Biomedical subjects

M L Nessly

Publications and source records attributed to M L Nessly.

26 records · Page 2Linked to original sources

PubMed1987

Hemodynamic effects of rapidly evacuating prolonged pneumothorax in rabbits.

Clinical observations suggest that systemic hypotension may be caused by rapid evacuation of persistent pneumothorax. This observation has not been substantiated experimentally and the mechanism(s) are unknown. In this study, we measured systemic hemodynamic parameters in rabbits before and for 2 h during negative pressure evacuation of a right-sided pneumothorax of 7-9 days duration. Three groups of animals were studied: 10 rabbits breathed room air and were hypoxemic during pneumothorax (hypoxemic pneumothorax = HP); 10 rabbits breathed 40% O2-60% N2, which prevented arterial hypoxemia during pneumothorax (supraoxemic pneumothorax = SP); seven normal control animals were untreated during this time period (NC). Pneumothoraces in HP and SP were evacuated by negative pressure applied to the right pleural space for 2 h while animals were anesthetized and mechanically ventilated. The NC group was anesthetized and ventilated without prior pneumothorax. Serial hemodynamic measurements were made before and during pleural suction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Extracellular fluid volume during pneumothorax and hypoxemia in rabbits.

This study was designed to test the hypothesis that persistent pneumothorax of greater than or equal to 6 days duration causes a decrease of extracellular fluid volume (ECF). Such changes are of interest as they may be causally related to persistent hypotension that has occurred in humans following pneumothorax evacuation. Experiments were done in rabbits to determine the effect on ECF of persistent pneumothorax with or without systemic hypoxemia. Animals were divided into four treatment groups: 1) pneumothorax with hypoxemia [fractional concentration of O2 in inspired gas (FIO2) = 0.21, n = 30], 2) pneumothorax without hypoxemia (FIO2 = 0.40, n = 25), 3) hypoxemia alone (FIO2 = 0.14, n = 11), and 4) normal controls (FIO2 = 0.21, n = 15). Measurements of ECF were made in the base-line control state and after 6 days of treatment using the dilution volume of thiocyanate sodium as an estimate of ECF volume. We found a reduction of ECF in 53% of animals with pneumothorax plus hypoxemia (range -47% to +13%) and in 54% of animals with hypoxemia alone (range -26% to +25%). ECF declined in only 7% of normal controls and 20% of animals with pneumothorax without hypoxemia. Arterial O2 tensions after 6 days of treatment were 58 +/- 12.6, 141 +/- 28, 60 +/- 5.1, and 97 +/- 9.3 Torr (mean +/- SD) in groups 1-4, respectively. The results suggest that pneumothorax with hypoxemia or hypoxemia alone may contribute to depletion of ECF, but this response is variable and unpredictable in individual animals.

Animals↗

PubMed1985

Endogenous plasma proteins in edematous lungs and alveolar fluid in rabbits.

In this study, we compared two methods of differentiating hydrostatic and permeability types of pulmonary edema. The first method entailed measurement of protein concentrations directly in samples of alveolar fluid (AF); the second method was an indirect technique in which protein concentration in extravascular extracellular water (EVECW) was calculated on the basis of separate measurements of the quantity of protein in the lung and the volume of EVECW. The concentration of albumin (Alb) and gamma-G-globulin was measured in EVECW and alveolar fluid in excised edematous rabbit lungs. Edema was caused by elevation of left ventricular end-diastolic pressure to 25 Torr (hydrostatic edema, HE) or by intravenous oleic acid, 0.09 ml/kg (permeability edema, PE). The volume of distribution of Na+ was utilized as a measure of EVECW in the lung. Protein concentration in EVECW and AF relative to plasma (EV/PL and AF/PL, respectively) was compared in the two types of edema. The EV/PL was 0.61 +/- 0.12 (SD) for Alb in He compared with 1.18 +/- 0.47 in PE (P less than 0.02). The AF/PL was 0.54 +/- 0.12 and 1.25 +/- 0.33 in HE and PE, respectively (P less than 0.001). There was good correlation between EV/PL and AF/PL for Alb (r = 0.74, P less than 0.001) but not for gamma-G-globulin. Thus EV/PL for Alb, AF/PL for Alb, and gamma-G-globulin all differentiated hydrostatic from permeability edema.

Animals↗

PubMed1983

The effects of prophylactic expiratory positive airway pressure on the resolution of oleic acid-induced lung injury in dogs.

It is not known whether positive end-expiratory airway pressure (PEEP) merely improves gas exchange in patients with the adult respiratory distress syndrome (ARDS) or if it also affects the resolution of their lung injury. The present investigation was performed to determine whether expiratory positive airway pressure (EPAP), a form of PEEP, is prophylactic in preventing the lung injury induced by oleic acid in dogs or in enhancing its resolution. Arterial and mixed venous blood gases and functional residual capacity (FRC) were measured in 14 pairs of mongrel dogs with indwelling catheters and permanent tracheostomies. One member of each pair was treated with 10 cm H2O EPAP through a valve attached to the tracheostomy tube. Both dogs received 0.06 ml/kg oleic acid intravenously at hour 0. Measurements were made at three, 12, and 24 hours, when EPAP was discontinued, and over the next six days. Five dog pairs were sacrificed at 72 hours; the other surviving animals were sacrificed at 168 hours. FRC was higher at three, 12, and 24 hours in dogs receiving EPAP than in the untreated dogs. The arterial oxygen tension (PaO2) was higher and the venous admixture (Qva/Qt) was lower at three and 12 hours in the dogs receiving EPAP than in the untreated dogs. However, after 24 hours, no differences were noted between the two groups in FRC, PaO2, Qav/Qt, mortality, final lung compliance to initial lung compliance differences, lung water to dry lung weight ratios, or histology. It is concluded that EPAP improves gas exchange during its administration, but has no demonstrable prophylactic effect on the resolution of lung injury in the oleic acid model of human ARDS.

