Posture primarily affects lung tissue distribution with minor effect on blood flow and ventilation

2007 ◽  
Vol 156 (3) ◽  
pp. 293-303 ◽  
Author(s):  
Johan Petersson ◽  
Malin Rohdin ◽  
Alejandro Sánchez-Crespo ◽  
Sven Nyrén ◽  
Hans Jacobsson ◽  
...  
2008 ◽  
Vol 295 (5) ◽  
pp. L756-L766 ◽  
Author(s):  
Peter E. Oishi ◽  
Dean A. Wiseman ◽  
Shruti Sharma ◽  
Sanjiv Kumar ◽  
Yali Hou ◽  
...  

Cardiac defects associated with increased pulmonary blood flow result in pulmonary vascular dysfunction that may relate to a decrease in bioavailable nitric oxide (NO). An 8-mm graft (shunt) was placed between the aorta and pulmonary artery in 30 late gestation fetal lambs; 27 fetal lambs underwent a sham procedure. Hemodynamic responses to ACh (1 μg/kg) and inhaled NO (40 ppm) were assessed at 2, 4, and 8 wk of age. Lung tissue nitric oxide synthase (NOS) activity, endothelial NOS (eNOS), neuronal NOS (nNOS), inducible NOS (iNOS), and heat shock protein 90 (HSP90), lung tissue and plasma nitrate and nitrite (NOx), and lung tissue superoxide anion and nitrated eNOS levels were determined. In shunted lambs, ACh decreased pulmonary artery pressure at 2 wk ( P < 0.05) but not at 4 and 8 wk. Inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). In control lambs, ACh and inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). Total NOS activity did not change from 2 to 8 wk in control lambs but increased in shunted lambs (ANOVA, P < 0.05). Conversely, NOxlevels relative to NOS activity were lower in shunted lambs than controls at 4 and 8 wk ( P < 0.05). eNOS protein levels were greater in shunted lambs than controls at 4 wk of age ( P < 0.05). Superoxide levels increased from 2 to 8 wk in control and shunted lambs (ANOVA, P < 0.05) and were greater in shunted lambs than controls at all ages ( P < 0.05). Nitrated eNOS levels were greater in shunted lambs than controls at each age ( P < 0.05). We conclude that increased pulmonary blood flow results in progressive impairment of basal and agonist-induced NOS function, in part secondary to oxidative stress that decreases bioavailable NO.


1979 ◽  
Vol 46 (6) ◽  
pp. 1207-1210 ◽  
Author(s):  
I. H. Young ◽  
P. D. Wagner

The solubility of sulfur hexafluoride (SF6), ethane, cyclopropane, halothane, diethyl ether, and acetone in homogenates of dog lung tissue were measured and compared with values obtained in dog blood. The measurements were made to provide data for a method for determining distribution of ventilation, blood flow, and tissue volume (Physiologist 20: 95, 1977) and for reasons discussed, the blood was not washed from the tissue prior to homogenization. All gases except SF6 were significantly more soluble in blood than lung tissue, whereas SF6 was 3.7 times more soluble in tissue than blood. It was further found that SF6 is 5 times more soluble, and ethane is twice as soluble in tissue obtained from lungs containing blood than in tissue obtained from rinsed lungs, suggesting that measurements of parenchymal solubility made on tissue from sinsed lungs may be considerably in error for some lipid-soluble gases.


2002 ◽  
Vol 88 (1) ◽  
pp. 63-68 ◽  
Author(s):  
Hiroshi Yamamoto ◽  
Tomonobu Koizumi ◽  
Masao Hirota ◽  
Toshimichi Kaneki ◽  
Hitoshi Ogasawara ◽  
...  

2001 ◽  
Vol 95 (1) ◽  
pp. 102-112 ◽  
Author(s):  
Kristina Hambraeus-Jonzon ◽  
Luni Chen ◽  
Filip Fredén ◽  
Peter Wiklund ◽  
Göran Hedenstierna

Background Inhaled nitric oxide (INO) is thought to cause selective pulmonary vasodilation of ventilated areas. The authors previously showed that INO to a hyperoxic lung increases the perfusion to this lung by redistribution of blood flow, but only if the opposite lung is hypoxic, indicating a more complex mechanism of action for NO. The authors hypothesized that regional hypoxia increases NO production and that INO to hyperoxic lung regions (HL) can inhibit this production by distant effect. Methods Nitric oxide concentration was measured in exhaled air (NO(E)), NO synthase (NOS) activity in lung tissue, and regional pulmonary blood flow in anesthetized pigs with regional left lower lobar (LLL) hypoxia (fraction of inspired oxygen [FIO2] = 0.05), with and without INO to HL (FIO2 = 0.8), and during cross-circulation of blood from pigs with and without INO. Results Left lower lobar hypoxia increased exhaled NO from the LLL (NO(E)LLL) from a mean (SD) of 1.3 (0.6) to 2.2 (0.9) parts per billion (ppb) (P &lt; 0.001), and Ca2+-dependent NOS activity was higher in hypoxic than in hyperoxic lung tissue (197 [86] vs. 162 [96] pmol x g(-1) x min(-1), P &lt; 0.05). INO to HL decreased the Ca2+-dependent NOS activity in hypoxic tissue to 49 [56] pmol x g(-1) x min(-1) (P &lt; 0.01), and NO(E)LLL to 2.0 [0.8] ppb (P &lt; 0.05). When open-chest pigs with LLL hypoxia received blood from closed-chest pigs with INO, NO(E)LLL decreased from 2.0 (0.6) to 1.5 (0.4) ppb (P &lt; 0.001), and the Ca2+-dependent NOS activity in hypoxic tissue decreased from 152 (55) to 98 (34) pmol x g(-1) x min(-1) (P = 0.07). Pulmonary vascular resistance increased by 32 (21)% (P &lt; 0.05), but more so in hypoxic (P &lt; 0.01) than in hyperoxic (P &lt; 0.05) lung regions, resulting in a further redistribution (P &lt; 0.05) of pulmonary blood flow away from hypoxic to hyperoxic lung regions. Conclusions Inhaled nitric oxide downregulates endogenous NO production in other, predominantly hypoxic, lung regions. This distant effect is blood-mediated and causes vasoconstriction in lung regions that do not receive INO.


