scholarly journals Fatty diabetic lung: functional impairment in a model of metabolic syndrome

2010 ◽  
Vol 109 (6) ◽  
pp. 1913-1919 ◽  
Author(s):  
Cuneyt Yilmaz ◽  
Priya Ravikumar ◽  
Dennis J. Bellotto ◽  
Roger H. Unger ◽  
Connie C. W. Hsia
Keyword(s):  
Blood Flow ◽  
Functional Impairment ◽  
Lung Volume ◽  
Pulmonary Blood Flow ◽  
Diffusing Capacity ◽  
Heterogeneous Distribution ◽  
Tissue Volume ◽  
Age Related ◽  
Wide Range ◽  
Different Ages

The Zucker diabetic fatty (ZDF fa/fa) rat with genetic leptin insensitivity develops obesity and Type 2 diabetes mellitus (T2DM) with age accompanied by hyperplastic changes in the distal lung ( Am J Physiol Lung Cell Mol Physiol 298: L392–L403, 2010). To determine the functional consequences of structural changes, we developed a rebreathing (RB) technique to simultaneously measure lung volume, pulmonary blood flow, lung diffusing capacity (DlCO), membrane diffusing capacity (DmCO), pulmonary capillary blood volume (Vc), and septal tissue volume in anesthetized tracheostomized male ZDF fa/fa and matched lean (+/+) control animals at 4, 8, and 12 mo of age. Results obtained by RB technique were compared with that measured by a single-breath (SB) technique and to that expected in a wide range of species. In fa/fa animals compared with +/+, lung volumes and compliance were 13–35% lower at different ages, and the normal age-related increase in lung compliance was no longer evident. Mean pulmonary blood flow declined with age in fa/fa but not in +/+ animals. DlCO measured at a given pulmonary blood flow was 20–43% lower at different ages due to reductions in both DmCO and Vc. Septal tissue volume was also reduced in older fa/fa rats. We conclude that obese rats with T2DM develop significant restrictive pulmonary defects with diffusion impairment in a pattern similar to that previously reported in obese human subjects with T2DM. Functional impairment became exaggerated with age and duration of T2DM. In both fa/fa and +/+ animals, DlCO measured by RB was systematically higher than by SB technique whereas lung volume was similar, a finding consistent with heterogeneous distribution of ventilation in the rat lung.

Temporal course of gas exchange and mechanical compensation after right pneumonectomy in immature dogs

1996 ◽  
Vol 80 (4) ◽  
pp. 1304-1312 ◽  
Author(s):  
S. Takeda ◽  
E. Y. Wu ◽  
M. Ramanathan ◽  
A. S. Estrera ◽  
C. C. Hsia
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Lung Volume ◽  
Pulmonary Blood Flow ◽  
Capillary Blood ◽  
Diffusing Capacity ◽  
Pulmonary Capillary ◽  
Capillary Blood Volume ◽  
Pulmonary Capillary Blood ◽  
Pulmonary Capillary Blood Volume

To determine the temporal progression and magnitude of functional compensation in immature dogs raised to maturity after extensive lung resection, we performed right pneumonectomy (R-Pnx) or right thoracotomy without pneumonectomy (Sham) in matched foxhounds at 2 mo of age. At 4, 8, 20, 40, and 60 wk after surgery, static transpulmonary pressure-lung volume relationships were determined. Lung diffusing capacity, membrane diffusing capacity, pulmonary capillary blood volume, pulmonary blood flow, septal lung tissue volume, and lung volumes were measured simultaneously by a rebreathing technique. During maturation, total lung capacity, lung volume at a given distending pressure, and compliance were lower in the R-Pnx group than in the Sham group (P < 0.05). Pulmonary viscous resistance at maturity was elevated after R-Pnx. There were no significant differences in total lung diffusing capacity, membrane diffusing capacity, pulmonary capillary blood volume, pulmonary blood flow, and septal lung tissue volume between groups. Compensation of alveolar-capillary gas exchange was complete by 4-8 wk after R-Pnx, but compensation of mechanical properties remained incomplete throughout maturation. Relative magnitude of compensation after R-Pnx was greater in immature dogs than in adult dogs studied previously by similar techniques.

Alveolar diffusion-perfusion interactions during high-altitude residence in guinea pigs

2007 ◽  
Vol 102 (6) ◽  
pp. 2179-2185 ◽  
Author(s):  
Cuneyt Yilmaz ◽  
D. Merrill Dane ◽  
Connie C. W. Hsia
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
High Altitude ◽  
Lung Volume ◽  
Guinea Pigs ◽  
Pulmonary Blood Flow ◽  
Ultrastructural Changes ◽  
Diffusing Capacity ◽  
Adaptive Responses ◽  
Structural Adaptation

