Effect of metabolic acidosis on pulmonary gas exchange of artificially ventilated dogs

1993 ◽  
Vol 74 (5) ◽  
pp. 2301-2308 ◽  
Author(s):  
A. Frans ◽  
T. Clerbaux ◽  
E. Willems ◽  
F. Kreuzer
Keyword(s):  
Metabolic Acidosis ◽  
Dynamic Method ◽  
Bohr Effect ◽  
Arterial Pco2 ◽  
Before And After ◽  
Two Factors ◽  
Simultaneous Decrease ◽  
Pulmonary Arterial ◽  
Co2 Excretion ◽  
Oxyhemoglobin Dissociation

It is well established that metabolic acidosis induces a reduction in alveolar-arterial O2 difference [(A-a)Do2] in artificially ventilated dogs by shifting the oxyhemoglobin dissociation curve (ODC) and/or by improving the distribution of the ventilation-to-perfusion ratio (VA/Q) throughout the lung. To assess the influence of these two factors we examined eight artificially ventilated dogs before and after induction of metabolic acidosis by a perfusion of 0.3 mol HCl. We measured classic indexes of cardiopulmonary function. VA/Q distribution was estimated using the multiple inert gas elimination technique (MIGET). ODC and Bohr effect of each dog were obtained by a dynamic method. Acidosis increased CO2 excretion, respiratory quotient, blood PO2 at 50% saturation, and arterial PCO2 and PO2 with a simultaneous decrease in (A-a)DO2. In seven dogs, the distribution of VA and Q, as assessed by MIGET, was not substantially modified by HCl perfusion. In the eighth dog the distribution of Q and VA became more homogeneous after acidosis. This led us to conclude that the Bohr effect is the most important and most consistently observed factor responsible for the decrease in (A-a)DO2 found in metabolic acidosis. In rare cases the increase in pulmonary arterial pressure may complement this action by improving the distribution of the VA/Q ratio.

Brain pH responses to sodium bicarbonate and Carbicarb during systemic acidosis

1989 ◽  
Vol 256 (5) ◽  
pp. H1316-H1321 ◽  
Author(s):  
J. I. Shapiro ◽  
M. Whalen ◽  
R. Kucera ◽  
N. Kindig ◽  
G. Filley ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Ammonium Chloride ◽  
Respiratory Acidosis ◽  
Arterial Pco2 ◽  
Bicarbonate Therapy ◽  
Brain Ph ◽  
Dose Dependent ◽  
Intracellular Alkalinization

Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.

Endothelin effects in isolated, perfused lamb lungs: role of cyclooxygenase inhibition and vasomotor tone

1991 ◽  
Vol 261 (2) ◽  
pp. H443-H450 ◽  
Author(s):  
H. Toga ◽  
J. Usha Raj ◽  
R. Hillyard ◽  
B. Ku ◽  
J. Anderson
Keyword(s):  
Vasomotor Tone ◽  
Cyclooxygenase Inhibition ◽  
Group Iii ◽  
Group I ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Group Ii ◽  
Sites Of Action ◽  
Arteries And Veins

We have determined the sites of action of endothelin-1 (ET) in the lamb pulmonary circulation. The influence of cyclooxygenase inhibition and baseline vasomotor tone on ET effects was also studied. Lungs of 14 lambs (6-9 wk of age, 12.1 +/- 0.6 kg body wt) were isolated and perfused with blood. Group I lungs (n = 5) were untreated, group II lungs (n = 5) were treated with indomethacin to inhibit cyclooxygenase, and group III lungs (n = 4) were treated with indomethacin and a thromboxane A2 analogue, U-46619, to elevate vasomotor tone. All lungs were perfused with constant flow in zone 3, with left atrial and airway pressures being 8 and 6 cmH2O, respectively. We measured pulmonary arterial pressure and, by the micropuncture servo-null method, pressures in 20- to 50-microns diameter subpleural venules, both before and after each dose of ET was infused (50, 100, 250, and 500 ng/kg). Group I lungs, with high baseline vasomotor tone, exhibited a biphasic response to ET; 50-100 ng/kg of ET dilated both arteries and veins, whereas 500 ng/kg of ET constricted both arteries and veins. In group II lungs with low vasomotor tone, all doses of ET caused constriction of arteries only. In group III lungs (indomethacin treated with elevated vasomotor tone), 50-100 ng/kg of ET caused dilation of arteries and veins, whereas 500 ng/kg of ET induced constriction, this time only in arteries. We conclude that ET has both dilator and constrictor effects in arteries and veins of isolated, perfused lamb lungs. ET-induced arterial and venous dilation is dependent on initial vasomotor tone but not on cyclooxygenase metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of pulmonary arterial PCO2 on breathing pattern

