Cardiorespiratory and cellular changes with interleukin 2 infusion in sheep

1989 ◽  
Vol 66 (1) ◽  
pp. 128-134 ◽  
Author(s):  
F. L. Glauser ◽  
D. E. Bechard ◽  
G. G. DeBlois ◽  
A. A. Fowler ◽  
R. E. Merchant ◽  
...  
Keyword(s):  
Interleukin 2 ◽  
Blood Gases ◽  
Base Line ◽  
Duration Of Treatment ◽  
Protein Ratio ◽  
Arterial Blood ◽  
Cellular Changes ◽  
Recombinant Interleukin 2 ◽  
Arterial Po2 ◽  
Lung Lymph

Recombinant interleukin 2 (rIL-2) administration, a new form of therapy for patients with far-advanced cancer, is associated with a "third space" syndrome, i.e., pulmonary edema, respiratory distress, and hypoxemia, which limits the dose and duration of treatment. To extend our knowledge regarding this toxicity, we established a sheep chronic lung lymph fistula model and measured hemodynamics, arterial blood gases, caudal mediastinal (lung) lymph flow (QL), and blood and lung lymph cellular changes before, during, and after (recovery) a 3-day continuous rIL-2 infusion (9 x 10(5) U/kg). Moderate systemic hypotension, mild pulmonary hypertension, and an increase in alveolar-arterial PO2 gradient was present on day 3 of rIL-2 infusion. QL increased from a base line of 1.9 +/- 0.2 to a maximum of 4.3 +/- 1.1 ml/15 min on day 3 of rIL-2 infusion. At no time was there a change in lymph-to-plasma protein ratio. The leukocyte count increased significantly to 16.1 +/- 4.5 x 10(3) cells/mm3 at recovery day 1. The percentage of blood lymphocytes decreased significantly by day 1 of rIL-2 infusion, returned to base-line levels on day 3, and significantly increased on day 2 of recovery. Lung lymph lymphocytes decreased significantly on days 1 and 2 of rIL-2 infusion. There was a shift in their size; i.e., their area increased from 32 +/- 7 to 57 +/- 19 micron 2 (P less than 0.05) by day 2 of rIL-2 infusion. By day 1 of recovery, lung lymph lymphocyte counts increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilation-perfusion relationships during induced normovolemic polycythemia in dogs

1988 ◽  
Vol 65 (4) ◽  
pp. 1686-1692 ◽  
Author(s):  
A. A. Balgos ◽  
D. C. Willford ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Base Line ◽  
Slight Improvement ◽  
Arterial Blood ◽  
The Mean ◽  
Arterial Po2

Previous studies on normal subjects and patients with polycythemia have given conflicting results of the effect of polycythemia on pulmonary gas exchange. We studied acutely induced normovolemic polycythemia in the dog and measured arterial blood gases and ventilation-perfusion (VA/Q) relationships using the multiple inert gas elimination technique. The mean base-line hematocrit of 43 +/- 5% was increased to 57 +/- 4 and 68 +/- 8%, respectively, after two exchange transfusions of packed erythrocytes. Subsequent plasma exchange transfusions returned the mean hematocrit to 44 +/- 4%. Polycythemia caused no significant arterial hypoxemia; indeed there was a slight improvement in the alveolar-arterial PO2 difference. The multiple inert gas elimination measurements showed no increase in VA/Q inhomogeneity with no increase in log SD ventilation (V) or log SD blood flow (Q). There was a shift of mean V and mean Q to high VA/Q areas because of a decrease in cardiac output, presumably caused by increased blood viscosity. This study showed no deleterious effects on pulmonary gas exchange within the hematocrit range of 36-76%.

