Biomedical subjects

R B Light

Publications and source records attributed to R B Light.

At least 37 records · Page 2Linked to original sources

PubMed1990

The effect of an increase in systemic arterial pressure in the newborn with right ventricular hypertension.

To evaluate the effect of an elevation in systemic arterial pressure upon pulmonary blood flow and arterial oxygenation during right ventricular hypertension (RVH), we acutely studied 13 1-d-old piglets. Catheters were positioned in the pulmonary artery, both atria, and the aorta for hemodynamic measurements. An electromagnetic probe was positioned in the main pulmonary artery for pulmonary blood flow measurement. Systemic and regional blood flow were measured with the radiolabeled microsphere technique. A balloon-mounted catheter was advanced in the aorta and maintained at the lower thoracic level. After induction of RVH (pulmonary artery banding), a significant decrease in arterial O2 pressure from 54.4 +/- 1.6 to 10.6 +/- 0.4 kPa (p less than 0.01), a 30% reduction in systemic arterial pressure, and a 44% decrease in pulmonary blood flow were observed. During RVH, partial inflation of the aortic balloon to restore the systemic arterial pressure to its initial value led to an increase in arterial O2 pressure to 23.5 +/- 3.1 kPa (p less than 0.01). Full inflation of the balloon further increased the arterial O2 pressure to 32.6 +/- 2.9 kPa (p less than 0.01). Aortic balloon inflation increased pulmonary blood flow in 11 and systemic O2 delivery in nine of the 13 animals. RVH was associated with a significant increase in cerebral and right ventricular myocardial free-wall blood flow and a decrease in renal and bowel blood flow and O2 delivery (p less than 0.01). Aortic balloon inflation during RVH did not change either the cerebral or myocardial free-wall blood flow, but further significantly decreased renal and bowel blood flow and O2 delivery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Early predictors of mortality for hospitalized patients suffering cardiopulmonary arrest.

Few if any prearrest or intraarrest variables have been identified as highly predictive of inhospital mortality following cardiopulmonary arrest. A total of 310 consecutive patients requiring advanced cardiac life support during the calendar years 1985 and 1986 were reviewed with respect to eight specific variables. These included age, diagnosis, location, mechanism of the event, duration of resuscitation, whether the event was witnessed or unwitnessed, the initial observed rhythm and medications administered. A total of 37.1 percent of the patients were successfully resuscitated, but only 9.7 percent survived until discharge. Factors strongly associated with inhospital mortality included unwitnessed events (p = 0.0316), the need for epinephrine (p = 0.0003), identification of electromechanical dissociation or asystole as initial rhythms (p = 0.0000), and cardiac vs respiratory mechanism of arrest (p = 0.0000).

Age Factors↗

PubMed1990

The effects of methoxamine and epinephrine on survival and regional distribution of cardiac output in dogs with prolonged ventricular fibrillation.

This study compares the effects of methoxamine, a pure alpha 1-agonist, and epinephrine on cerebral and myocardial blood flow, central hemodynamics, and survival in a randomized placebo-controlled fashion during prolonged ventricular fibrillation (VF) in a canine model. Twenty-four anesthetized and ventilated adult mongrel dogs were instrumented for regional blood flow determinations using radio-labeled microspheres. The dogs were randomized to receive either 20 mg of methoxamine as a single intravenous bolus or repeated boluses of 0.02 mg/kg of epinephrine, 0.2 mg/kg of epinephrine, or normal saline solution placebo beginning at three minutes following induction of VF and initiation of closed chest cardiac massage (CCCM). Organ blood flow measurements were determined during normal sinus rhythm and after five and 20 minutes of VF. All six dogs receiving methoxamine were successfully resuscitated in contrast to only one in each of the epinephrine-treated groups and none of the dogs receiving placebo (p less than .01). Although epinephrine was associated with significantly higher blood pressures than placebo during cardiopulmonary resuscitation (CPR), blood pressures achieved with methoxamine were significantly higher than those observed in the other three treatment groups (p less than .001). Cerebral blood flow was significantly higher with both methoxamine and high-dose epinephrine (p less than .05). Mean left and right ventricular myocardial flows were highest with methoxamine but this did not achieve statistical significance. In contrast, organ flows measured in the animals receiving the lowest dose of epinephrine were not significantly higher than those associated with placebo. Cardiac output after 20 minutes of CPR was significantly lower with high-dose epinephrine than with methoxamine or placebo (p less than .05). Our results suggest that methoxamine significantly improves regional cerebral blood flow and survival during CPR and although high-dose epinephrine is associated with comparable improvements in regional cerebral blood flow, this treatment is associated with deterioration in central hemodynamics during prolonged VF and does not enhance survival.

