Effects of acute prolonged hypoxia on cardiovascular dynamics in dogs

1977 ◽  
Vol 43 (5) ◽  
pp. 784-789 ◽  
Author(s):  
J. F. Borgia ◽  
S. M. Horvath
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiac Index ◽  
Carrying Capacity ◽  
Hemoglobin Concentration ◽  
Severe Hypoxia ◽  
Systemic Hypertension ◽  
Anesthetized Dogs ◽  
Oxygen Tensions ◽  
Oxygen Carrying Capacity

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.

Chronic hypoxia and the cerebral circulation

2006 ◽  
Vol 100 (2) ◽  
pp. 725-730 ◽  
Author(s):  
Kui Xu ◽  
Joseph C. LaManna
Keyword(s):  
Blood Flow ◽  
Carrying Capacity ◽  
Hemoglobin Concentration ◽  
Capillary Density ◽  
Hypoxic Exposure ◽  
Blood Oxygen ◽  
Brain Capillary ◽  
Blood Flow Increase ◽  
Time Courses ◽  
Oxygen Carrying Capacity

Exposure to mild hypoxia elicits a characteristic cerebrovascular response in mammals, including humans. Initially, cerebral blood flow (CBF) increases as much as twofold. The blood flow increase is blunted somewhat by a decreasing arterial Pco2 as a result of the hypoxia-induced hyperventilatory response. After a few days, CBF begins to fall back toward baseline levels as the blood oxygen-carrying capacity is increasing due to increasing hemoglobin concentration and packed red cell volume as a result of erythropoietin upregulation. By the end of 2 wk of hypoxic exposure, brain capillary density has increased with resultant decreased intercapillary distances. The relative time courses of these changes suggest that they are adjusted by different control signals and mechanisms. The CBF response appears linked to the blood oxygen-carrying capacity, whereas the hypoxia-induced brain angiogenesis appears to be in response to tissue hypoxia.

Consultation with the Specialist

1992 ◽  
Vol 13 (10) ◽  
pp. 379-380
Author(s):  
William B. Strong
Keyword(s):  
Cardiac Output ◽  
Oxygen Saturation ◽  
Carrying Capacity ◽  
Hemoglobin Concentration ◽  
Cyanotic Congenital Heart Disease ◽  
Compensatory Mechanism ◽  
Peripheral Tissues ◽  
Arterial Blood ◽  
Infant And Young Child ◽  
Oxygen Carrying Capacity

What is the likely pathophysiology of this event? What are the more common complications of hypoxemia in the older infant and young child? This clinical scenario is uncommon, but it represents one of the two feared central nervous system complications of cyanotic congenital heart disease, (ie, cerebrovascular accident and brain abscess). A uniform response to hypoxemia of cardiac etiology is the production of erythropoietin to produce more red blood cells. This is a compensatory mechanism to maintain oxygen delivery to the peripheral tissues. Normally, hemoglobin is about 96% saturated with oxygen. Therefore, the oxygen-carrying capacity of blood with a normal hemoglobin concentration of 15 g/dL is approximately 20.3 mL of oxygen per 100 mL of blood (ie, 15 g of hemoglobin x 1.35 mL of O2 per g of hemoglobin = 20.3). The oxygen content of blood equals the oxygen-carrying capacity multiplied by the oxygen saturation. At a normal oxygen saturation of 96%, the O2 content of arterial blood (Hgb 15 g/dL) equals 19.5 mL/dL (96% x 20.3 mm3/dL) or 195 mL per liter of cardiac output. The arterial O2 content of this child, assuming an average arterial saturation of 85%, will be 11.1 mL/dL. Therefore, every liter (10 dL) of cardiac output will carry 111 mL of O2 or 84 mL of O2 less than the child with a 15 g/dL hemoglobin level.

Whole body and hindlimb cardiovascular responses of the anesthetized dog during CO hypoxia

1984 ◽  
Vol 62 (7) ◽  
pp. 769-774 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Sympathetic Innervation ◽  
Cardiovascular Responses ◽  
The Body ◽  
Whole Body ◽  
Total Resistance ◽  
Intact Group ◽  
Anesthetized Dogs

To compare with earlier studies of anemic hypoxia obtained by hemodilution, O2 carring capacity was decreased by carbon monoxide (CO) hypoxia. Arterial O2 content was reduced either 50% (moderate CO) or 65% (severe CO). In two groups of anesthetized dogs (moderate and severe CO) hindlimb innervation remained intact while in a third group (moderate CO) the hindlimb was denervated. Measurements were obtained prior to and at 30 and 60 min of CO hypoxia. Cardiac output was elevated at 30 min of CO hypoxia in all groups (p < 0.01) and in the severe CO group at 60 min (p < 0.01). Hindlimb blood flow remained unchanged during CO hypoxia in the intact groups. In the denervated group, hindlimb blood flow was greater (p < 0.05) than that in the intact groups throughout the experiment. A decrease in mean arterial pressure (p < 0.01) in all groups was associated with a fall in total resistance (p < 0.01). Hindlimb resistance remained unchanged during moderate CO hypoxia in the intact group but increased (p < 0.05) in the denervated group. In the severe CO group hindlimb resistance was decreased (p < 0.05) at 60 min. The results indicate that the increase in cardiac output during CO hypoxia was directed to nonmuscle areas of the body and that intact sympathetic innervation was required to achieve this redistribution.