1988 ◽  
Vol 64 (5) ◽  
pp. 1844-1850 ◽  
Author(s):  
E. R. Schertel ◽  
D. A. Schneider ◽  
L. Adams ◽  
J. F. Green
Keyword(s):  
Breathing Pattern ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Middle Level ◽  
Positive Pressure ◽  
Breathing Patterns ◽  
Arterial Pco2 ◽  
Anesthetized Dogs ◽  
Steady State Levels ◽  
Pulmonary Arterial

We studied breathing patterns and tidal volume (VT)-inspiratory time (TI) relationships at three steady-state levels of pulmonary arterial PCO2 (PpCO2) in 10 anesthetized dogs. To accomplish this we isolated and then separately pump perfused the pulmonary and systemic circulations, which allowed us to control blood gases in each circuit independently. To ventilate the lungs at a rate and depth determined by central drive, we used an electronically controlled positive-pressure ventilator driven by inspiratory phrenic neural activity. Expiratory time (TE) varied inversely with PpCO2 over the range of PpCO2 from approximately 20 to 80 Torr. VT and TI increased with rising PpCO2 over the range from approximately 20 to 45 Torr but did not change further as PpCO2 was raised above the middle level of approximately 45 Torr. Thus minute ventilation increased as a function of TE and VT as PpCO2 was increased over the lower range and increased solely as a function of TE as PpCO2 was increased over the upper range. The VT-TI relationship shifted leftward on the time axis as PpCO2 was lowered below the middle level but did not shift in the opposite direction as PpCO2 was raised above the middle level. In addition to its effect on breathing pattern, we found that pulmonary hypocapnia depressed inspiratory drive.

scholarly journals Bioaktivitas ekstrak biji bintaro terhadap kutu daun Aphis gossypii GLOVER dan pengaruhnya terhadap tanaman cabai

Jurnal Agro ◽  
10.15575/8380 ◽  
2020 ◽  
Vol 7 (2) ◽  
pp. 179-192
Author(s):  
Rial Mustiarif ◽  
Djamilah Djamilah ◽  
Nanik Setyowati ◽  
Agustin Zakarni
Keyword(s):  
Insect Pest ◽  
Aphis Gossypii ◽  
Dry Weight ◽  
Seed Extract ◽  
Crop Damage ◽  
Time Of Application ◽  
Randomized Design ◽  
Aphis Gossypii Glover ◽  
Before And After ◽  
Two Factors

Aphis gossypii Glover hama penting tanaman cabai, dapat dikendalian dengan menggunakan pestisida nabati. Penelitian bertujuan untuk mengevaluasi waktu aplikasi dan konsentrasi ekstrak kasar biji bintaro (Cerbera odollam G.) dalam mengendalikan A. gossypii Glover serta pengaruhnya terhadap pertumbuhan tanaman cabai. Penelitian menggunakan Rancangan Acak Lengkap, dua faktor dan tiga ulangan. Faktor pertama adalah waktu aplikasi ekstrak (waktu sebelum dan waktu setelah infestasi A. gossypii Glover). Faktor kedua adalah konsentrasi ekstrak bintaro (0%, 1%, 2%, 3%, 4% dan 5%). Hasil penelitian menunjukkan konsentrasi 1% ekstrak biji bintaro menyebabkan mortalitas kutu daunnya 68% sedangkan pada konsentrasi 3% mortalitasnya mencapai 90%. Ekstrak biji bintaro yang diberikan sebelum hama diinfestasikan menyebabkan mortalitas kutu daun 59,5% sedangkan jika diberikan setelah hama diinfestasikan mortalitasnya meningkat menjadi 77,6%. Nilai LC50 dan LC90 ekstrak biji bintaro diaplikasikan sebelum dan setelah hama diinfestasikan secara berurutan adalah 1,8%; 4,4%; 0,57% dan 2,8%. A. gossypii Glover yang diinfestasikan pada tanaman berumur 4 minggu dan disemprot dengan ekstrak biji bintaro pada konsentrasi 1% dapat menurunkan intensitas kerusakan pada hari ke tujuh setelah infestasi dan tidak berpengaruh terhadap jumlah daun, bobot segar maupun bobot kering tanaman cabai. Ekstrak biji bintaro dapat dikembangkan sebagai pestisida nabati untuk mengendalikan hama A. gossypii Glover pada tanaman cabai. Aphis gossypii Glover is an important sucking insect pest of the pepper (Capsicum annum L.), Can be controlled by using natural pesticides. The study aimed to evaluate the application time and concentration of Cerbera odollam G. seed extract in controlling A. gossypii and their effects on pepper, C. annum. Complete randomized design was used in this experiment, with two factors, and was repeated three times. The first factor was the time of application of the extract, consisting of before and after A. gossypii infestation. The second factor was the concentration of C. odollam extract (0%, 1%, 2%, 3%, 4% and 5%). The results indicated the C. odollam seed extract affected the mortality of A. gossypii. At a concentration of 1% of C. odollam seed extract, the mortality of A. gossypii was 68% while at a concentration of 3% the mortality reached up to 90%. C. odollam seed extract applied before infestation, the mortality of A. gossypii was 59.5% whereas, after the infestation, the mortality increased up to 77.6%. LC50 and LC90 extract of C. odollam seeds applied before and after infestation were 1.8%; 4.4%; 0.57% and 2.8% respectively. A. gossypii infested at 8 weeks old pepper and sprayed with C. odollam seed extract at a concentration of 1% lowered the crop damage on the seventh day after infestation. On the other hand, the application of C. odollam seed extract did not affect the number of leaves, fresh weight, and dry weight of pepper. This study indicate that C. odollam seed extract can be developed as a natural pesticide to control A. gossypii on pepper..