Animals↗

PubMed1990

Intensive care management of pneumonia in the elderly.

Arterial hypoxemia, hypercapnic respiratory failure, hypotension, and depressed level of consciousness are the usual reasons for admitting a patient with pneumonia to an intensive care unit (ICU). Once the decision has been made to manage the patient in the ICU, age has little effect on the immediate goals of therapy, which include correction of hypoxemia, maintenance of adequate alveolar ventilation, and provision of sufficient blood pressure and cardiac output to support organ function until physiological homeostasis is restored as the pneumonia is controlled by appropriate antimicrobial therapy. Age-related decreases in physiological reserve are the major reasons specifically to consider ICU management of elderly pneumonia patients. These physiological changes increase the probability of major organ system failure with the development of pneumonia, and increase the likelihood that pneumonia will require ICU management. This has implications for the clinician regarding the selection and timing of therapeutic interventions. Unfortunately, the reduction of physiological reserve and the increased prevalence of coexistent chronic disease also result in significant mortality rates for elderly patients with pneumonia, potentially limiting the benefits of intensive care in this population. This raises a second issue: When, if ever, should intensive care not be used in the management of an elderly patient with severe pneumonia? A full discussion of the ethical issues surrounding this question is beyond the scope of this article, however, good medical ethics begin with sound medical judgment and are based upon solid clinical data. Accordingly, this article will also address the implications of age and underlying disease in the assessment of prognosis and use of the ICU in patients with pneumonia.

Aged↗

PubMed1989

Plasma volume expansion and PEEP in a canine model of acute Pseudomonas pneumonia.

Four groups of anesthetized, ventilated dogs (n = 6 in each group) inoculated endotracheally with Pseudomonas aeruginosa were studied over 5 h as bilateral, hemorrhagic pneumonia developed. Groups I and II were ventilated with zero end-expiratory pressure (ZEEP) and groups III and IV with positive end-expiratory pressure (PEEP) (8 cmH2O). Hetastarch (6%) in saline was infused intravenously to maintain similar transmural pulmonary wedge pressures (Pwtm) in groups I and III (approximately 5 mmHg) and groups II and IV (approximately 10 mmHg) throughout the experiment. The effects of plasma volume expansion were analyzed by comparing groups I and III with groups II and IV and of PEEP by comparing groups I and II with groups III and IV. The number of lobes with gross consolidation was greater in groups II (4.8 +/- 1.2) and IV (5 +/- 0.9) than in groups I (2 +/- 1.1) and III (3.3 +/- 1). The mean lung wet weight/body weight ratio was greater in groups II (40 +/- 11 g/kg) and IV (48 +/- 12 g/kg) than in groups I (19 +/- 3 g/kg) and III (32 +/- 6 g/kg) and in groups III and IV than in groups I and II. Plasma volume expansion, in the absence of PEEP (group II vs. group I), dramatically increased intrapulmonary shunt (Qs/Qt 5 h after inoculation: group II, 62 +/- 13%; group I, 25 +/- 12%). However, overall gas exchange 5 h after inoculation was not significantly different between PEEP-treated groups and ZEEP-treated groups despite more extensive disease in the former. Despite maintenance of Pwtm, cardiac output fell significantly over the 5 h study period in groups III (4.3 +/- 0.7 to 3.3 +/- 1.0 L/min) and IV (7.2 +/- 1.7 to 3.8 +/- 2.4 L/min) compared to groups I (3.8 +/- 1.0 to 3.5 +/- 1.2 L/min) and II (6.9 +/- 3.2 to 7.3 +/- 2.6 L/min). We conclude that plasma volume expansion, within the normal physiological range of Pwtm, increases the extent of pneumonia. Positive end-expiratory pressure with maintenance of Pwtm also independently increases pneumonia size, possibly by increasing pulmonary capillary hydrostatic pressure, but masks this effect by maintaining arterial oxygenation through recruitment of additional lung units for gas exchange. The data also suggest that PEEP adversely affects cardiac performance in this model of acute pneumonia.