The Influence of Nutritional State on the Circulatory and Respiratory Physiology of the Shore Crab, Carcinus Maenas

1985 ◽  
Vol 65 (1) ◽  
pp. 69-78 ◽  
Author(s):  
M. H. Depledge
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Salinity Stress ◽  
Carrying Capacity ◽  
Carcinus Maenas ◽  
Nutritional State ◽  
Respiratory Physiology ◽  
Shore Crab ◽  
Decapod Crustaceans ◽  
Oxygen Carrying Capacity

The oxygen-carrying capacity of the blood of decapod crustaceans fluctuates widely. Salinity stress results in doubling of haemocyanin concentration within 24–48 h in Carcinus maenas (Boone & Schoeffeniels, 1979) while in the lobster, Homarus gammarus respiratory pigment levels are very low prior to and following moulting (Spoek, 1974). In general, however, the most important factor regulating haemocyanin concentration is nutritional state. Following starvation low values are recorded (Wieser, 1965; Uglow, 1969; Djangmah, 1970) and there are concomitant reductions in ventilation, oxygen consumption and cardiac output (Ansell, 1973; Marsden, Newell & Ahsanullah, 1973; Wallace, 1973). The interrelationships between these events are poorly understood.

Distribution of cardiac output during induced isometric exercise in dogs

1979 ◽  
Vol 236 (2) ◽  
pp. H218-H224 ◽  
Author(s):  
S. C. Crayton ◽  
R. Aung-Din ◽  
D. E. Fixler ◽  
J. H. Mitchell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Adrenergic Receptor ◽  
Isometric Exercise ◽  
Peripheral Resistance ◽  
Minute Volume ◽  
Adrenergic Blockade ◽  
Limb Muscles ◽  
Anesthetized Dogs ◽  
Distribution Of Cardiac Output

Studies were designed to characterize the distribution of cardiac output during induced isometric exercise in anesthetized dogs. The response to isometric exercise involved significant increases in heart rate (+12 +/- 3%(SE)), mean arterial pressure (+13 +/- 2%), cardiac output (+26 +/- 8%), and respiratory minute volume (+75 +/- 26%); total peripheral resistance did not change significantly. Significant changes in blood flow were observed during isometric exercise in kidneys (-18 +/- 6%) and contracting limb muscles (+453 +/- 154%). Flow to liver (hepatic artery), spleen, brain, and myocardium remained near control values. Section of spinal dorsal roots L6-L7 abolished the responses to isometric exercise except for the increase in flow to exercising limb muscles. Alpha-adrenergic receptor blockade abolished the decrease in renal blood flow during isometric exercise; however, the increase in flow to exercising limb muscles was not affected by either alpha- or beta-adrenergic blockade.

Regional blood flow and cardiac output during acute hypoxia in the anesthetized dog

1963 ◽  
Vol 204 (6) ◽  
pp. 963-968 ◽  
Author(s):  
John F. Murray ◽  
I. Maureen Young
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Head Kidney ◽  
Arterial Oxygen ◽  
Circulatory Effects ◽  
Low Concentrations ◽  
Anesthetized Dogs

The circulatory effects of breathing low concentrations of oxygen were studied in ten anesthetized dogs. Simultaneous measurements were made of cardiac output (indicator dilution technique) and blood flow to the head, kidney, and hind limb (electromagnetic flowmeters). Four experiments were performed with the addition of succinylcholine to inhibit the ventilatory response to hypoxia and maintain pCO2 constant. A rise in cardiac output and mean arterial pressure occurred which was significantly correlated to the decrease in arterial oxygen saturation. No threshold for these responses was found. Blood flow tended to increase during hypoxia in the regions studied but the responses were variable and only the change in renal blood flow had a significant correlation to arterial oxygen unsaturation. Systemic and regional vascular resistances during hypoxia varied both in direction and magnitude of change. The preponderant effects of hypoxia influence cardiac output more than peripheral vascular resistance.