2009 ◽  
Vol 234 (5) ◽  
pp. 504-512 ◽  
Author(s):  
Xiaohui Li ◽  
Hongfang Jin ◽  
Geng Bin ◽  
Li Wang ◽  
Chaoshu Tang ◽  
...  

The mechanisms responsible for the structural remodeling of pulmonary vasculature induced by increased pulmonary blood flow are not fully understood. This study explores the effect of endogenous hydrogen sulfide (H2S), a novel gasotransmitter, on collagen remodeling of the pulmonary artery in rats with high pulmonary blood flow. Thirty-two Sprague-Dawley rats were randomly divided into sham, shunt, sham+PPG (D,L-propargylglycine, an inhibitor of cystathionine-γ-lyase), and shunt+PPG groups. After 4 weeks of shunting, the relative medial thickness (RMT) of pulmonary arteries and H2S concentration in lung tissues were investigated. Collagen I and collagen III were evaluated by hydroxyproline assay, sirius-red staining, and immunohistochemistry. Pulmonary artery matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and connective tissue growth factor (CTGF) were evaluated by immunohistochemistry. After 4 weeks of aortocaval shunting, resulting in an elevation of lung tissue H2S to 116.4%, rats exhibited collagen remodeling and increased CTGF expression in the pulmonary arteries. Compared with those of the shunt group, lung tissue H2S production was lowered by 23.4%, RMT of the pulmonary artery further increased by 39.5%, pulmonary artery collagen accumulation became obvious, and pulmonary artery CTGF expression elevated ( P < 0.01) in the shunted rats treated with PPG. However, pulmonary artery MMP-13 and TIMP-1 expressions decreased significantly in rats of shunt+PPG group ( P < 0.01). This study suggests that endogenous H2S exerts an important regulatory effect on pulmonary collagen remodeling induced by high pulmonary blood flow.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Raúl J Gazmuri ◽  
Herbert K Whitehouse ◽  
Alvin Baetiong ◽  
Karla Whittinghill ◽  
Jeejabai Radhakrishnan

Background: We have reported beneficial hemodynamic and survival effects of vasopressin (VP) infusion in swine models of hemorrhagic shock (HS), and attributed the effects to increases in peripheral vascular resistance. However, VP may also exert a minor effect on venous return. In the present study we used fluorescent microspheres to measure the effects of VP on blood flow to organs of interest during HS produced by liver laceration (LL). Methods: Forty male domestic pigs (32.3 to 40.3 kg) had their left lateral liver lobe lacerated with a sharpened steel, X-shaped 5 cm blade clamp. Thirty-two pigs received a second LL in the same lobe 7.5 minutes later and 24 pigs received a third LL in the left medial lobe at 15 minutes from the first LL. Pigs were randomized 1:1 to receive an infusion of VP (0.04 U/kg•min-1) or vehicle intraosseously starting 7 minutes after the first LL until the end of the experiment (240 min). Microspheres were injected into the left ventricle at baseline (BL) and during HS at times shown in the Table. Results: At 60 minutes of HS, VP infusion was associated with higher aortic blood pressure and lower cardiac index (both NS) along with overall reductions in blood flow to various organs (Table) coincident with a statistically significant reduction in heart rate (157±43 vs 184±29 min-1; p≤0.05). At 120 and 180 minutes of HS, the heart rate was only mildly reduced (NS). The aortic pressures remained high but without a reduction in cardiac index. Organ blood flows were all comparable or higher with VP than in control pigs attaining statistical significance for renal cortical blood flow. Conclusion: Contrary to the expected hemodynamic effects of VP redistributing blood flow away from “non-vital organs,” we observed a robust hemodynamic effect that adequately perfused vital and “non-vital” organs during HS without deterioration over time. Early and sustained VP infusion could represent a highly effective intervention for hemodynamic stabilization during severe HS.


1978 ◽  
Vol 44 (5) ◽  
pp. 795-802 ◽  
Author(s):  
M. F. Petrini ◽  
B. T. Peterson ◽  
R. W. Hyde
Keyword(s):  

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