Effect of changing venoarterial pH difference on in vivo arterial pH

1991 ◽  
Vol 70 (4) ◽  
pp. 1586-1592 ◽  
Author(s):  
E. Takahashi ◽  
E. A. Phillipson
Keyword(s):  
Computer Simulation ◽  
Significant Contribution ◽  
Regression Coefficient ◽  
Glass Electrode ◽  
Pulmonary Capillaries ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Unique Relationship

Plasma pH has been postulated to change slowly in blood leaving the pulmonary capillaries because of the uncatalyzed dehydration of CO2. If so, there could be a difference between in vivo and in vitro arterial pH, the magnitude of which would be dependent on the venoarterial pH difference (v-aDpH). We tested this hypothesis in anesthetized dogs by changing v-aDpH by airway CO2 loading and by comparing arterial pH measured in vivo by a rapidly responding intravascular pH electrode with that measured in vitro by a conventional glass electrode. Using a multiple regression analysis, we found a small but significant contribution of venous pH to in vivo arterial pH, with a regression coefficient of 0.0718 (P less than 0.0001), suggesting a postcapillary increase of in vivo arterial pH. When carbonic anhydrase was inhibited by the administration of acetazolamide, the effect of venous pH on arterial pH was abolished, and a unique relationship between in vivo and in vitro arterial pH was established (regression coefficient 1.02; P greater than 0.05, comparison with unity). These results could be accounted for in a computer simulation of gas exchange among alveolus, plasma, and erythrocyte. We conclude that there exists a small but measurable postcapillary increase in arterial pH.

Neutrophil kinetics in rabbits during infusion of zymosan-activated plasma

1989 ◽  
Vol 67 (1) ◽  
pp. 88-95 ◽  
Author(s):  
C. M. Doerschuk ◽  
M. F. Allard ◽  
J. C. Hogg
Keyword(s):  
Relative Size ◽  
Pulmonary Sequestration ◽  
Blood Velocity ◽  
Pulmonary Capillaries ◽  
In Vitro Activation ◽  
The Complement System ◽  
Kinetics In Vivo ◽  
Neutrophil Kinetics

Complement activation in vivo produces neutropenia and pulmonary sequestration of neutrophils (PMNs) whereas in vitro activation increases PMN adherence and decreases PMN deformability. The present study examined PMN kinetics in vivo to determine if this sequestration was specific to the lung. Venous or arterial injections of radiolabeled PMNs were given to animals receiving infusions of zymosan-activated plasma (ZAP) or saline, and the PMN distribution was evaluated 10 min later. In control animals, the relative size of the marginated and circulating PMN pools was similar after venous or arterial injection and regional PMN retention increased as blood velocity slowed. ZAP infusion produced threefold increases in PMNs within pulmonary capillaries after venous injection and PMN retention was independent of blood velocity. After arterial injection, ZAP infusion produced PMN sequestration in all organs. Rigid (glutaraldehyde-fixed) PMNs injected into control rabbits showed increased lung recoveries similar to those of fresh PMNs injected into ZAP-treated rabbits. We conclude that activation of the complement system causes PMN sequestration in both the pulmonary and the systemic microvasculature and that the decrease in PMN deformability that occurs with activation of the PMN may be important in the genesis of PMN sequestration.

In vivo characterization of vasocontractile activities in erythrocytes

1983 ◽  
Vol 58 (3) ◽  
pp. 356-361 ◽  
Author(s):  
Michael P. McIlhany ◽  
Lydia M. Johns ◽  
Thomas Leipzig ◽  
Nicholas J. Patronas ◽  
Frederick D. Brown ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Content Type ◽  
Control Value ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Chronic Cerebral Vasospasm ◽  
In Vivo Characterization

