The Generation of Kinins in the Blood of Dogs during Hypotension Due to Haemorrhage

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Venous Blood ◽  
Systemic Circulation ◽  
Substantial Effect ◽  
Mixed Venous Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Organ Technique

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.

Static filling pressure in patients during induced ventricular fibrillation

2003 ◽  
Vol 285 (6) ◽  
pp. H2510-H2515 ◽  
Author(s):  
J. D. Schipke ◽  
G. Heusch ◽  
A. P. Sanii ◽  
E. Gams ◽  
J. Winter
Keyword(s):  
Blood Pressure ◽  
Time Constant ◽  
Pressure Difference ◽  
Venous Pressure ◽  
Venous Blood ◽  
Central Venous ◽  
Equilibrium Pressure ◽  
Arterial Blood ◽  
Cardiac Pumping ◽  
Blood Pressure Difference

The static pressure resulting after the cessation of flow is thought to reflect the filling of the cardiovascular system. In the past, static filling pressures or mean circulatory filling pressures have only been reported in experimental animals and in human corpses, respectively. We investigated arterial and central venous pressures in supine, anesthetized humans with longer fibrillation/defibrillation sequences (FDSs) during cardioverter/defibrillator implantation. In 82 patients, the average number of FDSs was 4 ± 2 (mean ± SD), and their duration was 13 ± 2 s. In a total of 323 FDSs, arterial blood pressure decreased with a time constant of 2.9 ± 1.0 s from 77.5 ± 34.4 to 24.2 ± 5.3 mmHg. Central venous pressure increased with a time constant of 3.6 ± 1.3 s from 7.5 ± 5.2 to 11.0 ± 5.4 mmHg (36 points, 141 FDS). The average arteriocentral venous blood pressure difference remained at 13.2 ± 6.2 mmHg. Although it slowly decreased, the pressure difference persisted even with FDSs lasting 20 s. Lack of true equilibrium pressure could possibly be due to a waterfall mechanism. However, waterfalls were identified neither between the left ventricle and large arteries nor at the level of the diaphragm in supine patients. We therefore suggest that static filling pressures/mean circulatory pressures can only be directly assessed if the time after termination of cardiac pumping is adequate, i.e., >20 s. For humans, such times are beyond ethical options.

Hydrops fetalis in nephrectomized fetal lambs infused with angiotensin I

1994 ◽  
Vol 267 (6) ◽  
pp. R1522-R1527 ◽  
Author(s):  
J. J. Faber ◽  
D. F. Anderson
Keyword(s):  
Blood Pressure ◽  
Venous Pressure ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Hydrops Fetalis ◽  
Angiotensin I ◽  
Fetal Sheep ◽  
Gradual Rise ◽  
Arterial Blood ◽  
Excess Water

Nine bilaterally nephrectomized fetal sheep were infused for 6 days with angiotensin I in sterile water, and five nephrectomized fetal sheep were infused for 6 days with water alone. Total dose of angiotensin was 13.8 +/- 8.6 (SD) mg/kg fetal dry wt, and the total volumes of infused water were 303 +/- 201 and 423 +/- 164 ml, respectively. Of the fetuses infused with angiotensin I, one was of normal appearance, two showed moderate hydrops fetalis, and the remaining fetuses were grossly hydropic. All water-infused fetuses were normal. Their wet-to-dry weight ratios were 7.98 and 6.36 (P < 0.015), representing a 25% of normal body weight excess of water in the angiotensin I-infused fetuses. Six days of angiotensin I infusion caused a gradual rise in fetal arterial blood pressure from 37 +/- 15 to 81 +/- 15 mmHg (P < 0.05) and a gradual rise in venous blood pressure from 2.7 +/- 1.0 to 10.5 +/- 1.7 mmHg (P < 0.05). It was concluded that the fetal edema was due to the elevation in venous pressure. Plasma concentrations of Na+, K+, Cl-, HCO3-, total alpha-amino acids, fructose, glucose, and lactate in the fetus and the ewe did not identify an osmotically active solute responsible for the transplacental attraction of excess water into the conceptus, and the mechanism that attracted this excess water across the placenta remains unclear.

