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Biomedical subjects

I Mayers

Publications and source records attributed to I Mayers.

49 records · Page 3Linked to original sources
PubMed1990

The effects of halothane in hypoxic pulmonary vasoconstriction.

Human and animal experiments have not consistently shown halothane to inhibit hypoxic pulmonary vasoconstriction (HPV). The authors used a canine lung lobe perfused in situ to more precisely characterize the effects of halothane on HPV. The pulmonary vasculature can be divided into inflow, middle, and outflow segments by sequentially occluding the lobar inflow and outflow of blood. The lobes were ventilated with four different gas mixtures (normoxia, hypoxia, normoxia/halothane, hypoxia/halothane) and measured inflow, outflow, and middle segment (Rm) resistances using this stop-flow technique. All values are shown as means +/- standard deviation. The authors found that hypoxia increased Rm from normoxia values of .006 +/- .005 cmH2O.ml-1.min-1 to .025 +/- .008 cmH2O.ml-1.min-1 (P less than 0.05). During hypoxia/halothane Rm returned to .005 +/- .004 cmH2O.ml-1.min-1. The relationship between pressure and flow (P-Q) for the lobes for each gas mixture was also determined. The slopes of the P-Q lines by linear regression were all similar. The zero-flow pressure intercepts of the P-Q lines for normoxia (3.2 +/- .9 cmH2O) and hypoxia (4.4 +/- 1.1 cmH2O) were significantly decreased after the administration of halothane (1.7 +/- 1.0 cmH2O and 2.6 +/- 1.0 cmH2O, respectively). Since the zero-flow intercept likely reflects the tone at alveolar vessel level, the authors conclude that halothane inhibits HPV by decreasing the tone in the middle vascular segment.

Animals↗
PubMed1989

Cardiac output effects of high-frequency oscillatory ventilation in normal dogs.

We compared the hemodynamic effects of high-frequency oscillatory ventilation (HFOV) with conventional continuous positive pressure ventilation (CPPV). Six mongrel dogs were anesthetized with chloralose and evaluated over a range of mean airway pressures (Pao) during CPPV and HFOV. Pao during HFOV was measured by allowing alveolar pressure to come into equilibrium with airway opening pressure and was set to equal mean Pao during CPPV. Pao during CPPV was set by adding positive end-expiratory pressure (PEEP) of 0, 5, 10, and 15 cm H2O. Transmural pulmonary capillary wedge pressures (Pwp) were maintained at near 11 mm Hg in both groups during all four ventilatory periods. Cardiac output as measured in triplicate by thermal dilution was similar between HFOV and CPPV at each level of mean airway pressure. After matching mean airway pressure and transmural Pwp we were unable to find any sparing effect of HFOV on cardiac output over a wide range of airway pressures. We conclude that there is not an independent effect of HFOV on cardiac output.

Animals↗
PubMed1989

High-frequency oscillatory ventilation of a canine bronchopleural fistula.

We hypothesized that during high-frequency oscillatory ventilation (HFOV) of a central bronchopleural fistula (BPF), gas flow through the fistula (Vleak) should vary with ventilatory frequency. In six pentobarbital-anesthetized, open-chested dogs, we inserted a cannula into the left lower lobe bronchus. After 30 min of HFOV at 5 Hz (fistula closed), they received four periods of HFOV (fistula open) at frequencies of 5, 10, 15, and 20 Hz. With the fistula open, we could adequately ventilate at all four frequencies. Vleak ranged between 5.1 +/- 0.7 and 4.1 +/- 0.7 L/min and it was not significantly different at any frequency by analysis of variance. Airway opening pressure (Pao) was 3.9 +/- 0.6 cm H2O with the fistula closed. Pao decreased significantly to 1.9 +/- 0.2 cm H2O during 5 Hz ventilation (fistula open). Pao at the other frequencies was similar to fistula-closed ventilation. We believe that expiratory flow limitation at frequencies greater than 5 Hz may explain our findings.

Animals↗
PubMed1988

Treatment of canine aspiration pneumonitis: fluid volume reduction vs. fluid volume expansion.