Acute Disease↗

PubMed1989

Effect of increased afterload on right ventricular function in newborn pigs.

The effect of a progressive increase in right ventricular (RV) afterload was studied in pigs less than 24 h (group I) and 3-5 days old (group III). RV load was applied to increase mean pulmonary arterial pressure (Ppa) until right to left shunt was observed. Initially, pigs in group I had a significantly lower systemic arterial pressure (Psa = 63 +/- 2 vs. 82 +/- 5 mmHg) and higher Ppa (30 +/- 1 vs. 23 +/- 2 mmHg) even though the RV stroke work (RVSW) was similar (54.3 +/- 10.8 vs. 32.4 +/- 2.1 mmHg/ml) to group II. After a progressive rise in afterload, pigs in group I could maintain a higher RV stroke volume than those in group II (1.3 +/- 0.3 vs. 0.4 +/- 0.1 ml; P less than 0.05). At shunt condition, the RVSW was increased by 21 +/- 14% of the initial value in group I vs. a 32 +/- 8% decrease in group II (P less than 0.05). The ductus arteriosus was constricted and right-to-left shunt was observed in all animals at the foramen ovale level even though Ppa exceeded Psa before the rise in the right atrial pressure in group I. Thus, as RV afterload is increased in the pig, the older animals' right ventricle is progressively less capable of maintaining pulmonary blood flow than animals within 24 h of birth.

Animals↗

PubMed1989

Central hemodynamic and regional blood flow changes in the newborn with right ventricular hypertension.

To evaluate the central hemodynamic and regional blood flow changes associated with right ventricular hypertension in the newborn, 13 anesthetized, mechanically ventilated piglets less than 3 d old were acutely instrumented to permit measurements of central vascular pressures, cardiac output, and regional blood flow (radio-labeled microsphere technique). After initial measurements, right ventricular afterload was progressively increased by means of a pulmonary arterial mechanical occluder until right-to-left foramen ovale shunt was observed. An increase in pulmonary arterial pressure from 32 +/- 2 to 55 +/- 3 mm Hg was associated with a decrease in PaO2 from 364 +/- 16 to 88 +/- 9 mm Hg and an increase in the shunt fraction from 13 +/- 1 to 28 +/- 1% (p less than 0.01) during ventilation with oxygen. Right ventricular hypertension induced a significant decrease in systemic arterial pressure from 79 +/- 3 to 63 +/- 4 mm Hg, and left ventricular cardiac output from 156 +/- 10 to 112 +/- 11 mL.min-1.kg-1 (p less than 0.01), likely secondary to a reduction in left ventricular compliance. Oxygen delivery to the brain and heart were unaffected, due to a substantial increase in regional blood flow, but a significant reduction in delivery to the bowel and kidneys were observed. Contrary to what has been reported in the adult, myocardial blood flow to the right ventricle increased during hypertension. Metabolic acidosis was seen in all animals and the changes in serum bicarbonate and whole body oxygen consumption were directly related to the magnitude of decline in systemic O2 delivery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Effects of prolonged naloxone infusion in septic shock.

Fourteen patients suffering sixteen episodes of septic shock requiring inotrope and/or vasopressor support were randomised to receive a 30 micrograms/kg naloxone intravenous bolus followed by a 30 micrograms/kg/h infusion or an equivalent volume placebo bolus and infusion for 8-16 h in a double-blind study. pH and pulmonary wedge pressure were kept constant, and inotrope and/or vasopressor were titrated to maintain a preselected mean blood pressure. Inotrope/vasopressor requirements in the naloxone-treated group were significantly lower than those in the control group at 8 h (eight patients in each group, p less than 0.005) and at 16 h (five patients in each group, p less than 0.02). Late but significant improvements in stroke volume (p less than 0.02) and heart rate (p less than 0.05) were also noted in the eight naloxone-treated patients.