Pulmonary microvascular response to hemorrhagic shock, resuscitation, and recovery

1979 ◽  
Vol 46 (3) ◽  
pp. 498-503 ◽  
Author(s):  
R. H. Demling ◽  
G. Niehaus ◽  
J. A. Will
Keyword(s):  
Hemorrhagic Shock ◽  
Plasma Protein ◽  
Recovery Period ◽  
Blood Gases ◽  
Lymph Flow ◽  
Base Line ◽  
Protein Ratio ◽  
Fluid Filtration ◽  
Lung Lymph ◽  
Protein Permeability

We studied the effect of hemorrhagic shock, resuscitation, and recovery on the pulmonary microcirculation. We used lung lymph flow (QL) and lymph-to-plasma protein ratio as sensitive indices of transvascular fluid filtration rate and protein permeability. We measured pulmonary vascular pressures, cardiac output, blood gases, lymph flow, and lymph and plasma proteins before and during a 2-h period of shock, a 3-h period of resuscitation, and a 72-h period of recovery, in nine unanesthetized sheep with chronic lung lymph fistula. We found a 30% decrease in QL during early shock as animals were bled into bags containing an acetate citrate dextrose solution until aortic pressure was 50 Torr. QL gradually increased to or exceeded base line in five of nine animals during late shock as pulmonary vascula resistance increased by 250%. During the 3-h resuscitation period, mean QL increased by 110%, with the lymph-to-plasma protein ratio being significantly decreased, indicating no protein permeability change. In five of nine studies, lymph became visible bloody. The increased QL and lymph RBCs were felt to be secondary to an elevation in microvascular pressure. During the recovery period, pressures and QL returned to base line.

Naloxone alters the early response to an inspiratory flow-resistive load

1989 ◽  
Vol 67 (5) ◽  
pp. 1747-1753 ◽  
Author(s):  
A. T. Scardella ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Tidal Volume ◽  
Blood Gases ◽  
Inspiratory Flow ◽  
Abdominal Muscles ◽  
Base Line ◽  
Resistive Load ◽  
Endogenous Opioid ◽  
Transdiaphragmatic Pressure ◽  
Arterial Blood ◽  
Gastric Pressure

In a previous study in unanesthetized goats, we demonstrated that cerebrospinal fluid levels of beta-endorphin were significantly elevated after 2.5 h of inspiratory flow-resistive loading. Naloxone (NLX) (0.1 mg/kg) administration partially and transiently reversed the tidal volume depression seen during loading. In the current study, we tested the hypothesis that endogenous opioid elaboration results in depression of respiratory output to the diaphragm. In six studies of five unanesthetized goats, tidal volume (VT), transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi), and arterial blood gases were monitored. A continuous NLX (0.1 mg/kg) or saline (SAL) infusion was begun 5 min before an inspiratory flow-resistive load of 120 cmH2O.l-1.s was imposed. Our data show that the depression of VT induced by the load was prevented by NLX as early as 15 min and persisted for 2 h. At 2 h, Pdi was still 294 +/- 45% of the base-line value compared with 217 +/- 35% during SAL. There was no difference in EMGdi between the groups at any time. However, the augmentation of Pdi was associated with a greater increase in end-expiratory gastric pressure in the NLX group. We conclude that the reduction in VT and Pdi associated with endogenous opioid elaboration is not mediated by a decrease in neural output to the diaphragm, but it appears to be the result of a decrease in respiratory output to the abdominal muscles.

Hemodilution causes size-dependent constriction of pial arterioles in the cat

1989 ◽  
Vol 257 (3) ◽  
pp. H912-H917 ◽  
Author(s):  
M. L. Hudak ◽  
M. D. Jones ◽  
A. S. Popel ◽  
R. C. Koehler ◽  
R. J. Traystman ◽  
...  
Keyword(s):  
Blood Gases ◽  
Base Line ◽  
Isovolemic Hemodilution ◽  
Size Dependent ◽  
Cranial Window ◽  
Arterial Blood ◽  
Equal Importance ◽  
Pial Arterioles ◽  
Cerebral Arterioles ◽  
Cerebral Vasodilation