Regional blood flow distribution during the Cushing response: alterations with adrenergic blockade

1985 ◽  
Vol 248 (1) ◽  
pp. H98-H108
Author(s):  
D. G. van Wylen ◽  
L. G. D'Alecy
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Flow Distribution ◽  
Peripheral Tissue ◽  
Systemic Hypertension ◽  
Tissue Blood Flow ◽  
Blood Flow Distribution ◽  
Beta Receptor ◽  
Cushing Response

Regional blood flow distribution (microspheres) and cardiac output (CO, thermal dilution) were measured during the Cushing response in unblocked (UB), beta-receptor-blocked (BB, 2 mg/kg propranolol iv), or alpha-receptor blocked (AB, 0.5 mg/kg + 0.5 mg X kg-1 X min-1 phentolamine iv) chloralose-anesthetized dogs. Intracranial pressure was increased to 150 mmHg by infusion of temperature-controlled artificial cerebrospinal fluid into the cisterna magna. Similar increases in mean arterial pressure were seen in UB and BB, but in AB a Cushing response could not be sustained. In UB, cerebral blood flow (CBF) decreased 50%, coronary blood flow (CoBF) increased 120%, and peripheral tissue blood flow was reduced only in the kidneys (18%) and the intestines (small 22%, large 35%). Blood flow to the other viscera, skin, and skeletal muscle was unchanged. CO (16%) and heart rate (HR, 38%) decreased, and total peripheral resistance (TPR, 68%) and stroke volume (SV, 38%) increased. In BB, CBF decreased 50%, CoBF decreased 20%, and blood flow was reduced 40-80% in all peripheral tissues. CO (69%) and HR (62%) decreased, TPR increased 366%, and SV was unchanged. We conclude that the Cushing response in UB animals combines an alpha-receptor-mediated vasoconstriction with a beta-receptor cardiac stimulation. The beta-mechanism is neither necessary nor sufficient for the hypertension. However, the combination of alpha- and beta-adrenergic mechanisms maintains cardiac output and peripheral tissue blood flow relatively constant while producing a systemic hypertension.

Regional hemodynamic responses to hypoxia in polycythemic dogs

1988 ◽  
Vol 65 (5) ◽  
pp. 2069-2074 ◽  
Author(s):  
R. L. Stork ◽  
D. L. Bredle ◽  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Muscle Blood Flow ◽  
Regional Distribution ◽  
Experimental Conditions ◽  
Hypoxic Vasoconstriction ◽  
O2 Extraction ◽  
Anesthetized Dogs ◽  
O2 Delivery ◽  
Resting Muscle

Polycythemia increases blood viscosity so that systemic O2 delivery (QO2) decreases and its regional distribution changes. We examined whether hypoxia, by promoting local vasodilation, further modified these effects in resting skeletal muscle and gut in anesthetized dogs after hematocrit had been raised to 65%. One group (CON, n = 7) served as normoxic controls while another (HH, n = 6) was ventilated with 9% O2--91% N2 for 30 min between periods of normoxia. Polycythemia decreased cardiac output so that QO2 to both regions decreased approximately 50% in both groups. In compensation, O2 extraction fraction increased to 65% in muscle and to 50% in gut. When QO2 was reduced further during hypoxia, blood flow increased in muscle but not in gut. Unlike previously published normocythemic studies, there was no initial hypoxic vasoconstriction in muscle. Metabolic vasodilation during hypoxia was enhanced in muscle when blood O2 reserves were first lowered by increased extraction with polycythemia alone. The increase in resting muscle blood flow during hypoxia with no change in cardiac output may have decreased O2 availability to other more vital tissues. In that sense and under these experimental conditions, polycythemia caused a maladaptive response during hypoxic hypoxia.

Hemodynamic responses to dopamine and to isoproterenol following acute myocardial injury

1969 ◽  
Vol 47 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Keith L. MacCannell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Myocardial Injury ◽  
Left Renal Artery ◽  
Arterial Blood ◽  
Acute Myocardial Injury ◽  
Cardiac Slowing ◽  
Anesthetized Dogs ◽  
Higher Doses

Severe myocardial injury was produced in eight anesthetized dogs by the injection of microspheres into the coronary circulation. Cardiac output and renal blood flow were monitored continuously with electromagnetic flow probes around the ascending thoracic aorta and left renal artery respectively. Intravenous infusions of isoproterenol and of dopamine (0.01–0.64 and 0.4–32.0 μg/kg per minute respectively) produced an increase in the cardiac output. Renal blood flow increased with small doses of isoproterenol but tended to decrease with higher doses; in contrast, all doses of dopamine increased renal blood flow. Dopamine was more effective in raising the systemic arterial blood pressure, but also increased cardiac work. Occasional extrasystoles were induced at higher doses of both amines. In three unanesthetized dogs sensitized by prior ligation of a coronary artery, the largest doses of dopamine tested (24–64 μg/kg per minute) did not produce cardiac arrhythmias. However, when dopamine was given to anesthetized dogs during vagal-induced cardiac slowing (a condition conducive to the emergence of ventricular automaticity), arrhythmias were induced. These data suggest that dopamine can increase both cardiac output and renal blood flow after severe myocardial injury, and may be a rational agent in the treatment of cardiogenic shock. Its arrhythmogenic properties would not appear to restrict its use.

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