Influence of arterial oxygen tension on coronary vasodilator action of nitroglycerine

1969 ◽  
Vol 47 (1) ◽  
pp. 93-98 ◽  
Author(s):  
R. F. P. Cronin ◽  
A. Kovacs
Keyword(s):  
Vascular Resistance ◽  
Venous Blood ◽  
Arterial Oxygen Tension ◽  
Coronary Perfusion Pressure ◽  
Arterial Oxygen ◽  
Myocardial Segment ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Arterial Blood ◽  
Vasodilator Action

In 11 anesthetized open-chest dogs, controlled perfusion of the left circumflex coronary artery was accomplished by shunting blood from the femoral artery and vein via a peristaltic pump. The pO2 of the perfusing blood was altered by changing the proportion of arterial and venous blood reaching the inflow side of the pump. Coronary perfusion pressure (CPP) was measured during stepwise reduction in the left circumflex coronary flow (LCF) over the range 120–10 cc/min. Resistance to coronary blood flowin the perfused myocardial segment was calculated as the ratio CPP/LCF and plotted against flow. Resistance-flow curves for the perfused coronary segments were obtained at pO2 values ranging between 95 and 25 mm Hg. Lowering the pO2 of the perfusing blood caused a reduction in coronary vascular resistance (CVR) in the perfused segment. When nitroglycerine was infused in a dosage of 3–6 μg/kg per minute, arterial blood pressure and heart rate were unaltered but CVR was reduced. The reduction in CVR was inversely proportional to the pO2 of the perfusing blood, the maximal vasodilator effect being observed at pO2 > 60 mm Hg. Nitroglycerine caused no significant change in coronary vascular resistance at pO2 < 39 mm Hg and did not prevent or delay the appearance of excess lactate in the coronary venous blood.

Dynamics of myocardial oxygen consumption and coronary vascular resistance

1977 ◽  
Vol 233 (1) ◽  
pp. H34-H43 ◽  
Author(s):  
F. L. Belloni ◽  
H. V. Sparks
Keyword(s):  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Coronary Sinus ◽  
Myocardial Oxygen Consumption ◽  
Time Course ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Constant Flow

Coronary vascular resistance may be regulated in part by substances whose concentrations are determined by or reflect the rate of myocardial oxygen consumption (e.g., adenosine, vessel wall PO2). We tested this hypothesis by comparing the time course of changes in myocardial oxygen consumption and coronary vascular resistance following 20 beat/min changes in heart rate. Main left coronary arteries of in situ dog hearts were perfused with blood at constant flow. Coronary sinus O2 content was monitored continuously with a densitometer and reflected the time course of changes in oxygen consumption and also the effects of vascular transit between tissue and the coronary sinus. These transit effects were estimated from dye transit curves and added to the time course of changes in coronary perfusion pressure which was proportional to coronary vascular resistance at constant flow. Coronary sinus O2 content changes preceded the adjusted time course of vascular resistance. This supports the hypothesis that coronary vascular resistance is regulated in part by factors closely linked to oxidative metabolism.

scholarly journals Increases in coronary vascular resistance related to high arterial oxygen tension in dogs.

1980 ◽  
Vol 44 (9) ◽  
pp. 749-754 ◽  
Author(s):  
KINJI ISHIKAWA ◽  
KEN KANAMASA ◽  
TETSU YAMAKADO ◽  
YASUYUKI KOHASHI ◽  
ARATA KATO ◽  
...  
Keyword(s):  
Oxygen Tension ◽  
Vascular Resistance ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Coronary Vascular Resistance

Canine coronary vasodepressor responses to hypoxia are abolished by 8-phenyltheophylline

1989 ◽  
Vol 257 (4) ◽  
pp. H1043-H1048 ◽  
Author(s):  
H. M. Wei ◽  
Y. H. Kang ◽  
G. F. Merrill
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Systemic Hypoxia ◽  
Dose Dependent ◽  
Vasodepressor Response