Animals↗

PubMed1982

Extravascular, extracellular water in rabbit lung using Na and sucrose indicators.

We compared the volume of the pulmonary extravascular, extracellular water space using sodium and sucrose indicators in 8 normal and 11 edematous rabbit lungs by steady-state techniques. The volume of the extravascular, extracellular space (EVECW), expressed in milliliters per gram dry lung, was determined from the volume of distribution of 24Na, [3H]sucrose, or total sodium in 1) supernatant solutions obtained by centrifugation of homogenized lung or 2) intact lung fragments. There was no significant difference in EVECW measured in normal lungs [24Na 1.88 +/- (SD) 0.31; [3H]sucrose 1.84 +/- (SD) 0.27] or edematous lungs [24Na 4.78 +/- (SD) 1.44; [3H]sucrose 4.41 +/- (SD) 1.33] when comparing supernate solutions of homogenized lungs. Similarly, there was no significant difference between the volumes of distribution (EVECW) of these two isotopes when measured in intact fragments of normal lung [24Na 2.08 +/- (SD) 0.28; [3H]sucrose 1.68 +/- (SD) 0.37]. The volume of EVECW measured in supernates was less than in fragments with both isotopes. Washing the centrifuged tissue pellet and adding the wash activity to the initial supernate activity yielded results that were equal to the fragment technique. The failure to detect significant differences between 24Na and [3H]sucrose spaces in the lung suggests that the contribution on intracellular sodium to the measurement of lung water is small and relatively insignificant, at least within the confines of this experiment.

Animals↗

PubMed1982

The effects of expiratory positive airway pressure on the resolution of oleic acid-induced lung injury in dogs.

It is not known whether positive end-expiratory pressure (PEEP) merely improves gas exchange in patients with the adult respiratory distress syndrome or also affects the resolution of their lung injury. We examined the effects of expiratory positive airway pressure (EPAP), a form of PEEP, on 13 pairs of spontaneously breathing mongrel dogs with permanent tracheostomies that were subjected to acute lung injury from oleic acid. One member of each pair was treated with 10 cm H2O EPAP by means of a special valve attached to its tracheostomy tube; the other member breathed through the tracheostomy tube alone. The EPAP was applied 3 h after an intravenous injection of 0.06 ml/kg oleic acid and continued for a total of 21 h. Functional residual capacity (FRC) was increased to preinjury values in the EPAP-treated dogs at 3, 12, and 24 h compared with that in the untreated dogs. The PaO2 was higher and the venous admixture (Qva/QT) was lower in the EPAP-treated dogs compared with that in the untreated dogs at 3 and at 12 h. However, over the 7 days after removal of EPAP no significant differences were noted between the 2 groups in FRC, PaO2, Qva/QT, inert gas elimination profiles, mortality, final lung compliance to initial lung compliance differences, lung water to dry lung weight ratios, or histologic features. We conclude that EPAP improves gas exchange during its administration but has no demonstrable effect on the resolution of lung injury induced by oleic acid in dogs.

Animals↗

PubMed1981

Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits.

In order to study the mechanism(s) underlying re-expansion edema, we measured the concentration of labeled albumin (RISA) in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of rabbit lungs that had been collapsed for 1 wk by pneumothorax. The RISA in EVECW was expressed as a fraction of its plasma concentration: (RISA)L/(RISA)PL. The volume of EVECW (ml/gm dry lung) was measured using a 24Na indicator. Results in re-expansion edema were compared with normal control lungs and with oleic acid edema as a model of permeability edema. In re-expanded lungs, EVECW (3.41 +/- SD 1.24 ml/g) and (RISA)L/(RISA)PL 0.84 +/- SD 0.15) were significantly increased when compared with normal control lungs (2.25 +/- 0.41 ml/g and 0.51 +/- 0.20, respectively). Results in oleic acid edema (5.66 +/- 2.23 ml/g and 0.84 +/- 0.23) were similar to re-expansion edema. This suggested that re-expansion edema is due to increased pulmonary vascular permeability caused by mechanical stresses applied to the lung during re-expansion.

Animals↗

PubMedDate not supplied

Randomized, double-blind trial comparing indinavir alone, zidovudine alone and indinavir plus zidovudine in antiretroviral therapy-naive HIV-infected individuals with CD4 cell counts between 50 and 250/mm3.

Treatment with indinavir has been shown to result in marked decreases in viral load and increases in CD4 cell counts in HIV-infected individuals. A randomized double-blind study to evaluate the efficacy of indinavir alone (800 mg q8h), zidovidine alone (200 mg q8h) or the combination was performed to evaluate progression to AIDS. 996 antiretroviral therapy-naive patients with CD4 cell counts of 50-250/mm3 were allocated to treatment. During the trial the protocol was amended to add lamivudine to the zidovudine-containing arms. The primary endpoint was time to development of an AIDS-defining illness or death. The study was terminated after a protocol-defined interim analysis demonstrated highly significant reductions in progression to a clinical event in the indinavir-containing arms, compared to the zidovudine arm (p<0. 0001). Over a median follow-up of 52 weeks (up to 99 weeks), percent reductions in hazards for the indinavir plus zidovudine and indinavir groups compared to the zidovudine group were 70% and 61%, respectively. Significant reductions in HIV RNA and increases in CD4 cell counts were also seen in the indinavir-containing groups compared to the zidovudine group. Improvement in both CD4 cell count and HIV RNA were associated with reduced risk of disease progression. All three regimens were generally well tolerated.

Adult↗