scholarly journals Age, but not short-term intensive swimming, affects chondrocyte turnover in zebrafish vertebral cartilage

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5739 ◽  
Author(s):  
Quan-Liang Jian ◽  
Wei-Chun HuangFu ◽  
Yen-Hua Lee ◽  
I-Hsuan Liu
Keyword(s):  
Critical Factor ◽  
The Body ◽  
Micro Computed Tomography ◽  
Mineral Density ◽  
Short Term ◽  
Cartilage Homeostasis ◽  
Intensive Exercise ◽  
Before And After ◽  
Two Factors ◽  
Brdu Labeling

Both age and intensive exercise are generally considered critical risk factors for osteoarthritis. In this work, we intend to establish zebrafish models to assess the role of these two factors on cartilage homeostasis. We designed a swimming device for zebrafish intensive exercise. The body measurements, bone mineral density (BMD) and the histology of spinal cartilages of 4- and 12-month-old zebrafish, as well the 12-month-old zebrafish before and after a 2-week exercise were compared. Our results indicate that both age and exercise affect the body length and body weight, and the micro-computed tomography reveals that both age and exercise affect the spinal BMD. However, quantitative analysis of immunohistochemistry and histochemistry indicate that short-term intensive exercise does not affect the extracellular matrix (ECM) of spinal cartilage. On the other hand, the cartilage ECM significantly grew from 4 to 12 months of age with an increase in total chondrocytes. dUTP nick end labeling staining shows that the percentages of apoptotic cells significantly increase as the zebrafish grows, whereas the BrdU labeling shows that proliferative cells dramatically decrease from 4 to 12 months of age. A 30-day chase of BrdU labeling shows some retention of labeling in cells in 4-month-old spinal cartilage but not in cartilage from 12-month-old zebrafish. Taken together, our results suggest that zebrafish chondrocytes are actively turned over, and indicate that aging is a critical factor that alters cartilage homeostasis. Zebrafish vertebral cartilage may serve as a good model to study the maturation and homeostasis of articular cartilage.

Pulmonary pressor response after prostaglandin synthesis inhibition in conscious dogs

1982 ◽  
Vol 52 (3) ◽  
pp. 705-709 ◽  
Author(s):  
B. R. Walker ◽  
N. F. Voelkel ◽  
J. T. Reeves
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Conscious Dogs ◽  
Pulmonary Pressure ◽  
Time Control ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial

Recent studies have shown that vasodilator prostaglandins are continually produced by the isolated rat lung. We postulated that these vasodilators may contribute to maintenance of normal low pulmonary arterial pressure. Pulmonary pressure and cardiac output were measured in conscious dogs prior to and 30 to 60 min following administration of meclofenamate (2 mg/kg iv, followed by infusion at 2 mg . kg-1 . h-1) or the structurally dissimilar inhibitor RO–20–5720 (1 mg/kg iv, followed by infusion at 1 mg . kg-1 . h-1). The animals were also made hypoxic with inhalation of 10% O2 before and after inhibition. Time-control experiments were conducted in which only the saline vehicle was administered. Meclofenamate or RO–20–5720 caused an increase in mean pulmonary arterial pressure and total pulmonary resistance. Cardiac output and systemic pressure were unaffected. The mild hypoxic pulmonary pressor response observed was not affected by meclofenamate. Animals breathing 30% O2 to offset Denver's altitude also demonstrated increased pulmonary pressure and resistance when given meclofenamate. It is concluded that endogenous vasodilator prostaglandins may contribute to normal, low vascular tone in the pulmonary circulation.

Changes in efferent pulmonary sympathetic nerve activity during systemic hypoxia in anesthetized cats

1995 ◽  
Vol 269 (6) ◽  
pp. R1404-R1409 ◽  
Author(s):  
M. Shirai ◽  
K. Matsukawa ◽  
N. Nishiura ◽  
A. T. Kawaguchi ◽  
I. Ninomiya
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Peripheral Chemoreceptor ◽  
Renal Sympathetic Nerve Activity ◽  
O2 Partial Pressure ◽  
Systemic Hypoxia ◽  
Before And After ◽  
The Central Nervous System ◽  
Pulmonary Arterial

Changes in efferent sympathetic nerve activity to the pulmonary vessels during systemic hypoxia have yet to be elucidated. The purpose of this study was to determine the pulmonary sympathetic nerve activity (PSNA) changes in response to acute systemic hypoxia before and after sinoaortic denervation plus vagotomy in anesthetized cats. The denervation was performed to estimate the central nervous system-mediated peripheral chemoreceptor- and baroreceptor-independent PSNA change. PSNA was recorded from the central end of the cut nerve bundle, which was isolated from the lobar artery supplying the diaphragmatic lobe. Renal sympathetic nerve activity (RSNA) and systemic and pulmonary arterial pressures were also measured simultaneously. The animals were submitted to approximately 3-min periods of graded hypoxia (16, 12, 8, 5, and 3% O2 inhalations). PSNA did not change from normoxia down to an arterial O2 partial pressure (PaO2) of approximately 45 Torr (with 12-21% O2 inhalations). Below this level, PSNA began to increase, and markedly so (approximately 2.5-fold) at a PaO2 of approximately 15 Torr (with 3% O2). The hypoxic PSNA increase was significantly larger than that for RSNA, with a PaO2 of less than approximately 30 Torr (with 3-8% O2). Particularly at a PaO2 of approximately 15 Torr, the magnitude of the PSNA increase was two times greater than that for RSNA. After denervation, the hypoxic PSNA increase was significantly attenuated at a PaO2 of approximately 25 to approximately 45 Torr (with 5-12% O2), but the attenuation was very small; therefore most of the PSNA increase persisted. The hypoxic RSNA increase, in contrast, was mostly abolished after denervation. The data indicate that the neural reflex effect of systemic hypoxia on PSNA is significantly greater than that on RSNA and suggest that the hypoxic PSNA increase is mostly mediated by central mechanisms, whereas that for RSNA is chiefly caused by peripheral chemoreceptors.

Ventilation-induced release of prostaglandinlike material from fetal lungs

1980 ◽  
Vol 238 (3) ◽  
pp. H282-H286 ◽  
Author(s):  
C. W. Leffler ◽  
J. R. Hessler ◽  
N. A. Terragno
Keyword(s):  
Pulmonary Blood Flow ◽  
Inferior Vena ◽  
Fetal Lung ◽  
Inferior Vena Caval ◽  
Pulmonary Vasodilation ◽  
Flow Characterization ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Near Term ◽  
Layer Chromatography

Effects of indomethacin upon ventilation-induced pulmonary vasodilation of fetal goats suggest prostaglandins may be important in perinatal transition of the pulmonary circulation. To further test this hypothesis, left pulmonary arterial and pulmonary venous samples were taken before and after ventilation from anesthetized exteriorized fetal (near-term) goats and sheep utilizing, in different animals, either constant or variable left pulmonary blood flow. Characterization and quantification of prostaglandinlike compounds were accomplished utilizing extraction of acidic lipids, thin-layer chromatography, and tissue cascade bracket bioassay. The primary vascular prostaglandinlike material in both fetal and neonatal animals was PGI2-like (PGI). On passage through the fetal lung, concentrations of prostaglandin I- and E-like compounds decreased considerably. After ventilation and ligation of the umbilical cord, concentrations of both PGE2-like (PGE) and PGI in inferior vena caval blood fell, and there was net production of PGI by the newly ventilated lung. Production of PGI2 by newly ventilated lung could provide an important vasodilator influence that would establish and maintain the low pulmonary vascular resistance that is necessary for successful adaptation to extrauterine life.