Anesthetized randomsource mongrel dogs of either sex were instrumented to investigate the effects of 8-phenyltheophylline on changes in coronary perfusion pressure caused by systemic hypoxia under conditions of controlled constant coronary blood flow. In the absence of 8-phenyltheophylline, coronary perfusion pressure decreased from 98 +/- 10 to 69 +/- 4 mmHg (P less than 0.05) at the end of 3 min of systemic hypoxia [arterial partial pressure of oxygen (PO2) = 23 +/- 2 mmHg]. Calculated coronary vascular resistance decreased concomitantly by 30 +/- 5% (P less than 0.05). In the presence of continuously infused 8-phenyltheophylline, equally severe hypoxia increased coronary perfusion pressure from 112 +/- 10 to 129 +/- 13 mmHg (P less than 0.05). Under these conditions, calculated coronary vascular resistance increased 14 +/- 3% (P less than 0.05). Dose-dependent attenuation of the coronary vasodilator response to exogenous adenosine under normoxic conditions was produced by 8-phenyltheophylline. In vehicle-treated dogs, repeat bolus injections of adenosine consistently lowered coronary perfusion pressure by 45 +/- 15%. The vasodepressor response did not vary from one injection to the next. These data demonstrate that under conditions of controlled constant coronary blood flow, treatment with 8-phenytheophylline abolishes coronary vasodilation caused by systemic hypoxia.

Effect of cardiac cooling on coronary vascular resistance in normothermic dogs

1960 ◽  
Vol 199 (1) ◽  
pp. 163-166 ◽  
Author(s):  
Robert A. Hardin ◽  
Jerry B. Scott ◽  
Francis J. Haddy
Keyword(s):  
Vascular Resistance ◽  
Control Level ◽  
Coronary Perfusion Pressure ◽  
Effect Of Temperature ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
External Work ◽  
Cold Blood ◽  
Warm Blood ◽  
Arch Of The Aorta

Coronary vascular resistance was observed while the temperature of the heart was lowered to 25°C. The heart was beating but performing no external work. This was accomplished by shunting the blood around the heart and lungs, clamping the arch of the aorta and perfusing cold or warm blood at a constant rate into the ascending aorta. In most instances, coronary perfusion pressure decreased during perfusion with cold blood. The pressure suddenly fell further as perfusion with warm blood was restarted and then gradually returned to the control level. The heart spent an increased proportion of time in systole during perfusion with cold blood. These findings indicate that local cardiac cooling by the method utilized causes active dilatation of the coronary vascular bed of the dog. This dilatation may result from some direct effect of temperature change upon vascular smooth muscle.

Action of nicotine on coronary vascular resistance in dogs

1962 ◽  
Vol 203 (4) ◽  
pp. 621-625 ◽  
Author(s):  
Floyd E. Leaders ◽  
J. P. Long
Keyword(s):  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Force Of Contraction ◽  
Parasympathetic Nerve ◽  
Intracoronary Administration ◽  
Chromaffin Tissue

The effect of nicotine, norepinephrine, acetylcholine, and sympathetic and parasympathetic nerve stimulation on perfusion pressure in the left descending coronary artery has been evaluated. Nicotine administered intra-arterially produced an increase in coronary vascular resistance as indicated by an increase in coronary perfusion pressure. It was concluded that this results from sympathetic nervous system activity or release of catecholamines from chromaffin tissue. Ganglia or ganglion-like structures are apparently involved. Other drugs and procedures that were used in attempting to localize the site of nicotine action are discussed. The experimental procedures were also used with preparations that measured myocardial force of contraction. The contractile force of the myocardium, as well as coronary perfusion pressure, was increased with intracoronary administration of nicotine or norepinephrine and sympathetic nerve stimulation. Coronary vascular resistance was increased by these agents and procedures. Vagal nerve stimulation or intracoronary administration of acetylcholine usually decreased the force of contraction and coronary perfusion pressure.