✓ Partially purified protein from washed and artificially hemolyzed erythrocytes, known to cause significant contractions of isolated canine cerebral vessels in vitro, was injected into the cisterna magna of intact anesthetized dogs. Cerebral blood flow, measured by the xenon-133 washout technique, decreased from a control value of 49.5 ± 1.17 ml/100 gm/min to an experimental value of 34.1 ± 1.65 ml/100 gm/min at 2 hours. Cerebral vascular resistance rose from a control value of 2.05 ± 0.17 PRU (peripheral resistance units) to an experimental value of 2.91 ± 0.25 PRU at 2 hours. Mean arterial blood pressure, heart rate, intracranial pressure, and cerebral perfusion pressure remained stable. Cardiac output also fell significantly (in 2-hour control animals it was 2.89 ± 0.37 liter/min, and in 2-hour experimental animals 1.43 ± 0.13 liter/min) and peripheral vascular resistance rose. These changes were evident by 10 minutes after the cisternal injection of the hemolysate protein, and remained for the duration of the 2-hour monitoring period. Serial vertebrobasilar angiograms demonstrated marked narrowing of the intracranial basilar artery when compared to control values. The narrowing persisted for several days in most animals, and tended to increase with time. Relaxation occurred by the 10th through the 14th day. The authors conclude that this experimental preparation may be a useful model for both in vitro and in vivo investigation of chronic cerebral vasospasm.

In vivo and in vitro correlation of trachealis muscle contraction in dogs

1992 ◽  
Vol 73 (4) ◽  
pp. 1486-1493 ◽  
Author(s):  
M. Okazawa ◽  
K. Ishida ◽  
J. Road ◽  
R. R. Schellenberg ◽  
P. D. Pare
Keyword(s):  
Isometric Force ◽  
Optimal Length ◽  
Linear Elastic ◽  
Elastic Load ◽  
Muscle Shortening ◽  
Anesthetized Dogs ◽  
Trachealis Muscle ◽  
Isotonic Shortening

Maximal trachealis muscle shortening in vivo was compared with that in vitro in seven anesthetized dogs. In addition, the effect of graded elastic loads on the muscle was evaluated in vitro. In vivo trachealis muscle shortening, as measured using sonomicrometry, revealed maximal active shortening to be 28.8 +/- 11.7% (SD) of initial length. Trachealis muscle preparations from the same animals were studied in vitro to evaluate isometric force generation, isotonic shortening, and the effect of applying linear elastic loads to the trachealis muscle during contraction from optimal length. Maximal isotonic shortening was 66.8 +/- 8.4% of optimal length in vitro. Increasing elastic loads decreased active shortening and velocity of shortening in vitro in a hyperbolic manner. The elastic load required to decrease in vitro shortening to the extent of the shortening observed in vivo was similar to the estimated load provided by the tracheal cartilage. We conclude that decreased active shortening in vivo is primarily due to the elastic afterload provided by cartilage.

The Hemoglobin-Deficit Mouse: Analysis of Phenotype and Hematopoiesis in the Transplant Model

Blood ◽  
1997 ◽  
Vol 90 (5) ◽  
pp. 2062-2067 ◽  
Author(s):  
Michael L. Bloom ◽  
Karen L. Simon-Stoos
Keyword(s):  
Autosomal Recessive ◽  
Significant Contribution ◽  
Erythroid Differentiation ◽  
Microcytic Anemia ◽  
Mouse Mutant ◽  
In Vivo Assays ◽  
Transplant Model ◽  
Autosomal Recessive Manner

Abstract The mouse mutant hemoglobin deficit (gene symbol hbd ) is characterized by a severe microcytic anemia that is inherited in an autosomal-recessive manner. To assess the mutation's effect on hematopoiesis, unfractionated bone marrow (BM) from either a mutant C57BL6/J-hbd/hbd, Gpi1b/Gpi1b (phenotype symbol HBD), or normal C57BL6/J -+hbd/+hbd, Gpi1b/Gpi1b mouse was injected intravenously into irradiated congenic C57BL6/J-+hbd/+hbd, Gpi1a/Gpi1a, Igha/Igha, Thy1a/Thy1a mice. The congenic recipients of mutant or normal marrow obtained complete red blood cell (RBC) and leukocyte reconstitution, with the exception of one recipient of HBD marrow. After 24 weeks posttransplantation, the normal recipients of HBD marrow obtained a microcytic anemia similar to the donor. These results suggest that the HBD phenotype is caused by a BM defect. We observed that the erythroid lineage derived from donor HBD marrow repopulated more slowly than the normal marrow at 4 weeks posttransplantation. To determine if this difference was a result of an erythropoietic defect, competitive repopulation was performed using either mutant or normal marrow competed against normal congenic marrow. For the erythroid lineage, no significant contribution from HBD marrow was observed. To assess if the RBC block was based on a deficiency of myeloid progenitors, both in vitro and in vivo assays were performed: absolute numbers of bone progenitors were increased, suggesting that the defect results in a late block to erythroid differentiation.