Cerebral blood flow (CBF) rises as hematocrit (Hct) falls. We previously attributed this rise in CBF to two independent factors of equal importance, decreased arterial O2 content and decreased blood viscosity. We hypothesized that decreased arterial O2 content would dilate cerebral arterioles and that the magnitude of the vasodilation would depend on the magnitude of the passive fall in vascular resistance attributable to decreased viscosity. The present study was designed to test the hypothesis that anemia is accompanied by cerebral vasodilation. Using a closed cranial window, we measured the diameters of 42 pial arterioles (35-305 microns) in 7 cats as serial isovolemic hemodilution lowered Hct by 44% from 31 +/- 4 to 17 +/- 3%. Hemodilution increased CBF (microsphere technique) but did not change mean arterial blood pressure or arterial blood gases. Anticipated vasodilation did not occur; instead, pial arterioles constricted as Hct fell. Maximum vasoconstriction was observed when Hct reached 65-70% of the initial value. Vasoconstriction lessened as Hct was lowered further, but arteriolar diameters at the lowest Hcts remained less than base-line levels. Constriction was greater in small (less than 100 microns) than in large (greater than or equal to 100 microns) arterioles. The initial constriction of pial arterioles may represent myogenic vasoconstriction in response to flow-induced vasodilation of more proximal portions of the cerebrovascular bed and/or to washout of an endogenous vasodilator. Arteriolar relaxation with more profound hemodilution may reflect superimposed metabolic vasodilation.

Furosemide in the Intraoperative Reduction of Intracranial Pressure in the Patient with Subarachnoid Hemorrhage

Neurosurgery ◽  
1982 ◽  
Vol 10 (2) ◽  
pp. 167-169 ◽  
Author(s):  
Duke Samson ◽  
Chester W. Beyer
Keyword(s):  
Mean Arterial Pressure ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Blood Gases ◽  
Base Line ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Ruptured Intracranial Aneurysm ◽  
Intracranial Lesions ◽  
Sequential Measurements

Abstract The effect of furosemide in the intraoperative reduction of intracranial pressure was measured in 25 patients undergoing the operative repair of a ruptured intracranial aneurysm. Seven patients with similar intracranial lesions served as controls. A single bolus of 80 mg of furosemide was administered intravenously after the induction of anesthesia, and sequential measurements were made of intracranial pressure, mean arterial pressure, and arterial blood gases. A mean decrease of intracranial pressure of 56% was measured in the furosemide-treated patients, whereas the control patients demonstrated a mean decline of subarachnoid pressures of 18%. These changes are significant at the P < 0.005 confidence level, whereas changes in mean arterial pressure, mean arterial pCO2, and base line arterial pCO2 were statistically insignificant. This study suggests that intravenous furosemide is a quick, dependable, and effective mechanism for the intraoperative reduction of intracranial pressure in the postsubarachnoid hemorrhage aneurysm patient.

Granulocytes mediate the increase in pulmonary vascular permeability after thrombin embolism

1983 ◽  
Vol 54 (6) ◽  
pp. 1489-1495 ◽  
Author(s):  
M. V. Tahamont ◽  
A. B. Malik
Keyword(s):  
Vascular Permeability ◽  
Control Group ◽  
Base Line ◽  
Protein Ratio ◽  
Pulmonary Vascular Permeability ◽  
Pulmonary Capillary ◽  
Cellular Factors ◽  
Pulmonary Embolization ◽  
Lung Lymph