Roles of intra- and extracellular carbonic anhydrase in alveolar-capillary CO2 equilibration

1994 ◽  
Vol 77 (2) ◽  
pp. 697-705 ◽  
Author(s):  
T. A. Heming ◽  
E. K. Stabenau ◽  
C. G. Vanoye ◽  
H. Moghadasi ◽  
A. Bidani
Keyword(s):  
Carbonic Anhydrase ◽  
Driving Forces ◽  
Excretion Rate ◽  
Blood Gas ◽  
Gas Barrier ◽  
Arterial Pco2 ◽  
Co2 Diffusion ◽  
Chemical Equilibration ◽  
Co2 Excretion ◽  
Alveolar Capillary

Alveolar-capillary CO2 equilibration involves diffusive equilibration of CO2 across the blood-gas barrier and chemical equilibration of perfusate CO2-HCO-3-H+ reactions. These processes are governed by different, but related, driving forces and conductances. The present study examined the importance of pulmonary carbonic anhydrase (CA) for diffusive and reactive CO2 equilibration in isolated rat lungs. Lungs were perfused with salines containing membrane-impermeant or -permeant inhibitors of CA. Measurements of CO2 excretion rate, equilibrated venous and arterial PCO2 and pH, and postcapillary pH and PCO2 disequilibria were used, together with our previous model of CO2-HCO-3-H+ reactions and transport in saline-perfused capillaries (Bidani et al. J. Appl. Physiol. 55: 75–83, 1983), to compute the relevant driving forces and conductances. Reactive CO2 equilibration was markedly affected by extracellular (vascular) CA activity but not by the activity of intracellular (cytosolic) CA. The driving force for CO2 diffusion was strongly influenced by vascular CA activity. The conductance for CO2 diffusion was independent of CA activity. The minimum conductance for CO2 diffusion was estimated to be 700–800 ml.min-1.Torr-1. The results indicate that extracellular vascular CA activity influences both diffusive and reactive CO2 equilibration. However, cytosolic CA has no detectable role in alveolar-capillary CO2 equilibration.

Effect of inhaled and intravenous acetylcholine on bronchial blood flow in anesthetized sheep

1996 ◽  
Vol 80 (1) ◽  
pp. 341-344 ◽  
Author(s):  
M. Scuri ◽  
V. McCaskill ◽  
A. D. Chediak ◽  
W. M. Abraham ◽  
A. Wanner
Keyword(s):  
Blood Flow ◽  
Systemic Arterial Pressure ◽  
Bronchial Mucosa ◽  
Anatomic Site ◽  
Bronchial Wall ◽  
Mechanically Ventilated ◽  
Lung Resistance ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Increased Blood Flow

The reported effects of cholinergic agonists on bronchial blood flow (Qbr) have been inconsistent. The aim of the present study was to determine whether the inconsistency could be due to the mode of agonist administration (systemic vs. aerosol) or the anatomic site of blood flow in the bronchus (mucosal vs. deep wall). In 10 anesthetized mechanically ventilated adult sheep, we measured Qbr in main bronchi by color-coded microspheres, systemic and pulmonary arterial pressures, cardiac output, and lung resistance (RL) before and after acetylcholine (ACh) administered either as an aerosol (nebulized dose 100 micrograms) or as an intravenous bolus (2 micrograms/kg). Before drug administration, 72% of mean Qbr was distributed to the bronchial mucosa and the remainder was distributed to the deep bronchial wall. For a comparable increase in mean RL (150% for intravenous ACh and 205% for aerosol ACh), mean total Qbr normalized for systemic arterial pressure increased by 291% after intravenous ACh (P < 0.05) and decreased by 9% after aerosol ACh (not significant). Mucosal and deep wall Qbr increased proportionally. Atropine (0.2 microgram/kg) prevented the changes in Qbr and RL after intravenous ACh. Thus intravenous but not aerosol ACh increased blood flow in the mucosa and deep wall of extrapulmonary bronchi. This suggests that the muscarinic receptors mediating vasodilation are more accessible to intravascular than intrabronchial ACh.

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