CO binding to hemoglobin and myoglobin in equilibrium with a gas phase of low PO2 value

1988 ◽  
Vol 65 (6) ◽  
pp. 2513-2517 ◽  
Author(s):  
A. Agostoni ◽  
M. Perrella ◽  
L. Sabbioneda ◽  
U. Zoni
Keyword(s):  
Computer Simulation ◽  
Gas Phase ◽  
Qualitative Agreement ◽  
Significant Proportion ◽  
In Vitro System

The aim of this paper was to measure the binding of CO to myoglobin and hemoglobin at various PO2 values. For this purpose we have studied an "in vitro" system made up of solutions of hemoglobin and myoglobin equilibrated in two connected tonometers with the same gas phase of various PO2 and PCO. The results indicate that a significant proportion of CO is released by hemoglobin and binds myoglobin at low PO2 values (approximately 2-3 Torr), in qualitative agreement with the predictions of a previous computer simulation of the "in vivo" system.

Computer simulation of neutrophil transit through the pulmonary capillary bed

1993 ◽  
Vol 74 (4) ◽  
pp. 1647-1652 ◽  
Author(s):  
C. C. Hanger ◽  
W. W. Wagner ◽  
S. J. Janke ◽  
T. C. Lloyd ◽  
R. L. Capen
Keyword(s):  
Computer Simulation ◽  
Computer Model ◽  
Pulmonary Circulation ◽  
Cell Deformation ◽  
In Vivo Microscopy ◽  
Pulmonary Capillaries ◽  
Pulmonary Capillary ◽  
Capillary Bed ◽  
Diameter Distributions

One-half of the neutrophils that enter the pulmonary circulation become temporarily trapped in capillaries. The neutrophils that are impeded make complete stops between free-flowing movements. These observations, based on in vivo microscopy, suggest that pulmonary margination is caused by neutrophils being impeded at focal sites in the capillary bed. To investigate the frequency with which impeding sites had to occur in the pulmonary capillaries to trap one-half of the circulating neutrophils, we developed a computer model to simulate neutrophils encountering discrete obstructions in a capillary-like network. Surprisingly, if only 1% of the capillaries in the network acted as traps, one-half of the neutrophils stopped at least once. The trapping ability of a given percentage of obstructions was independent both of the geometry of the network was whether the obstructions occurred in the segments or junctions. To simulate neutrophil transit more realistically, both neutrophil and capillary diameters were randomly selected from published diameter distributions. Every neutrophil was trapped multiple times by this model, suggesting that cell deformation contributes importantly to neutrophil passage through the pulmonary capillary bed.

Presynaptic inhibition of canine renal adrenergic nerves by acetylcholine in vivo

1979 ◽  
Vol 237 (3) ◽  
pp. H326-H331
Author(s):  
N. W. Robie
Keyword(s):  
Nerve Stimulation ◽  
Neurotransmitter Release ◽  
Intact Animal ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Renal Vasculature ◽  
Anesthetized Dogs ◽  
Renal Sympathetic

Experiments were performed in anesthetized dogs to determine whether previously reported in vitro inhibition of sympathetic neurotransmitter release by acetylcholine could be demonstrated in the renal vasculature of the intact animal. Vasoconstrictor responses to renal sympathetic nerve stimulation at varying frequencies were compared to intra-arterial injections of norepinephrine before and during intra-arterial infusions of acetylcholine, 2.5--80 micrograms/min. The vasoconstrictor responses to nerve stimulation were inhibited to a greater extent than were responses to norepinephrine during infusions of acetylcholine. The inhibitory effects of acetylcholine on nerve stimulation were dose and frequency dependent. The inhibition was blocked by atropine but not altered by physostigmine. Changes in renal blood flow per se did not contribute to the inhibitory effect of acetylcholine, since another vasodilator agent, sodium acetate, did not affect the nerve stimulation-norepinephrine vasocontriction relationship. Thus, acetylcholine produced inhibition of in vivo renal sympathetic vasoconstrictor responses, and the receptor involved appears to be muscarinic.