On venous pressure in arterial and "isolated" venous hypertension

1927 ◽  
Vol 23 (6-7) ◽  
pp. 632-640
Author(s):  
P. N. Nikolaev
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Venous Blood ◽  
Venous Hypertension ◽  
Clinical Use ◽  
Arterial Blood

If the determination of arterial blood pressure has entered clinical use as an indispensable method for the recognition and interpretation of various diseases, the same cannot be said about the determination of venous blood pressure. Only the first steps are still being taken.

scholarly journals Outflow occlusion for circulatory arrest in dogs

2009 ◽  
Vol 29 (2) ◽  
pp. 137-142
Author(s):  
James N.B.M. de Andrade ◽  
Angelo J. Stopiglia ◽  
Denise T. Fantoni ◽  
Maria C. Abduch ◽  
Marcia Kahvegian
Keyword(s):  
Circulatory Arrest ◽  
Venous Pressure ◽  
Venous Blood ◽  
Pulmonary Trunk ◽  
Mixed Venous Blood ◽  
Stroke Work ◽  
Arterial Blood ◽  
Group I ◽  
Group Ii ◽  
Mixed Venous

The purpose of this study was to evaluate the possibility of producing circulatory arrest by occlusion of the pulmonary trunk as an alternative to the venous inflow occlusion through the left hemithorax. Eight healthy mongrel dogs were divided in two groups. Group I underwent 4 minutes of outflow occlusion and Group II was submitted to 8 minutes of circulatory arrest. Outflow occlusion was performed through left thoracotomy and pericardiotomy by passing a Rumel tourniquet around the pulmonary trunk. Physical examination, electrocardiography, echocardiography, blood gas analyses, hemodynamic, and oxygen transport variables were obtained before and after the procedure. The dogs from Group I did not have any clinical, electrocardiographic, echocardiographic, or hemo-dynamic abnormalities after anesthetic recover. In the Group II, only one dog survived, which had no clinical, electrocardiographic, or echocardiographic abnormalities. In this last dog, just after releasing the occlusion, it was detected increases in the following parameters: heart rate (HR), systolic, diastolic and mean arterial blood pressure (SAP; DAP; MAP), pulmonary artery pressure (PAP), pulmonary wedge pressure (PWP), central venous pressure (CVP), cardiac output (CO), systolic index (SI), cardiac index (CI), left and right ventricular stroke work (LVSW; RVSW), oxygen delivery index (DO2), oxygen consumption index (VO2), and oxygen extraction (O2 ext). Moreover, the oxygen content of arterial and mixed venous blood (CaO2; CvO2), and the arterial and mixed venous partial pressure of oxygen (PaO2; PvO2) were decreased 5 minutes after circulatory arrest. Outflow occlusion is a feasible surgical procedure for period of 4 minutes of circulatory arrest.

scholarly journals Respiratory and cardiovascular responses of the exercising chicken to spinal cord cooling at different ambient temperatures. I. Cardiovascular responses and blood gases

1985 ◽  
Vol 114 (1) ◽  
pp. 415-426
Author(s):  
G. M. Barnas ◽  
M. Gleeson ◽  
W. Rautenberg
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Treadmill Exercise ◽  
Venous Blood ◽  
Blood Gases ◽  
Cardiovascular Responses ◽  
Mixed Venous Blood ◽  
Ambient Temperatures ◽  
Arterial Blood ◽  
Exercise Period

We measured oxygen consumption (VO2), heart rate (HR), stroke volume (SV), cardiac output (CO) and mean arterial blood pressure (MBPa) of chickens during 15 min treadmill exercise at 0.5 ms-1 and 0.8 ms-1 at thermoneutral (23 degrees C), low (9 degrees C) and high (34 degrees C) ambient temperature (Ta); the vertebral canal was cooled to 34 degrees C during the middle 5 min of each exercise period. PO2, PCO2, pH and oxygen content (CO2) of the arterial and mixed venous blood were also measured. VO2 during exercise was not significantly affected by Ta. Spinal cord cooling produced definite increases in VO2, CO and SV during 0.5 ms-1 exercise at 9 degrees C; otherwise, effects of spinal cord cooling were not significant. HR, SV and CO were all linearly related to VO2; these relationships were unaffected by spinal cord cooling or Ta. Blood pressure did not increase during exercise. PaCO2 and P-vCO2 did not increase significantly during exercise. The arterial-venous CO2 difference was increased by exercise only at 34 degrees C. The chickens generally hyperventilated at 34 degrees C Ta compared to the other Ta values. No consistent effect on blood gases or on pH and CO2 of the blood could be attributed to spinal cord cooling.