We previously reported in weanling guinea pigs raised at high altitude (HA; 3,800 m) an elevated lung diffusing capacity estimated by morphometry from alveolar-capillary surface area, harmonic mean blood-gas barrier thickness, and pulmonary capillary blood volume (Vc) compared with litter-matched control animals raised at an intermediate altitude (IA; 1,200 m) (Hsia CCW, Polo Carbayo JJ, Yan X, Bellotto DJ. Respir Physiol Neurobiol 147: 105–115, 2005). To determine if HA-induced alveolar ultrastructural changes are associated with improved alveolar function, we measured lung diffusing capacity for carbon monoxide (DlCO), membrane diffusing capacity for carbon monoxide (DmCO), Vc, pulmonary blood flow, and lung volume by a rebreathing technique in litter-matched male weanling Hartley guinea pigs raised at HA or IA for 4 or 12 mo. Separate control animals were also raised and studied at sea level (SL). Resting measurements were obtained in the conscious nonsedated state. In HA animals compared with corresponding IA or SL controls, lung volume and hematocrit were significantly higher while pulmonary blood flow was lower. At a given pulmonary blood flow, DlCO and DmCO were higher in HA-raised animals than in control animals without a significant change in Vc. We conclude that 1) HA residence enhanced physiological diffusing capacity corresponding to that previously estimated on the basis of structural adaptation, 2) adaptation in diffusing capacity and its components should be interpreted with respect to pulmonary blood flow, and 3) this noninvasive rebreathing technique could be used to follow adaptive responses in small animals.

scholarly journals Pulmonary blood flow and tissue volume.

Anaesthesia ◽  
1980 ◽  
Vol 35 (11) ◽  
pp. 1054-1059 ◽  
Author(s):  
J.C. SALT ◽  
J.W.W. GOTHARD ◽  
M.A. BRANTHWAITE
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Tissue Volume

The effects of artificial lung inflation on pulmonary blood flow and heart rate in the turtle Trachemys scripta.

1997 ◽  
Vol 200 (19) ◽  
pp. 2539-2545
Author(s):  
J Herman ◽  
T Wang ◽  
A W Smits ◽  
J W Hicks
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Lung Volume ◽  
Pulmonary Blood Flow ◽  
Trachemys Scripta ◽  
Spontaneous Ventilation ◽  
Lung Inflation ◽  
Cardiovascular Changes ◽  
Blood Flows ◽  
Stimulation Of

As for most ectothermic vertebrates, the breathing pattern of turtles is episodic, and pulmonary blood flow (Qpul) and heart rate (fH) normally increase several-fold during spontaneous ventilation. While some previous studies suggest that these cardiovascular changes are caused by stimulation of pulmonary stretch receptors (PSRs) during ventilation, it has been noted in other studies that blood flows often change prior to the initiation of breathing. Given the uncertainty regarding the role of PSRs in the regulation of central vascular blood flows, we examined the effect of manipulating lung volume (and therefore PSR stimulation) on blood flows and heart rate in the freshwater turtle Trachemys scripta. Turtles were instrumented with blood flow probes on the left aortic arch and the left pulmonary artery for measurements of blood flow, and catheters were inserted into both lungs for manipulation of lung volume. In both anaesthetized and fully recovered animals, reductions or increases in lung volume by withdrawal of lung gas or injection of air, N2, O2 or 10% CO2 (in room air) had no effect on blood flows. Furthermore, simulations of normal breathing bouts by withdrawal and injection of lung gas did not alter Qpul or fH. We conclude that stimulation of PSRs is not sufficient to elicit cardiovascular changes and that the large increase in Qpul and fH normally observed during spontaneous ventilation are probably caused by a simultaneous feedforward control of central origin.

Splenectomy impairs diffusive oxygen transport in the lung of dogs

2006 ◽  
Vol 101 (1) ◽  
pp. 289-297 ◽  
Author(s):  
D. Merrill Dane ◽  
Connie C. W. Hsia ◽  
Eugene Y. Wu ◽  
Richard T. Hogg ◽  
Deborah C. Hogg ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Pulmonary Blood Flow ◽  
Compensatory Mechanism ◽  
Diffusing Capacity ◽  
Restrictive Lung Disease ◽  
Before And After ◽  
Capillary Blood Volume ◽  
Exercise Induced ◽  
Experimental Findings

The spleen acts as an erythrocyte reservoir in highly aerobic species such as the dog and horse. Sympathetic-mediated splenic contraction during exercise reversibly enhances convective O2 transport by increasing hematocrit, blood volume, and O2-carrying capacity. Based on theoretical interactions between erythrocytes and capillary membrane (Hsia CCW, Johnson RL Jr, and Shah D. J Appl Physiol 86: 1460–1467, 1999) and experimental findings in horses of a postsplenectomy reduction in peripheral O2-diffusing capacity (Wagner PD, Erickson BK, Kubo K, Hiraga A, Kai M, Yamaya Y, Richardson R, and Seaman J. Equine Vet J 18, Suppl: 82–89, 1995), we hypothesized that splenic contraction also augments diffusive O2 transport in the lung. Therefore, we have measured lung diffusing capacity (DlCO) and its components during exercise by a rebreathing technique in six adult foxhounds before and after splenectomy. Splenectomy eliminated exercise-induced polycythemia, associated with a 30% reduction in maximal O2 uptake. At any given pulmonary blood flow, DlCO was significantly lower after splenectomy owing to a lower membrane diffusing capacity, whereas pulmonary capillary blood volume changed variably; microvascular recruitment, indicated by the slope of the increase in DlCO with respect to pulmonary blood flow, was also reduced. We conclude that splenic contraction enhances both convective and diffusive O2 transport and provides another compensatory mechanism for maintaining alveolar O2 transport in the presence of restrictive lung disease or ambient hypoxia.

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