggested by others on the basis of a decline in the pHi along the gastrointestinal tract in animals subjected to vascular occlusion or circulatory shock. Moreover, tissue PCO2 depends on the PCO2 of supplying blood. Conversely, the bicarbonate concentration in ischemic mucosa may not equal that in arterial blood. Taken together, an elevated tonometer fluid arterial blood PCO2-gradient might be a more sensitive and specific indicator of mucosal ischemia than a decrease in the pHi, analogous to an increase in tissue PCO2 and widening of the venoarterial PCO2 gradient during various types of hypoperfusion, in animals and humans. Although splanchnic ischemia is an early event in shock, the sensitivity and specificity of this index for mucosal ischemia and its clinical value, relative to that of the pHi, have not been formally evaluated yet. Nevertheless, the pHi has been suggested to be of predictive value for gastrointestinal complications, multiple organ failure, success or failure of weaning from mechanical ventilation, and outcome in critically ill patients. Tonometry may be a useful monitoring technique to guide treatment and to improve survival. Splanchnic tonometry is a relatively simple, noninvasive, and thereby promising technique to monitor the critically ill. However, some aspects need further evaluation before the technique can be advocated for routine use.

Acid-Base Equilibrium↗

PubMed1994

High volume hemofiltration improves hemodynamics and survival of pigs exposed to gut ischemia and reperfusion.

This study assesses the influence of high volume continuous hemofiltration on hemodynamics of pigs subjected to bowel ischemia/reperfusion. Twelve anesthetized and ventilated pigs were studied for 60 min during clamping of the superior mesenteric artery (SMA) and subsequently for 90 min after release of the clamp, while measuring global hemodynamics, SMA flow, and jejunal pCO2. They were randomly divided into two groups: pigs in "control" group were subjected to SMA clamping only. Pigs in "hemofiltered" group received zero-balanced, high volume, veno-venous hemofiltration with the removal of 6000 ml of ultrafiltrate/h, starting 30 min before clamping until 90 min after removal of the SMA clamp. Thereafter, pigs were allowed to awake and sacrificed after 24 h for macroscopic assessment of bowel damage. The drop in cardiac output (CO) during SMA clamping in the hemofiltered group was 2.5 +/- .3 L/min (mean +/- SE) (1.1/4.0; 95% confidence interval) smaller than in the control group. At the end of the experiment, mean arterial pressure (MAP) in the hemofiltered group was 33 +/- 6 (19/48) mmHg higher than in the control group, CO was 2.0 +/- .2 (1.2/2.8) L/min higher in the hemofiltered group. After 60 min of SMA clamping, left ventricular stroke work in the hemofiltered group was 35 +/- 4 (14/56) g higher than in the control group, and higher by 33 +/- 3 (21/46) g at 90 min after release of the SMA clamp. The mean pulmonary artery pressure, right atrial pressure, pulmonary artery wedge pressure, SMA flow and bowel wall pCO2 at different time points did not differ between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Effect of ranitidine on basal and bicarbonate enhanced intragastric PCO2: a tonometric study.

A high intragastric PCO2 (iPCO2), determined tonometrically, is the main factor participating in a low gastric intramucosal pH (pHi) and may point to gastric mucosal ischaemia. iPCO2 might also increase, however, after buffering of gastric acid by bicarbonate; the magnitude of this effect and the efficacy of H2 blockers to prevent it are unclear. Ten healthy volunteers (20-24 years) were studied at baseline and after oral ingestion of 500 mg sodium bicarbonate. The same test was carried out one hour after intravenous injection of 100 mg ranitidine. A glass pH electrode for continuous gastric juice pH measurements and a Tonomitor catheter were placed 10 cm distally from the gastro-oesophageal junction. iPCO2 was measured in saline boluses, infused at 30 minute intervals in the balloon at the tip of the Tonomitor. Before ranitidine was given, basal iPCO2 (mean (SD)) was 8.40 (2.53) kPa, and increased to 19.20 (5.87) kPa after sodium bicarbonate (p < 0.001). After ranitidine, the gastric juice pH increased from 1.8 (0.9) to 5.6 (1.3) (p < 0.05), while basal iPCO2 was 5.60 (0.67) kPa (p < 0.01) and did not change after sodium bicarbonate (6.27 (2.67) kPa)). iPCO2 values after acid secretion suppression were similar to those in capillary blood (5.60 (0.40 kPa)). The difference between intragastric and blood PCO2 during normal acid secretion probably results from buffering of gastric acid by gastric bicarbonate, rather than by duodenogastric reflux or saliva entering the stomach. During acid secretion suppression, intragastric equals blood PCO2, even after oral ingestion of sodium bicarbonate. Hence, acid secretion inhibition is mandatory for proper assessment of iPCO2 and pHi as specific measures of the adequacy of gastric mucosal blood flow.