Abstract P22: An Impedance Threshold Device Combined with an Automated Active Compression Decompression CPR Device (LUCAS) Improves the Chances For Survival in Pigs in Cardiac Arrest

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Timothy R Matsuura ◽  
Scott H McKnite ◽  
Anja K Metzger ◽  
Demetris Yannopoulos ◽  
Tom P Aufderheide ◽  
...  
Keyword(s):  
Venous Blood ◽  
Blood Gases ◽  
Intrathoracic Pressure ◽  
Organ Damage ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Adverse Outcomes ◽  
Coronary Perfusion ◽  
Threshold Device ◽  
Impedance Threshold Device

Background: By lowering intrathoracic pressure during the chest recoil phase of CPR, the impedance threshold device (ITD) increases circulation and the rate of return of spontaneous circulation (ROSC). This study evaluated the ITD combined with a new automated CPR device, the US version of the LUCAS, that compresses the chest and then pulls upwards with a 3 lb force. Methods and Results: After 6 min of untreated ventricular fibrillation, anesthetized female pigs (40.0±0.7 kg) were randomized to 6 min of CPR (100 compressions/min with LUCAS and ventilation: 1.0 FiO2, tidal volume of 10ml/kg, rate 12/min) with an active (−10 cm H2O resistance) (n=12) or sham ITD (n=12), and then shocked once with 120 joules of direct current. Epinephrine (0.04 mg/kg) and more CPR and shocks were used if ROSC was not achieved. Results (in mmHg) after 6 min of CPR with an active vs. sham ITD were: coronary perfusion pressure (PP) 20.8±1.2 vs. 21.0±0.9 (p=0.94); cerebral PP 8.8±1.0 vs. 10.0±0.9 (p=0.62); and end tidal CO2 38.1±1.5 and 37.1±1.3 (p=0.61). Peak and mean carotid artery blood flow (ml/min) was 323.9±15.2 vs. 256.6±21.1 (p=0.17) and 95.3±5.4 vs. 77.0±6.0 (p=0.22) with an active vs. sham ITD, respectively. Mean endotracheal pressures (mmHg) during chest recoil with an active vs. sham ITD were −2.0±0.5 vs. −0.2±0.2 (p<0.01). Arterial and venous blood gases were similar after 6 min of CPR between groups. ROSC, the primary survival endpoint for comparing the active vs. sham ITD, was 7/12 vs. 2/12 after 1 shock (p= 0.09), 12/12 vs. 5/12 after 2 shocks (p<0.01), and 12/12 vs. 7/12 after 3 shocks (p=0.04). With up to 14 shocks, 10/12 sham animals had a ROSC. All animals with ROSC lived for 30 min. There was no evidence of pulmonary edema or organ damage on autopsy with either ITD. Conclusions: After 6 min of CPR, LUCAS and active ITD resulted in lower mean airway pressures during chest recoil versus controls but hemodynamic findings were similar. However, ROSC was significantly easier to achieve with an active ITD; with up to 3 shocks twice as many animals were resuscitated with an active ITD. This benefit is most likely explained by carotid blood flows that trended higher with the active ITD. These positive findings and lack of any adverse outcomes support the safety and efficacy of this device combination.

ARTERIAL BLOOD GAS AND ACID-BASE DISORDERS IN INFANTS AND CHILDREN WITH STATUS ASTHMATICUS

PEDIATRICS ◽  
1968 ◽  
Vol 42 (2) ◽  
pp. 238-249
Author(s):  
John J. Downes ◽  
David W. Wood ◽  
Theodore W. Striker ◽  
Joffie C. Pittman
Keyword(s):  
Status Asthmaticus ◽  
Clinical Signs ◽  
Arterial Oxygen Tension ◽  
Base Deficit ◽  
Infants And Children ◽  
Clinical Severity ◽  
Arterial Oxygen ◽  
Acid Base ◽  
Arterial Blood ◽  
Arterial Ph

The course of arterial oxygen tension (Pao2), pH, carbon dioxide tension (Paco2) and base deficit (negative base excess) was studied in 45 episodes of status asthmaticus occurring in 32 infants and children. The data indicate that arterial hypoxemia occurs in these patients due to alveolar hypoventilation and pulmonary arterial-venous shunts. Three fourths of the patients tested demonstrated a base deficit which was related in part to ketonemia. The Paco2 varied from below normal to 168 mm Hg, and arterial pH varied from 6.89 to 7.41 at the time of peak clinical severity. Clinical signs of respiratory failure associated with a Paco2 above 65 mm Hg occurred in 13 patients (18 episodes), all of whom were successfully managed by mechanical ventilation. These studies indicate the variability in alveolar ventilation and acid-base balance during an asthmatic episode and the need for repeated assessment of arterial pH and blood gases if one is to provide optimal management.