Adult↗

PubMed1988

The pulmonary vascular effects of dopamine, dobutamine, and isoproterenol in unilobar pulmonary edema in dogs.

Although catecholamine inotropic drugs are often used to support the circulation of critically ill patients with hypoxemic respiratory failure, their effect on the pulmonary circulation and on gas exchange is incompletely understood. In order to improve our understanding of the effects of these drugs on the pulmonary circulation, we made measurements of total and regional intrapulmonary shunt (Qs/Qt), distribution of pulmonary blood flow, and pulmonary hemodynamics before and after infusions of dopamine (n = 6, 5 micrograms/kg/min), dobutamine (n = 6, 10 micrograms/kg/min), isoproterenol (n = 6, 0.1 micrograms/kg/min), or saline in dogs with unilobar oleic acid-induced pulmonary edema. In addition to permitting determination of the overall hemodynamic and gas exchange effects of these drugs, this preparation allowed measurement of changes in distribution of pulmonary blood flow between normal and edematous lung. In 6 dogs given dobutamine, mean cardiac output (CO) increased by 1 liter/min, while pulmonary arterial pressure (PPA) increased by 2 mm Hg with no change in pulmonary vascular resistance (PVR) or distribution of pulmonary blood flow. There was a 5% increase in mean Qs/Qt which, because of the lack of evidence of pulmonary vasoactivity, was attributed to time or to increased CO. Isoproterenol produced a similar increase in CO, but reduced PPA and PVR indicating pulmonary vasodilator activity. Pulmonary vasodilation was most prominent in edematous lung, resulting in an increase in relative blood flow to the edema lung lobe and a substantial increase in Qs/Qt, exceeding the increase in all other groups. Dopamine, similarly increasing CO, did not change overall PVR but reduced fractional blood flow to the edema lobe by 3.4% of CO. Neither Qs/Qt nor PaO2 changed significantly in this group. The differing effects of these agents on pulmonary hemodynamics, intrapulmonary blood flow distribution, and gas exchange have potentially significant implications affecting the choice of drug used for circulatory support in hypoxemic respiratory failure.

Animals↗

PubMed1988

Intrapulmonary oxygen consumption in experimental pneumococcal pneumonia.

To test the hypothesis that lung affected by acute bacterial pneumonia consumes significant amounts of O2, whole-body O2 consumption (VO2) was measured simultaneously by collection of expired gas (VO2exp) and by the Fick principle (VO2Fick) in five dogs with acute experimental pneumococcal pneumonia and in five uninfected controls. This approach is based on the premise that VO2Fick will not detect lung VO2, whereas the expired gas measurement represents the true whole-body VO2, including the lung. In controls VO2 exp averaged 110 +/- 20 ml/min (4.78 +/- 0.78 ml.min-1.kg-1), and VO2Fick was nearly identical at 114 +/- 21 ml/min (4.96 +/- 0.79 ml.min-1.kg-1). The VO2Fick in the pneumonia group was 127 ml/min, similar to both control group values when indexed for body weight (4.91 +/- 1.17 ml.min-1.kg-1). VO2exp, however, was 146 +/- 46 ml/min (5.74 +/- 1.57 ml.min-1.kg-1), exceeding VO2Fick by an average of 20 +/- 9 ml/min (P less than 0.01). This between-method difference of 20 +/- 9 ml/min (or 24 ml/min if the difference in the control group is assumed to apply to the pneumonia group) amounted to 13-15% of whole-body VO2 and can be attributed to VO2 in the lung, presumably by cells involved in the acute inflammatory response. Implications include the potential for significant underestimate of whole-body VO2 by the Fick method when used in the presence of lung inflammation and overestimate of blood flow to shunting or low ventilation-perfusion ratio lung units by the O2 method of measuring venous admixture-like perfusion. This observation may also explain the disproportionate hypoxemia sometimes seen in patients with severe pneumonia.