The aspiration of gastric acid causes pulmonary edema and hypoxemia. One approach to the management of this syndrome is to raise cardiac output (Qt) and O2 delivery (QO2) to ensure tissue oxygenation (VO2) at the risk of increasing the edema. Another approach reduces the edema by reducing pulmonary microvascular pressure (Pmv) at the risk of reducing QO2 and VO2. We compared these approaches in 24 anesthetized, ventilated dogs with pulmonary wedge pressure (Ppw), a clinical approximation of Pmv, of 12.5 mmHg. Before and again 1 h after endobronchial instillation of 0.1 N HCl, we measured Qt, QO2, VO2, venous admixture, and in vivo extravascular lung liquid. The dogs were then randomly divided into four equal groups: 1) 12.5 mmHg Ppw, high Qt; 2) 7.5 mmHg Ppw, intermediate Qt; 3) 4.5 mmHg Ppw, low Qt; and 4) 4.5 mmHg Ppw plus dopamine, intermediate Qt. Measured values were followed for 4 more h, after which the lungs were excised to compare wet weight-to-body weight ratios (W/B). When plasmapheresis reduced Ppw at 1 h, edema did not increase further and W/B of groups 2 (21 +/- 3), 3 (18 +/- 3), and 4 (22 +/- 3) were significantly less than in group 1 (27 +/- 3) (P less than 0.001). Although Qt decreased with Ppw, increased hematocrit and reduced venous admixture maintained QO2 in group 2 but not in group 3. In group 4 an intermediate Qt maintained QO2 even at 4.5 mmHg Ppw but edema increased to the group 2 level presumably because Pmv rose with Qt on dopamine. VO2 remained constant over time in each group. These data demonstrate that canine HCl-induced pulmonary edema, measured in vivo or gravimetrically, is very sensitive to reductions in Pmv. Moreover, the lowest Pmv (and QO2) was well tolerated because an O2 supply dependency of VO2 was not observed.

Animals↗
PubMed1987

The effects of indomethacin on edema and gas exchange in canine acid aspiration.

Previous studies have suggested that prostaglandin synthesis inhibition might alter lung water accumulation in low pressure pulmonary edema. Therefore we studied the effects of indomethacin administration on edema formation, hemodynamics, and gas exchange in canine acid aspiration. Fourteen pentobarbital anesthetized dogs received 1 ml/kg of 0.1 N HCl intratracheally and then 7 received indomethacin (5 mg/kg) and 7 served as time controls. Lung liquid was measured in vivo by a double indicator technique and at the end of the experiment by gravimetric determinations. Following HCl administration, venous admixture (Qva/Qt) increased in both groups. Over the succeeding 4 h Qva/Qt decreased after indomethacin administration by 4.1 +/- 14.2%, but increased in the control group by 10.9 +/- 11.5% (P less than 0.05). Cardiac index remained constant in the control group but decreased after indomethacin from 232 +/- 89 ml X kg-1 X min-1 to 167 +/- 75 ml X kg-1 X min-1. Lung liquid accumulation, however, was similar between both groups. We believe that the changes in Qva/Qt associated with indomethacin can be explained by the known observations that decreases in cardiac output are associated with decreases in intrapulmonary shunt.

Analysis of Variance↗
PubMed1987

Canine bronchoconstriction, gas trapping, and hypoxia with methacholine.