Continuous Monitoring of Arterial Oxygen Tension Using a Catheter-Tip Polarographic Electrode in Infants

PEDIATRICS ◽  
1976 ◽  
Vol 57 (2) ◽  
pp. 244-250
Author(s):  
M. Conway ◽  
G. M. Durbin ◽  
D. Ingram ◽  
N. McIntosh ◽  
D. Parker ◽  
...  
Keyword(s):  
Oxygen Tension ◽  
Continuous Monitoring ◽  
Newborn Infants ◽  
Arterial Oxygen Tension ◽  
Oxygen Electrode ◽  
Arterial Oxygen ◽  
Respiratory Illnesses ◽  
Arterial Blood ◽  
Reliable Instrument ◽  
Catheter Tip

An oxygen electrode mounted in the tip of an umbilical artery catheter was used in 36 newborn infants with severe respiratory illnesses, 28 of whom survived. Thirty-seven electrodes were used. The median age at insertion was 4 hours (range, 30 minutes to 122 hours). Three electrodes failed to work and they were removed or replaced, and two could not be properly evaluated. Thirty-two electrodes functioned satisfactorily for 10 to 190 hours (mean, 75 hours) after a one-point calibration against blood sampled through the catheter. Twenty-two did not need recalibrating before they were removed after 10 to 190 hours (mean, 88 hours). Four of the remaining ten electrodes were recalibrated once after 33 to 97 hours and then functioned until removed 15 to 55 hours later. The other six electrodes failed after 32 to 105 hours (mean, 49 hours). Complications were few. A total of 356 arterial blood samples, obtained after the initial calibration and before any recalibration was necessary, gave a correlation coefficient of 0.93 (P &lt; .0001) against an independent system for measuring arterial oxygen tension (Pao2) (Radiometer Type E.5046 oxygen electrode). We conclude that the catheter-tip electrode is a safe and reliable instrument for continuously recording Pao2 in newborn infants which much simplifies the management of serious respiratory illnesses.

scholarly journals Bidirectional Ductal Shunting and Preductal to Postductal Oxygenation Gradient in Persistent Pulmonary Hypertension of the Newborn

Children ◽  
2020 ◽  
Vol 7 (9) ◽  
pp. 137
Author(s):  
Amy Lesneski ◽  
Morgan Hardie ◽  
William Ferrier ◽  
Satyan Lakshminrusimha ◽  
Payam Vali
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Pulmonary Blood Flow ◽  
Ductus Arteriosus ◽  
Arterial Oxygen Tension ◽  
Persistent Pulmonary Hypertension ◽  
Arterial Oxygen ◽  
Meconium Aspiration ◽  
Arterial Blood Gas ◽  
Arterial Blood

Background: The aim was to evaluate the relationship between the direction of the patent ductus arteriosus (PDA) shunt and the pre- and postductal gradient for arterial blood gas (ABG) parameters in a lamb model of meconium aspiration syndrome (MAS) with persistent pulmonary hypertension of the newborn (PPHN). Methods: PPHN was induced by intermittent umbilical cord occlusion and the aspiration of meconium through the tracheal tube. After delivery, 13 lambs were ventilated and simultaneous 129 pairs of pre- and postductal ABG were drawn (right carotid and umbilical artery, respectively) while recording the PDA and the carotid and pulmonary blood flow. Results: Meconium aspiration resulted in hypoxemia. The bidirectional ductal shunt had a lower postductal partial arterial oxygen tension ([PaO2] with lower PaO2/FiO2 ratio—97 ± 36 vs. 130 ± 65 mmHg) and left pulmonary flow (81 ± 52 vs. 133 ± 82 mL/kg/min). However, 56% of the samples with a bidirectional shunt had a pre- and postductal saturation gradient of < 3%. Conclusions: The presence of a bidirectional ductal shunt is associated with hypoxemia and low pulmonary blood flow. The absence of a pre- and postductal saturation difference is frequently observed with bidirectional right-to-left shunting through the PDA, and does not exclude a diagnosis of PPHN in this model.

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