Animals↗

PubMed1988

Effect of alveolar hypoxia on pulmonary fluid filtration in in situ dog lungs.

We have studied the effect of alveolar hypoxia on fluid filtration characteristics of the pulmonary microcirculation in an in situ left upper lobe preparation with near static flow conditions (20 ml/min). In six dogs (group 1), rate of edema formation (delta W/delta t, where W is weight and t is time) was assessed over a wide range of vascular pressures under two inspired O2 fraction (FIO2) conditions (0.95 and 0.0 with 5% CO2-balance N2 in both cases). delta W/delta t was plotted against vascular pressure, and the best-fit linear regression was obtained. There was no significant difference (paired t test) in either threshold pressure for edema formation [18.3 +/- 1.8 and 17.1 +/- 1.2 (SE) mmHg, respectively] or the slopes (0.067 +/- 0.008 and 0.073 +/- 0.017 g.min-1. mmHg-1.100g-1, respectively). In another seven dogs (group 2), delta W/delta t was obtained at a constant vascular pressure of 40 mmHg under four FIO2 conditions (0.95, 0.21, 0.05, and 0.0, with 5% CO2-balance N2). Delta W/delta t for the four conditions averaged 0.60 +/- 0.11, 0.61 +/- 0.11, 0.61 +/- 0.10, and 0.61 +/- 0.10 (SE) g.min-1.mmHg-1.100g-1, respectively. No significant differences (ANOVA for repeated measures) were noted. We conclude that alveolar hypoxia does not alter the threshold for edema formation or delta W/delta t at a given microvascular pressure.

Animals↗

PubMed1988

Role of prostacyclin and thromboxane in the circulatory changes of acute bacteremic Pseudomonas pneumonia in dogs.

We investigated the role of prostacyclin (PGI2) and thromboxane A2 (TxA2), as evidenced by changes in their stable metabolites, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2), in the pathophysiology of acute bacteremic gram-negative pneumonia. Three groups of dogs were inoculated endotracheally: Group I (n = 5) with sterile broth, and Groups II (n = 5) and III (n = 10) with Pseudomonas aeruginosa. Gas exchange, hemodynamics, and plasma prostaglandins were measured before inoculation and hourly thereafter for 5 h in Groups I and II but only once in Group III, 5 h after inoculation. All animals were then killed, and the extent of pneumonia was assessed by lung wet weight and measurement of the percentage of cardiac output (CO) perfusing pneumonic lung using radionuclide-labeled microspheres. None of these measurements changed significantly in Group I, but all dogs in Groups II and III developed severe pneumonia. In Group II, mean arterial oxygen tension fell from 575 +/- 17 to 237 +/- 59 mm Hg (FIO2 = 1.0), with an increase in pulmonary shunt from 6 +/- 2% to 24 +/- 6%. Although TxB2 levels did not change, plasma 6-keto-PGF1 alpha rose progressively as pneumonia developed from baseline levels (less than 100 pg/ml) to a peak level of 890 +/- 114 pg/ml 5 h after inoculation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1988

Hyperventilation in the newborn piglet does not increase whole body oxygen consumption as seen in mature animals.

Hyperventilation has been shown to cause increased whole body oxygen consumption (VO2) and lactic acid production in human and animal mature subjects, but limited data are available in neonates. We investigated the effect of hypocarbic and normocarbic hyperventilation during normoxia and hypoxia (fractional inspired oxygen concentration = 0.14) upon the VO2 in anesthetized and paralyzed piglets. Systemic arterial, pulmonary arterial, and left and right atrial pressures as well as cardiac output and body temperature were continuously recorded. Hypocarbic hyperventilation (PaCO2 = 19 +/- 1 mm Hg; pH = 7.58 +/- 0.02) was associated with a significant decrease in systemic and pulmonary arterial pressures and cardiac output. These measurements returned to values similar to the initial normoventilation ones when PaCO2 was increased by adding CO2 to the inspired gas, whereas hyperventilation was continued. Neither hyperventilation alone nor in combination with hypoxia induced any significant change in VO2. We conclude that in the newborn pig, unlike what has been reported in mature subjects, cellular metabolic function is unaffected by hyperventilation as evidenced by the unchanged VO2.