Carbon Dioxide Equilibration in Canine Lungs during Rebreathing and Acute Alkalosis

1979 ◽  
Vol 57 (5) ◽  
pp. 385-388 ◽  
Author(s):  
R. D. Latimer ◽  
G. Laszlo
Keyword(s):  
Whole Blood ◽  
Base Excess ◽  
Venous Blood ◽  
Main Pulmonary Artery ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Significant Difference ◽  
Venous Pco2 ◽  
Pulmonary Arterial ◽  
Gas Pressures

1. The left lower lobe of the lungs of six anaesthetized dogs were isolated by the introduction of a bronchial cannula at thoracotomy. Catheters were introduced into the main pulmonary artery and a vein draining the isolated lobe. 2. Blood-gas pressures and pH were measured across the isolated lobe and compared with gas pressures in alveolar samples from the lobe. 3. When the isolated lobe was allowed to reach gaseous equilibrium with pulmonary arterial blood for 30 min, there was no significant difference between alveolar and pulmonary venous Pco2. Mean values of whole-blood base excess were similar in pulmonary arterial and pulmonary venous blood. 4. After injection of 20 ml of 8·4% sodium bicarbonate solution into a peripheral vein, Pco2, pH and plasma bicarbonate concentrations rose in the mixed venous blood. There was no change of whole-blood base excess across the lung, indicating that HCO−3, as distinct from dissolved CO2, did not enter lung tissue in measurable amounts. 5. No systematic alveolar—pulmonary venous Pco2 differences were demonstrated in this preparation other than those explicable by maldistribution of lobar blood flow.

Respiratory measurements of cardiac output: from elegant idea to useful test

2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo
Keyword(s):  
Cardiac Output ◽  
Human Subjects ◽  
Venous Blood ◽  
The Body ◽  
Mixed Venous Blood ◽  
Indirect Determination ◽  
Arterial Blood ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Mixed Venous

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.

Insights into Dahl salt-sensitive hypertension revealed by temporal patterns of renal medullary gene expression

2003 ◽  
Vol 12 (3) ◽  
pp. 229-237 ◽  
Author(s):  
Mingyu Liang ◽  
Baozhi Yuan ◽  
Elizabeth Rute ◽  
Andrew S. Greene ◽  
Michael Olivier ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Injury ◽  
Time Course ◽  
Expression Patterns ◽  
Renal Medulla ◽  
Temporal Patterns ◽  
Reference Distribution ◽  
Arterial Blood ◽  
Renal Tubular ◽  
Salt Sensitive Hypertension

Dahl salt-sensitive SS and consomic, salt-resistant SS-13BN/Mcw rats possess a highly similar genetic background but exhibit substantial differences in blood pressure salt sensitivity. We used cDNA microarrays to examine sequential changes of mRNA expression of ∼2,000 currently known rat genes in the renal medulla (a tissue critical for long-term blood pressure regulation) in SS and SS-13BN/Mcw rats in response to a high-salt diet (16 h, 3 days, or 2 wk). Differentially expressed genes in each between-group comparison were identified based on a threshold determined experimentally using a reference distribution that was constructed by comparing rats within the same group. A difference analysis of 54 microarrays identified 50 genes that exhibited the most distinct temporal patterns of expression between SS and SS-13BN/Mcw rats over the entire time course. Thirty of these genes could be linked to the regulation of arterial blood pressure or renal injury based on their known involvement in functional pathways such as renal tubular transport, metabolism of vasoactive substances, extracellular matrix formation, and apoptosis. Importantly, the majority of the 30 genes exhibited temporal expression patterns that would be expected to lower arterial pressure and reduce renal injury in SS-13BN/Mcw compared with SS rats. The phenotypic impact of the other 20 genes was less clear. These 50 genes are widely distributed on chromosome 13 and several other chromosomes. This suggested that primary genetic defects, although important, are unlikely to be solely responsible for the full manifestation of this type of hypertension and associated injury phenotypes. In summary, the results of this study identified a number of pathways potentially important for the amelioration of hypertension and renal injury in SS-13BN/Mcw rats, and these results generated a series of testable hypotheses related to the role of the renal medulla in the complex mechanism of salt-sensitive hypertension.

Lactate, pyruvate, glucose, and free fatty acid in mixed venous and arterial blood

1963 ◽  
Vol 18 (5) ◽  
pp. 933-936 ◽  
Author(s):  
P. Harris ◽  
T. Bailey ◽  
M. Bateman ◽  
M. G. Fitzgerald ◽  
J. Gloster ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cardiac Output ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Venous Blood ◽  
Average Concentration ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Acquired Heart Disease ◽  
Mixed Venous

The concentrations of lactic acid, pyruvic acid, glucose, and free fatty acids have been measured simultaneously in the blood from the pulmonary and brachial arteries at rest and during exercise in a group of patients with acquired heart disease. The arteriovenous differences in the concentration of lactate, pyruvate, and free fatty acid were such as could be attributed to chance. The average concentration of glucose was slightly but significantly higher in the brachial arterial blood than in the mixed venous blood. cardiac output; lung metabolism; exercise Submitted on January 15, 1963

Sign in / Sign up

Export Citation Format

Share Document