Cardiac output and peripheral blood flow during occlusion of carotid arteries

1961 ◽  
Vol 200 (6) ◽  
pp. 1185-1190 ◽  
Author(s):  
C. Polosa ◽  
G. Rossi
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Pressure Rise ◽  
Blocking Agent ◽  
Carotid Occlusion ◽  
Peripheral Blood Flow ◽  
Cardiac Work ◽  
Anesthetized Dogs

Cardiac output and blood flow to the kidney, hind limb, and splanchnic area were studied in anesthetized dogs during the arterial pressure rise due to carotid occlusion. All the vascular beds studied exhibited an increased resistance to flow. Cardiac output was maintained constant through an increased cardiac work in spite of the increased arterial pressure. This increased cardiac work was reflexly produced as evidenced by the action of the adrenergic blocking agent dichloroisoproterenol (DCI). This drug allowed the reflex vasoconstriction and the consequent pressure rise, but preventing the reflex chronotropic and inotropic sympathetic effects on the heart resulted in a fall of cardiac output during carotid occlusion. It is concluded a) that the reflex increase in vasomotor tone is the main factor in the pressor response to carotid occlusion and b) that the reflex effect on the myocardium is an important factor in regulating cardiac output in this situation.

Inhibition of carotid pressor response by left aortic depressor nerve in dogs

1981 ◽  
Vol 240 (4) ◽  
pp. H555-H560 ◽  
Author(s):  
S. C. Walgenbach ◽  
D. E. Donald ◽  
A. Melcher
Keyword(s):  
Arterial Pressure ◽  
Pressor Response ◽  
The Other ◽  
Carotid Occlusion ◽  
Aortic Depressor Nerve ◽  
Vagal Nerves ◽  
Isolated Aorta ◽  
Anesthetized Dogs ◽  
The Mean ◽  
Aortic Baroreceptors

In 12 conscious dogs, the mean increase of 26 mmHg in arterial pressure during carotid occlusion was augmented by 52 mmHg after section of the left cervical vagus nerve and 6 mmHg after right vagal section. In 18 anesthetized dogs, in which the cervical vagal nerves were reversibly cold blocked, corresponding values were 33, 28, and 6 mmHg, respectively. In nine of these dogs, this left-sided dominance was present after bilateral section of the vagal cardiopulmonary afferents; it was absent after bilateral section of the aortic nerves in the other nine dogs. In five dogs on cardiopulmonary bypass with heart and lungs excluded, pressure within the isolated aorta and major intrathoracic arteries was raised from 120 to 220 mmHg. The resultant hypotension reflexly induced by activation of aortic baroreceptors was reduced by left but not by right vagal cold block. It was concluded that, in the dog, the left aortic nerve provided the major inhibition of the increase in arterial pressure after carotid occlusion.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

Improved cardiac output and peripheral blood flow after correcting neonatal hyperviscosity

1985 ◽  
Vol 110 (3) ◽  
pp. 707
Author(s):  
Sydney Swetnam ◽  
Dale Alverson ◽  
Steven M. Yabek ◽  
Pam Angelus ◽  
Connie Bakstrom ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Blood ◽  
Peripheral Blood Flow

Cardiac Output Changes in Newborns With Hyperbilirubinemia Treated With Phototherapy

PEDIATRICS ◽  
1985 ◽  
Vol 76 (6) ◽  
pp. 918-921
Author(s):  
Frans J. Walther ◽  
Paul Y. K. Wu ◽  
Bijan Siassi
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Skin Blood Flow ◽  
Peripheral Blood ◽  
Cardiovascular Effects ◽  
Tissue Perfusion ◽  
Peripheral Blood Flow ◽  
Limb Blood Flow ◽  
Term Infants