Adult↗

PubMed1994

Delayed resolution of pulmonary oedema after cocaine/heroin abuse.

Pulmonary oedema lasting six days occurred in a 68 year old man after sniffing cocaine. He also had evidence of parenteral self-administration of heroin. Pulmonary microvascular filtration pressure and permeability were normal. Delayed resolution of the pulmonary oedema may have been caused by a cocaine-induced impairment of sodium and thus fluid transport across alveolar epithelium. Recognition may be important, since lowering filtration pressure with diuretics may not hasten resolution of oedema.

Aged↗

PubMed1994

Pathogenesis of acute renal failure during sepsis.

Acute renal failure (ARF) is often a component of multiple organ system failure in critically ill patients. Sepsis (i.e. systemic bacterial infection) is a major factor in the aetiology of ARF and this is primarily caused by sepsis-induced cardiovascular and pulmonary failure. This association suggests that systemic haemodynamic factors, leading to severe and persistent renal hypoperfusion, play a key role in the development of ARF. However, ARF in the course of sepsis or endotoxaemia may not be solely due systemic or renal haemodynamic changes, since humoral and cellular reactions may also have an adverse effect on renal function. This review will address the haemodynamic and non-haemodynamic factors and their interaction in the development of ARF during sepsis.

Acute Kidney Injury↗

PubMed1993

Infusion of ultrafiltrate from endotoxemic pigs depresses myocardial performance in normal pigs.

We previously showed a beneficial effect of hemofiltration on hemodynamics of endotoxic shock pigs. To test the hypothesis that this effect of hemofiltration is caused by convective removal of factors that adversely affect hemodynamics during endotoxemia, we infused ultrafiltrate from endotoxic shock pigs into healthy pigs. Their hemodynamics were compared with those of pigs who were infused with ultrafiltrate from healthy pigs. Twelve anesthetized and ventilated pigs were hemodynamically monitored for 150 minutes following the infusion of 2 L of ultrafiltrate from 12 donor pigs. The acceptor pigs were randomly divided into two groups; group 1 received ultrafiltrate from pigs who were hemofiltered after the infusion of 0.5 mg/kg endotoxin over 30 minutes; group 2 served as a control group, receiving ultrafiltrate from healthy donor pigs. Group 1 showed a decrease in mean arterial pressure of 28 +/- 7 mm Hg (mean +/- SEM) versus an increase of 17 +/- 3 mm Hg in group 2 (P < 0.4). Mean pulmonary artery pressure increased more in group 1 than in group 2 (9 +/- 2 mm Hg versus 1 +/- 1 mm Hg, P < .04). The decrease in cardiac output in group 1 was greater than in group 2 (3.3 +/- 0.2 L/min v 0.3 +/- 0.3 L/min, P < .02) and was due to a decrease in stroke volume. The decrease in right ventricular ejection fraction was also greater (0.15 +/- 0.02 v 0.01 +/- 0.00, P < .01). Systemic vascular resistance, right atrial pressure, right ventricular end-diastolic volume, pulmonary wedge pressure and heart rate did not differ between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Transvascular transport of 67Ga in the lungs after cardiopulmonary bypass surgery.

STUDY OBJECTIVE: To examine the effect of cardiac surgery with cardiopulmonary bypass (CPB) on pulmonary vascular permeability. DESIGN: A prospective, serial study. SETTING: Department of nuclear medicine and intensive care units of a university hospital. PATIENTS: Twelve consecutive patients were studied, before and immediately after elective cardiac surgery using CPB (group 1), and 4 consecutive, artificially ventilated patients with acute cardiogenic pulmonary edema (group 2). MEASUREMENTS AND RESULTS: The kinetics in blood and over both lungs were measured, using two mobile probes at the bedside, of intravenously injected 67Ga, assumed to bind to circulating transferrin, and in vitro 99mTc-labeled red blood cells to account for pulmonary blood volume. From data recorded in time (1 h), a pulmonary leak index (PLI), the time constant of transport of 67Ga from the intravascular to the extravascular space of the lung, was calculated and values for both lungs were averaged. In group 1, the PLI (.10(-3).min-1, mean +/- SD) was 8.2 +/- 3.7 before and 17.0 +/- 13.5 after CPB surgery (p < 0.01) and changes directly related to the duration of CPB. In four patients with a CPB duration > or = 120 min, the PLI, 31.1 +/- 16.3.10(-3).min-1, exceeded 2 SD plus mean preoperative PLI. Changes in PLI tended to relate inversely to changes in arterial WBC, which, in turn, inversely related to CPB duration. The PaO2/FIO2 ratio decreased and tended to relate inversely to PLI after surgery. No patient developed alveolar pulmonary edema on chest radiograph. In group 2, the PLI was 11.1 +/- 3.1.10(-3).min-1 (NS from group 1 preoperative PLI). CONCLUSIONS: Cardiopulmonary bypass induces a pulmonary vascular leak, as assessed by 67Ga kinetics using a bedside detection technique, in some cardiac surgery patients with prolonged CPB. This leak may reflect pulmonary vascular injury and increased permeability, following activation of leukocytes by CPB and subsequent pulmonary sequestration, rather than increased filtration through pressure factors. It may contribute to impaired gas exchange, even in the absence of manifest alveolar edema of the lungs, after surgery.