Animals↗

PubMed1987

Effect of indomethacin on arterial oxygenation in critically ill patients with severe bacterial pneumonia.

The effect of indomethacin (1 mg/kg) on gas exchange was studied in ten patients with hypoxaemic respiratory failure precipitated by bacterial pneumonia. Mean arterial oxygen tension (PaO2) improved significantly (79 +/- 16 mm Hg to 98 +/- 20 mm Hg) but the response varied between patients: five showed substantial responses (27-42 mm Hg), three lesser responses (7-9 mm Hg), and two no response. Similar changes were found in the alveolar-arterial oxygen gradient and the ratio of PaO2 to fractional inspired oxygen concentration. In two responders studied further, PaO2 had fallen to baseline values 4-6 h later and a repeat indomethacin challenge again increased PaO2 by greater than 25 mm Hg with concomitant changes in pulmonary shunt. There were no significant changes in the other gas-exchange or haemodynamic variables measured and there was no clear reason for the variability in response to indomethacin. These results suggest a role for products of the cyclo-oxygenase pathway of arachidonic acid metabolism in the pathogenesis of hypoxaemia in patients with severe bacterial pneumonia.

Acute Disease↗

PubMed1987

Lung mechanics, gas exchange, pulmonary perfusion, and hemodynamics in a canine model of acute Pseudomonas pneumonia.

Acute bilateral hemorrhagic pneumonia was induced in 6 dogs (pneumonia group) by endotracheal inoculation with Pseudomonas aeruginosa. Measurements of lung mechanics, gas exchange, distribution of pulmonary blood flow, and hemodynamics were made prior to inoculation and 5 hr later when pneumonia was established. These findings were compared to the same measurements in 6 other dogs inoculated with a sterile broth (control group). While there were no significant changes in lung mechanics in the control group, pneumonia caused a significant and proportional reduction (42%) in total lung capacity (TLC) and functional residual capacity (FRC). Although tidal lung compliance was reduced in the pneumonia group, neither the specific compliance nor the deflation pressure-volume curve, with lung volume expressed as a percentage of observed TLC, changed significantly. Pneumonia caused marked hypoxemia with a mean increase in shunt and venous admixture of 35% and 52%, respectively, while the control group developed only minimal abnormalities in gas exchange. Perfusion of the consolidated lung region, determined by radioactive microspheres and expressed as a percentage of total pulmonary blood flow, showed a small but significant decrease from baseline (53 +/- 13%) to established pneumonia (44 +/- 14%), while no change in lobar perfusion was seen in the control group. Only the infected animals showed significant changes in hemodynamics with a rise in cardiac output and fall in mean systemic arterial pressure and vascular resistance. We conclude that acute experimental Pseudomonas pneumonia causes reduction of FRC by filling of alveoli with inflammatory exudate and further reduction of TLC by preventing these alveoli from inflating at higher lung volumes without evidence for a change in the elastic properties of the remaining inflated lung; marked hypoxemia caused by maintenance of perfusion of consolidated lung with reduced or absent ventilation; and a hyperdynamic septic hemodynamic state similar to that seen in humans.

Animals↗

PubMed1987

Effect of cyclooxygenase blockade on gas exchange and hemodynamics in Pseudomonas pneumonia.