We examined the effect of pulmonary embolization with microthrombi on the lung vascular permeability to proteins and the role of platelets and granulocytes as putative cellular factors in mediating the alterations in permeability. Anesthetized artificially ventilated sheep were prepared with lung lymph fistulas. Pulmonary embolization was induced using thrombin. Pulmonary vascular resistance (PVR) was increased approximately threefold from baseline. Pulmonary lymph flow (Qlym) increased 2 h after thrombin, but the lymph-to-plasma protein ratio (L/P) did not change significantly from base line. Raising the pulmonary capillary pressure (Pc) by inflating a left atrial balloon produced a large increase in Qlym but no change in L/P, indicating a permeability-increasing effect of thrombin. Reduction of platelet count with antiplatelet serum before thrombin also produced an increase in Qlym without a change in L/P. Raising Pc in this group resulted in changes comparable with those in the control group, i.e., increased Qlym without a change in L/P. In contrast to both control and platelet-depleted groups, reduction of the granulocyte count with hydroxyurea did not affect Qlym or L/P after thrombin. Raising Pc in this group increased Qlym but decreased L/P, indicating normal capillary sieving of proteins. Therefore embolization of pulmonary vessels with microthrombi increases pulmonary vascular permeability, and the increase is mediated by granulocytes.

Effect of a single air dive on pulmonary diffusing capacity in professional divers

1993 ◽  
Vol 74 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Z. Dujic ◽  
D. Eterovic ◽  
P. Denoble ◽  
G. Krstacic ◽  
J. Tocilj ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Time Course ◽  
Blood Gases ◽  
Diffusing Capacity ◽  
Pulmonary Diffusing Capacity ◽  
Sequence Of Events ◽  
Arterial Blood ◽  
Bubble Detection ◽  
Venous Gas Embolism ◽  
Arterial Po2

The aim of this study was to determine whether venous gas embolism after a single air dive, evaluated using precordial Doppler monitoring, was associated with alterations in spirometry, lung volumes, arterial blood gases, or pulmonary diffusing capacity for carbon monoxide (DLCO). Postdive time course monitoring of pulmonary function was undertaken in 10 professional divers exposed to absolute air pressure of 5.5 bar for 25 min in a dry walk-in chamber. The US Navy decompression table was followed. Venous bubbles were detected by precordial Doppler monitoring. Two types of decompression were used: air and 100% O2 applied for 21 min during decompression stops. Spirometry, flow-volume, and body plethysmography parameters were unchanged after the dive with air decompression (AD) as well as with O2 decompression (OD). A significant reduction in arterial PO2, on average 20 Torr, was found after the dive with AD. DLCO was decreased in all divers 20, 40, 60, and 80 min after diving with AD (P < 0.001), whereas it was not significantly decreased after diving with OD. Maximal DLCO decrease of approximately 15% occurred 20 min postdive. In AD diving, maximum bubble grade for each individual vs. maximum DLCO reduction correlated significantly (r = 0.85, P = 0.002), as well as DLCO vs. arterial PO2 (r = 0.64, P = 0.017). In conclusion, a reduction in pulmonary diffusing capacity is observed in parallel with the appearance of venous bubbles detected by precordial Doppler. We suggest that bubbles cause pulmonary microembolization, triggering a complex sequence of events that remains to be resolved. Measuring DLCO complements Doppler bubble detection in postdiving assessment of pulmonary function.

Role of barometric pressure in pulmonary fluid balance and oxygen transport

1988 ◽  
Vol 64 (1) ◽  
pp. 419-428 ◽  
Author(s):  
B. D. Levine ◽  
K. Kubo ◽  
T. Kobayashi ◽  
M. Fukushima ◽  
T. Shibamoto ◽  
...  
Keyword(s):  
Hypobaric Hypoxia ◽  
Barometric Pressure ◽  
Significant Rise ◽  
Lymph Flow ◽  
Base Line ◽  
Protein Ratio ◽  
Hypoxic Conditions ◽  
Normal Atmospheric Pressure ◽  
Lung Lymph