Adenosine regulates blood flow and glucose uptake in adipose tissue of dogs

1986 ◽  
Vol 250 (6) ◽  
pp. H1127-H1135
Author(s):  
S. E. Martin ◽  
E. L. Bockman
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
Indirect Effect ◽  
Glycerol Release ◽  
Anesthetized Dogs ◽  
Tissue Contents ◽  
Fat Pads

Intravenous norepinephrine increases glycerol release and blood flow in adipose tissue. The vasodilation may be an indirect effect of norepinephrine through the production of adenosine. Adenosine increases glucose uptake and inhibits lipolysis in vitro. To test whether adenosine regulates blood flow and/or metabolism in vivo, adenosine deaminase (ADA) was infused intra-arterially into the inguinal fat pads of anesthetized dogs. In unstimulated tissues, ADA (n = 7) significantly increased vascular resistance and significantly decreased glucose uptake compared with the effects of a control (boiled deaminase, n = 6) infusion. ADA completely blocked the norepinephrine-induced vasodilation (n = 6). No potentiation of basal or catecholamine-stimulated lipolysis was observed with ADA. The presence of ADA in the interstitial space was verified by analysis of lymph effluents. Interstitial levels of ADA were inversely correlated with the tissue contents of adenosine. These data support the hypothesis that adenosine is a regulator of blood flow in basal and stimulated adipose tissue. Adenosine also appears to regulate glucose uptake, but not lipolysis, in vivo.

Catecholamine release: mechanism of mercury-induced vascular smooth muscle contraction

1975 ◽  
Vol 229 (1) ◽  
pp. 8-12 ◽  
Author(s):  
HS Solomon ◽  
NK Hollenberg
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Electromagnetic Flowmeter ◽  
Smooth Muscle Contraction ◽  
Release Mechanism ◽  
Adrenergic Blockade ◽  
Mercuric Ion ◽  
Anesthetized Dogs

The mechanism by which mercuric ion (HgCl2) induces contraction of vascular smooth muscle was defined in the kidney of anesthetized dogs and in rabbit aortic strips. In vivo, HgCl2 injected into the renal artery induced a dose-related reduction in renal blood flow (electromagnetic flowmeter) and glomerular filtration rate (creatinine clearance). An intra-arterial infusion of phenoxybenzamine (POB) significantly reduced the vascular response to HgCl2 (P less than 0.001). In vitro, alpha-adrenergic blockade with phentolamine and POB prevented mercury-induced contraction, whereas agents that block serotonin, histamine, acetylcholine, and angiotensin did not do so. Norepinephrine receptor "protection" from phenoxybenzamine blockade sustained the response to HgCl2. Reserpine pretreatment produced a parallel reduction in the response of the aorta to tyramine and mercury. The results are consistent with an indirect action of mercuric ion via release of endogenous catecholamines.

Nitric oxide as a putative nonadrenergic noncholinergic inhibitory transmitter in the canine pylorus in vivo

1992 ◽  
Vol 262 (4) ◽  
pp. G695-G702 ◽  
Author(s):  
H. D. Allescher ◽  
G. Tougas ◽  
P. Vergara ◽  
S. Lu ◽  
E. E. Daniel
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Vagal Stimulation ◽  
Inhibitory Effect ◽  
Field Stimulation ◽  
Neural Inhibition ◽  
Anesthetized Dogs ◽  
Inhibitory Transmitter

Antropyloroduodenal motility was recorded in seven anesthetized dogs to assess the role of nitric oxide and L-arginine metabolites in nonadrenergic noncholinergic (NANC) mediation of pyloric relaxation. Pyloric activity induced by duodenal field stimulation was inhibited by antral field stimulation and electrical vagal stimulation. Intra-arterial NG-L-arginine-methyl-ester (L-NAME) reduced the inhibition from antral or vagal stimulation (P less than 0.05). Intravenous infusion of L-NAME also blocked the inhibitory effect of vagal and antral stimulation but left the tetrodotoxin-insensitive action of intra-arterial vasoactive intestinal peptide (VIP) and sodium nitroprusside unchanged. L-Arginine reversed the effect of L-NAME whereas D-arginine did not. L-NAME enhanced pyloric contractions to intra-arterial acetylcholine. The NANC inhibition of the substance P-stimulated pyloric response in vitro was blocked by L-NAME and reversed by addition of L-arginine. Sodium nitroprusside was effective as a relaxant in vitro but VIP was not. These data suggest that metabolites of L-arginine mediate neural inhibition of canine pyloric motor activity.

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