Acute bilateral Pseudomonas aeruginosa pneumonia was induced in 10 anesthetized dogs, after which five dogs received intravenous indomethacin (2 mg/kg) (indomethacin group), whereas five others were infused with saline (2 ml/kg) (control group). Plasma levels of 6-ketoprostaglandin F1 alpha(6-keto-PGF1 alpha) and thromboxane B2 (TxB2), stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TxA2), respectively, were measured by radioimmunoassay. Although TxB2 levels were not different before and after inoculation in either group, 6-keto-PGF1 alpha levels increased from their base-line value in each animal as pneumonia developed (indomethacin group: less than 100 to 330 +/- 90 pg/ml; control group: less than 100 to 630 +/- 300 pg/ml). Both prostaglandins fell to less than 100 pg/ml in each dog after indomethacin infusion, whereas they remained elevated in the control group after infusion of normal saline. Perfusion of consolidated lung regions (Qp/QT), measured with radioactive microspheres and expressed as a percent of total pulmonary blood flow, was dramatically reduced after indomethacin (35 +/- 3 to 16 +/- 1%) with consequent improvement in pulmonary shunt (Qs/QT: 30 +/- 8 to 18 +/- 6%) and arterial O2 tension (PaO2: 123 +/- 25 to 274 +/- 77 Torr). These parameters remained unchanged or deteriorated further in the control group after infusion of saline. Three additional dogs with Pseudomonas pneumonia were studied in which the indomethacin-induced reduction in Qp/QT was substantially but not completely reversed by intravenous infusion of PGI2.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1987

Perfluorochemical artificial blood as a volume expander in hypoxemic respiratory failure in dogs.

The perfluorochemical O2-transport fluid, Fluosol-DA 20 percent (PFC), is being clinically evaluated as a volume expander in patients who are unable to receive blood products. Since patients treated with Fluosol-DA may be at risk of developing adult respiratory distress syndrome (ARDS) as a complication of the original disorder for which they were transfused, we examined central hemodynamics and gas exchange in anesthetized O2-ventilated dogs with oleic-acid induced pulmonary edema before and after transfusion with 400 ml of either PFC (n = 5) or whole blood (n = 5). Transfusion produced similar increases in cardiac output, pulmonary and systemic vascular pressures and intrapulmonary shunt in the two groups. Arterial O2 tension, however, fell from 209 +/- 117 to 172 +/- 81 mmHg in the blood transfused group but increased from 219 +/- 145 to 302 +/- 138 mmHg in the PFC group. Arterial O2 content, on the other hand, increased in the blood transfused group due to an increase in hematocrit, but fell with PFC because of hemodilution. This lower total arterial O2 content in the PFC group was, however, compensated for by more efficient O2 transport by the PFC in that the PFC arteriovenous O2 content difference accounted for 26 percent of the total arteriovenous O2 content difference, making it about four times as efficient as hemoglobin in tissue O2 delivery. Fluosol DA, 20 percent, is an effective volume expander in this model of hypoxemic respiratory failure, and it can transport significant amounts of O2 even in the presence of a substantial intrapulmonary shunt.

Animals↗

PubMed1986

Indomethacin and acetylsalicylic acid reduce intrapulmonary shunt in experimental pneumococcal pneumonia.

Arterial hypoxemia in acute experimental pneumococcal pneumonia is caused primarily by persistence of pulmonary blood flow to lung regions consolidated by pneumonia, which results in an intrapulmonary shunt. In order to test the hypothesis that in acute pneumonia indomethacin or acetylsalicylic acid (ASA) would improve gas exchange, as has been observed in some other disease models, 15 pentobarbital-anesthetized dogs with acute lobar pneumonia caused by Streptococcus pneumoniae type 3 were studied. After baseline measurements of pulmonary gas exchange, central hemodynamics and radionuclide-labeled microsphere determination of regional distribution of pulmonary blood flow, the dogs were randomly assigned to receive an intravenous infusion of indomethacin (2 mg/kg, n = 5), ASA, (100 mg/kg, n = 5) or a saline infusion (control, n = 5). All measurements were then repeated 30 and 60 min after infusion. Although there were no significant changes in the control group, PaO2 during O2 ventilation increased from a mean +/- SD value of 104 +/- 46 mmHg at baseline to 180 +/- 73 mmHg after ASA and from 262 +/- 173 to 361 +/- 134 mmHg after indomethacin. These improvements in PaO2 were associated with a decrease in shunt from 0.38 +/- 0.12 to 0.23 +/- 0.03 with ASA and from 0.29 +/- 0.21 to 0.21 +/- 0.08 with indomethacin. The reduction in shunt in both treatment groups was attributable to a fall in the fraction of the pulmonary blood flow perfusing the consolidated lung regions, from 33 +/- 8 to 21 +/- 5% after ASA and from 33 +/- 12 to 22 +/- 9% after indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