To examine the role of barometric pressure in high-altitude pulmonary edema, we randomly exposed five unanesthetized chronically instrumented sheep with lung lymph fistulas in a decompression chamber to each of three separate conditions: hypobaric hypoxia, normobaric hypoxia, and normoxic hypobaria. A combination of slow decompression and/or simultaneous adjustment of inspired PO2 provided three successive stages of simulated altitudes of 2,600, 4,600, and 6,600 m during which hemodynamics and lymph flow were monitored. Under both hypoxic conditions we noted significant and equivalent elevations in pulmonary arterial pressure (Ppa), cardiac output, and heart rate, with left atrial and systemic pressures remaining fairly constant. Normoxic hypobaria was also accompanied by a smaller but significant rise in Ppa. Lymph flow increased to a highly significant maximum of 73% above base line, accompanied by a slight but significant decrease in lung lymph-to-plasma protein ratio, only under conditions of combined hypobaric hypoxia but not under equivalent degrees of alveolar hypoxia or hypobaria alone. Arterial hypoxemia was noted under all three conditions, with arterial PO2 being uniformly lower under hypobaric conditions than when identical amounts of inspired PO2 were delivered at normal atmospheric pressure. We therefore hypothesize that alveolar pressure significantly alters the Starling forces governing transcapillary fluid flux in the lung and may affect the alveolar-arterial gradient for O2 as well.

Effects of increased ventilation on lung lymph flow in unanesthetized sheep

1986 ◽  
Vol 60 (6) ◽  
pp. 2063-2070 ◽  
Author(s):  
S. M. Albelda ◽  
J. H. Hansen-Flaschen ◽  
P. N. Lanken ◽  
A. P. Fishman
Keyword(s):  
Cardiac Output ◽  
Dead Space ◽  
Total Protein ◽  
Minute Ventilation ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Base Line ◽  
Arterial Blood ◽  
Lung Lymph ◽  
Lung Lymph Flow

To determine the effect of an increase in spontaneous minute ventilation on lung fluid balance, we added external dead space to the breathing circuit of six tracheostomized, unanesthetized, spontaneously breathing sheep in which lung lymph fistulas had been created surgically. The addition of 120–180 ml of dead space caused minute ventilation to increase by 50–100% (secondary to increases in both tidal volume and frequency), without changing pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac output, or arterial blood gas tensions. The increase in spontaneous ventilation was associated with an average increase of 27% in lung lymph flow (P less than 0.05) and an average reduction of 11% in the lymph-to-plasma concentration ratio (L/P) for total protein (P less than 0.05). Lymph flow and L/P for total protein approached stable values after 2–3 h of hyperpnea, and the increase in lymph flow persisted for at least 18 h of dead-space breathing. Removal of dead space was associated with a rapid return (within 45 min) of lymph flow to base-line levels. These results suggest that hyperpnea increases the pulmonary transvascular filtration rate. Since no changes in vascular pressures or cardiac output were observed, this increase in transvascular filtration is most likely due to a fall in interstitial fluid pressure.

Chest Physiotherapy in the Neonate: A Controlled Study

PEDIATRICS ◽  
1978 ◽  
Vol 61 (2) ◽  
pp. 282-285 ◽  
Author(s):  
N. N. Finer ◽  
J. Boyd
Keyword(s):  
Respiratory Distress ◽  
Blood Gases ◽  
Chest Physiotherapy ◽  
Significant Alteration ◽  
Controlled Study ◽  
Arterial Blood Gases ◽  
Gradual Improvement ◽  
Arterial Blood ◽  
Postural Drainage ◽  
Arterial Po2

The effect of postural drainage alone was compared to postural drainage with chest percussions on the arterial blood gases of 20 neonates with respiratory distress. There was no significant alteration in the arterial PO2 following postural drainage alone, with a significant increase (14.5 mm Hg) following postural drainage with chest percussions. The PO2 midway through postural drainage with percussions showed a small (5 mm Hg) but nonsignificant rise in the PO2, suggesting a gradual improvement throughout the use of this form of therapy. There was no significant change in the pH or PCO2 with either procedure. Appropriately performed chest percussions will result in an improvement in oxygenation in neonates with respiratory distress.

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