The effects of an intravenous methacholine infusion on cardiovascular-pulmonary function were measured in seven mongrel dogs (22.0 +/- 2.8 kg), anesthetized with chloralose and urethan and beta-adrenergically blocked with propranolol. In a volume-displacement plethysmograph, physiological measurements were made at base line and 25 min after establishing a methacholine infusion (0.1-1.0 mg X kg-1 X h-1). Methacholine significantly (P less than 0.05) increased airways resistance (1.9 +/- 0.8 to 8.2 +/- 2.9 cmH2O X l-1 X s), decreased static lung compliance (84.7 +/- 18.5 to 48.2 +/- 9.4 ml/cmH2O), depressed arterial PO2 (81 +/- 17 to 56 +/- 10 Torr), and lowered blood pressure (132 +/- 10 to 69 +/- 18 Torr) and cardiac output (5.7 +/- 1.9 to 4.1 +/- 1.2 l/min). These effects persisted during a further 80 min of methacholine infusion conducted in five of the animals. During the initial 25-min period of methacholine, the end-expired volume (volume-displacement Krogh spirometer) rose in all animals, indicating an increase in functional residual capacity from 997 +/- 115 to 1,623 +/- 259 ml (P less than 0.0005). Analysis of pulmonary pressure-volume curves revealed no change in total lung capacity but an increase in residual volume from 489 +/- 168 to 1,106 +/- 216 ml (P less than 0.001). Thus methacholine caused 617 ml of gas trapping, which was not detected by the Boyle's law principle, presumably because gas was trapped at high transpulmonary pressure. We suggest that intravenous methacholine-induced canine bronchoconstriction, which causes gas trapping and hypoxia, may be a useful animal model of clinical status asthmaticus.

Animals↗
PubMed1987

Delayed resolution of high-pressure pulmonary edema or capillary leak.

Both clinical and experimental evidence suggest that the time course of edema formation is different from that of edema resolution. To better describe and quantify this difference, we followed the accumulation of high-pressure pulmonary edema in live dogs with the thermal-green dye (TGD) double-indicator technique at steady-state levels of lung liquid. We raised left atrial pressure (PLa) in steps of 5 to 10 mm Hg as high as 25 mm Hg and followed edema to steady-state levels. Lung water was then measured as PLa was lowered to initial values. By plotting steady-state edema against PLa, pressure-volume relationships were constructed. There was little change in edema until PLa reached approximately 15 mm Hg, at which point further changes in PLa were associated with large increases in lung liquid. At PLa = 25 mm/kg, the average lung water had increased by 10 ml/kg. In each animal there was slow resolution of edema with decreases in PLa from its peak back to its initial value, but in no animal was edema fully reabsorbed even though PLa was maintained at about 5 mm Hg for as long as 10 hours. Several possible explanations account for these observations. Water could be trapped in alveolar and central interstitial spaces. In addition, vessel closure in edematous lung units could further influence water reabsorption. These observations raise the possibility that pulmonary edema in the presence of normal filling pressures may represent resolution of a transient high-pressure edema as opposed to a capillary leak syndrome.

Animals↗
PubMed1986

Artificial ventilation of a canine model of bronchopleural fistula.

The authors studied the abnormalities of gas exchange and lung mechanics in a canine model of bronchopleural fistula during intermittent positive pressure ventilation (IPPV) and high-frequency oscillatory ventilation (HFOV). The left lower lobe bronchus was opened to atmosphere and it was determined that end expired volume was best maintained at frequencies of 45-50 breaths/min. during IPPV. Comparing alternating periods of IPPV and HFOV in six dogs (Group I) at matched airway opening pressure (Pao), we found that Pao2 decreased significantly to 68 +/- 14 mmHg and 69 +/- 24 mmHg, respectively, on opening the fistula. In a second group of six dogs (Group 2), when Pao was increased by additional bias flow into the ventilatory circuit during both IPPV and HFOV, Pao2 increased significantly to 89 +/- 12 mmHg and 87 +/- 8 mmHg, respectively. Repeating Group 2 studies after induction of oleic acid low-pressure pulmonary edema demonstrated that conventional IPPV was associated with large intrapulmonary shunts. HFOV, however, maintained gas exchange at near baseline values. For both Group 1 and Group 2, the calculated gas flow through the fistula was significantly less at all levels of airway pressure during HFOV. The authors conclude that HFOV offers advantages over conventional IPPV in the maintenance of oxygenation and in the reduction of gas leak through the fistula.

Animals↗
PubMed1985

Increased cardiac output increases shunt: role of pulmonary edema and perfusion.