Phototherapy is known to increase peripheral blood flow in neonates, but information on the associated cardiovascular effects is not available. Using pulsed Doppler echocardiography we evaluated cardiac output and stroke volume in 12 preterm and 13 term neonates during and after phototherapy. We concomitantly measured arterial limb blood flow by strain gauge plethysmography and skin blood flow by photoplethysmography. Cardiac output decreased by 6% due to reduced stroke volume during phototherapy, whereas total limb blood flow and skin blood flow increased by 38% and 41%, respectively. Peripheral blood flow increments tended to be higher in the preterm than in the term infants. The reduced stroke volume during phototherapy may be an expression of reduced activity of the newborn during phototherapy. For healthy neonates the reduction in cardiac output is minimal, but for sick infants with reduced cardiac output, this reduction may further aggravate the decrease in tissue perfusion.

Cardiovascular responses to insulin in the absence of hypoglycemia

1962 ◽  
Vol 202 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Santiago A. Pereda ◽  
John W. Eckstein ◽  
François M. Abboud
Keyword(s):  
Pressor Response ◽  
Direct Action ◽  
Cardiovascular Responses ◽  
Blocking Agent ◽  
Neuromuscular Blocking ◽  
Right Atrial ◽  
Systemic Vein ◽  
Anesthetized Dogs ◽  
Adrenergic Blocking ◽  
The Brain

Cardiovascular responses to intravenous administration of insulin were studied in lightly anesthetized dogs treated with a neuromuscular blocking agent. An early transient pressor response was observed. This abrupt increase in arterial pressure appeared 2–9 min after insulin was given. It was accompanied by increases in cardiac output and right atrial pressure. It occurred in the presence of hyperglycemia and in the absence of hypoglycemia. It was not altered by glucagon but it could be antagonized by ganglionic and adrenergic blocking drugs and by pentobarbital. The response could be produced when insulin was given in the carotid artery in doses that caused no effect when injected in a systemic vein. The experiments suggest that insulin may have a direct action on the brain.

Cerebral blood flow and evoked potentials during Cushing response in sheep

1989 ◽  
Vol 256 (3) ◽  
pp. H779-H788
Author(s):  
R. C. Koehler ◽  
J. E. Backofen ◽  
R. W. McPherson ◽  
M. D. Jones ◽  
M. C. Rogers ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Evoked Potentials ◽  
Aortic Pressure ◽  
Base Line ◽  
Auditory Evoked Responses ◽  
Cushing Response

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.

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.

Effects of hypoxia, hyperoxia and hypercapnia on graded cerebral ischemic responses in rabbits

1992 ◽  
Vol 263 (6) ◽  
pp. H1839-H1846
Author(s):  
T. Takeuchi ◽  
J. Horiuchi ◽  
N. Terada ◽  
M. Nagao ◽  
H. Terajima
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Arterial Pressure ◽  
Internal Carotid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Left Internal Carotid Artery ◽  
Renal Nerve ◽  
Tissue Po2 ◽  
Cerebral Ischemic

This study was designed to determine how several factors interact to modify the cerebral ischemic pressor response (CIR) in anesthetized rabbits. After the carotid sinus and aortic nerves were bilaterally sectioned, blood flow through the left internal carotid artery (ICF), which was surgically restricted as the sole route of blood supply to the brain, was reduced by a servo-controller during ventilation with room air, and 8% and 90% O2 and 2 and 5% CO2 gas mixtures. Blood flow (MBF), tissue PO2, PCO2, and interstitial pH were measured in the rostral ventrolateral medulla. Internal carotid arterial pressure, tissue PO2, and MBF decreased proportionately as ICF decreased in the range from 4 to 0 ml/min. Hypoxia significantly increased the rise in renal nerve activity (RNA) and CIR caused by cerebral ischemia, while hyperoxia significantly decreased them. Hypercapnia had almost no influence on the increases in RNA and mean arterial pressure produced by cerebral ischemia. CIR showed a much higher correlation with changes in tissue PO2 than with the other factors. We examined how these factors interact to modify CIR and found that central hypoxia is the main factor in producing CIR.

Sign in / Sign up

Export Citation Format

Share Document