Acute Disease↗

PubMed1993

Time course and variability of the endocrine and metabolic response to severe sepsis.

BACKGROUND: In trauma patients a specific pattern of the hormone endocrine response to injury has been described. Conflicting data exist regarding the hormonal changes during sepsis. We studied the time course and variability of the hormonal and metabolic responses to severe sepsis in twelve medical patients. METHODS: Hormone levels were measured every 6 hours. Urinary nitrogen and 3-methylhistidine excretion were measured daily. Indirect calorimetry was used to calculate energy production rate (EPR). RESULTS: None of the hormones measured showed a time course in individual patients. Growth hormone (1.69 +/- 0.17 ng/ml) and insulin (48 +/- 5 mU/L) values were within normal range. Cortisol value (474 +/- 44 nmol/L) was in the upper normal range. Insulin-like growth factor 1 level (12.5 +/- 5.7 nmol/L) was decreased. Nitrogen balance was negative and did not change during the study period. Neither oxygen consumption (VO2) (318 +/- 20 ml/min), carbon dioxide output (283 +/- 10 ml/min), EPR (2064 +/- 435 kcal/day), nor fuel utilization showed a time course. The variability during the study period compared with values on admission ranged from 20% (insulin-like growth factor 1) to 74% (growth hormone). The variability of calculated fuel utilization ranged from 35% (protein) to 180% (fat). The variability of VO2, carbon dioxide production, and EPR was for less, 8%. CONCLUSIONS: A specific pattern in the endocrine and metabolic responses as observed in trauma patients does not occur in medical patients with severe sepsis. Hormones and calculated fuel utilization show large variations when compared with values on admission. VO2 and EPR vary for less. Nutritional needs in patients with sepsis, therefore, can be calculated on admission and need not be recalculated during the first week after admission.

Adult↗

PubMed1993

Vasodilating prostaglandin E1 decreases critical oxygen delivery by increasing critical oxygen extraction in anesthetized pigs.

The abnormal dependence of O2 uptake (VO2) on O2 delivery (QO2) during severe sepsis, and the adult respiratory distress syndrome (ARDS) may be caused by impaired vascular reactivity, following release of vasodilating prostaglandins. Infusion of these compounds, however, may improve tissue oxygenation. We studied the effect of vasodilating prostaglandin E1 (PGE1; 0.2 microgram/kg/min) on the critical O2 extraction ratio (ERO2c) and the critical QO2 (QO2c) in a saline-controlled, crossover study in 12 barbiturate-anesthetized pigs. QO2, VO2 (independently from QO2), and blood lactate concentrations were measured during graded cardiac output reductions by incremental positive end-expiratory pressure (0-20 cm H2O PEEP, raised by 5 cm H2O at 15 min intervals). At 0 cm H2O PEEP, PGE1 decreased arterial blood pressure, mainly due to a fall in systemic vascular resistance. From 0 to 20 cm H2O PEEP, the fall in QO2 was greater in the PGE1 than in the saline series (P < 0.005), since ventricular filling and the rise in heart rate were less in the former. The decrease in VO2 (P < 0.005) did not differ between series. As estimated from bilinear regression on paired VO2/QO2 data in individual pigs, the QO2c was 9.8 +/- 3.6 (mean +/- SD) during PGE1 and 14.6 +/- 3.8 ml/kg/min during saline infusion (P = 0.008), with ERO2c 68% +/- 16% and 48% +/- 12%, respectively (P < 0.005). The QO2c, estimated from bilinear regression on paired lactate/QO2 data during the first treatment period, was 7.1 +/- 1.2 for PGE1 and 12.8 +/- 4.5 ml/kg/min for saline (P < 0.05), at similar lactate concentrations (2.0 +/- 0.5 and 1.7 +/- 0.5 mmol/liter, respectively). PGE1-induced vasodilation thus decreases QO2c, because of increased ERO2c, probably resulting from capillary recruitment, an increased surface area available for O2 exchange, and decreased O2 diffusion distances. Hence, a reduced ERO2 and abnormal supply dependence of VO2 during severe sepsis and ARDS are not caused by release of vasodilating prostaglandins. In contrast, our results partly explain improved tissue oxygenation with these compounds during abnormal VO2 supply dependence, following sepsis and ARDS.

Alprostadil↗