In low-pressure pulmonary edema increased cardiac output (QT) increases shunt (Qs/QT); we tested whether the mechanism is an increase in extravascular lung water in turn mediated by the accompanying increase in microvascular pressure. In six pentobarbital sodium-anesthetized dogs ventilated with O2 we administered oleic acid into the right atrium. From base line to 2 h post-oleic acid we measured concurrent significant increases in Qs/QT (6-29%, O2 technique) and extravascular thermal volume (ETV, 2.6-7.1 ml/g dry intravascular blood-free lung wt, thermal-green dye indicator technique) that were stable by 90 min. Then, bilateral femoral arteriovenous fistulas were opened and closed in 30-min periods to cause reversible increases in QT and associated Qs/QT. When fistulas were open the time-averaged QT increased from 5.1 to 6.9 min (P less than 0.05), the simultaneous Qs/QT rose from 30.7 to 38.4% (P less than 0.05), but ETV did not increase. We conclude that increasing lung edema does not account for our rise in Qs/QT when QT increased.

Animals↗
PubMedDate not supplied

Lazaroids--not nitric oxide synthetase inhibitors--improve hemodynamics after thermal injury in anesthetized guinea pigs.

Our objective was to study the effects of a lipid peroxidation inhibitor (U74389G) and nitric oxide synthetase inhibitor (NG-methyl-L-arginine) on hemodynamic stability in burn shock. The design was a prospective, placebo control, randomized, and masked multigroup study in a research laboratory of a university hospital. We used 24 guinea pigs (N = 24), and induced burn shock by a scalding thermal injury (75 degrees C) to 35% of their body surface area. Hemodynamics and gas exchange were observed for 90 minutes after the burn injury in the four groups: no burn, burn-control, burn-U74 (10 mg/kg U74389G), and burn-LNMA (20 mg/Kg NG-methyl-L-arginine). The percentage of mean arterial pressure, normalized for the initial value at 30 minutes after the burn injury, decreased in all groups over time but was not significantly different in any group. The normalized percentage of flow also decreased over time in all groups with the slope of the linear regression significantly less in the burn-U74 group (-0.32 95% CI, -0.05, -0.15) and the no burn group (-0.37 95% CI, -0.48, -0.26), compared with the burn-control group (-0.66 95% CI, -0.77, -0.56) and the burn-LNMA group (-0.66 95% CI, -0.77, -0.56). The slope of the linear regression for the normalized percentage of systemic vascular resistance was significantly more marked in the burn-control group (2.45 95% CI, 1.35, 3.54) and the burn-LNMA group (1.22 95% CI, 0.89, 1.55) compared with the no burn group (0.16 95% CI, 0.11, 0.44) or the burn-U74 group (0.34 95% CI, 0.06, 0.74). The burn shock resulted in hemodynamic instability as measured with increased systemic vascular resistance, decreased cardiac output, and mean arterial pressure. Use of a lazaroid (U74389G), not a nitric oxide synthetase inhibitor (NG-methyl-L-arginine), altered the clinical course after thermal injury. These data suggest the importance of lipid peroxidation and free radicals as secondary mediators in the evolution of burn shock.

Analysis of Variance↗
PubMedDate not supplied

The effects of U-74389G, a 21-aminosteroid, on pulmonary vascular resistance after a scald.

We tested U-74389G (C37H50N6O2-CH4O4), a 21-aminosteroid, to determine whether it ameliorates the pulmonary vascular effects of a surface scald. We studied 24-anesthetized rabbits mechanically ventilated with 100% and then 13% O2. Twelve rabbits received a scald (75 degrees C water applied to the shaved ventral surface for 90 seconds), and 12 served as control (20 degrees C water). Six control and six scalded animals additionally received U-74389G (5 mg/ kg intravenously). We measured hemodynamics and blood gases prescald, 30 minutes postscald, and 30 minutes after U-74389G or placebo administration. The strength of hypoxic pulmonary vasoconstriction (HPV) was assessed as the difference between pulmonary vascular resistance measured during 13% O2 ventilation and during 100% O2 ventilation. Hemodynamics and gas exchange were similar between groups. The strength of HPV was significantly diminished postscald, but U-74389G treatment restored HPV to baseline values. We conclude that a scald reduces the strength of HPV, and the response to U-74389G suggests this may be mediated by free radicals.

Animals↗