Effects of l-Epinephrine and l-Norepinephrine on the Splanchnic Bed of Intact Dogs

1957 ◽  
Vol 189 (3) ◽  
pp. 576-579 ◽  
Author(s):  
E. Allbaugh Farrand ◽  
R. Larsen ◽  
Steven M. Horvath
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Splanchnic Blood Flow ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Metabolic Functions ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Change In Mean ◽  
Infusion Period

The changes in splanchnic blood flow and related metabolic functions which occurred as the result of the infusion of 0.1 µg/kg/min. of l-epinephrine and l-norepinephrine for 10 minutes were measured in anesthetized dogs. l-Epinephrine elicited a marked increase in estimated splanchnic blood flow and no change in mean arterial pressure. While a significantly increased mean arterial blood pressure was observed following the administration of l-norepinephrine, no change in estimated splanchnic blood flow occurred. Arterial oxygen content was increased significantly with both drugs. Utilization of oxygen by the splanchnic bed was not changed during the infusion of either drug but was increased during the postepinephrine infusion period.

Peripheral chemoreflex activation and cardiac function during hypoxemia in near term fetal sheep without placental compromise

2021 ◽  
Author(s):  
Juulia Lantto ◽  
Tiina Erkinaro ◽  
Mervi Haapsamo ◽  
Heikki Huhta ◽  
Leena Alanne ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Carotid Artery ◽  
Arterial Oxygen ◽  
Sheep Model ◽  
Fetal Sheep ◽  
Descending Aorta ◽  
Arterial Blood ◽  
Near Term ◽  
Peripheral Chemoreflex

A drop in arterial oxygen content activates fetal chemoreflex including an increase in sympathetic activity leading to peripheral vasoconstriction and redistribution of blood flow to protect the brain, myocardium, and adrenal glands. By using a chronically instrumented fetal sheep model with intact placental circulation at near-term gestation, we investigated the relationship between peripheral chemoreflex activation induced by hypoxemia and central hemodynamics. 17 Åland landrace sheep fetuses at 115-128/145 gestational days were instrumented. Carotid artery was catheterised in 10 fetuses and descending aorta in 7 fetuses. After a 4-day recovery, baseline measurements of fetal arterial blood pressures, blood gas values, and fetal cardiovascular hemodynamics by pulsed Doppler ultrasonography were obtained under isoflurane-anesthesia. Comparable data to baseline was collected 10 (acute hypoxemia) and 60 minutes (prolonged hypoxemia) after maternal hypo-oxygenation to saturation level of 70-80% was achieved. During prolonged hypoxemia, pH and base excess (BE) were lower, and lactate levels higher in the descending aorta than in the carotid artery. During hypoxemia mean arterial blood pressure (MAP) in the descending aorta increased, while in the carotid artery MAP decreased. In addition, right pulmonary artery pulsatility index values increased, and the diastolic component in the aortic isthmus blood flow velocity waveform became more retrograde. Both fetal ventricular cardiac outputs were maintained even during prolonged hypoxemia when significant fetal metabolic acidemia developed. Fetal chemoreflex activation induced by hypoxemia decreased the perfusion pressure in the cerebral circulation. Fetal weight-indexed LVCO or AoI Net Flow-ratio did not correlate with a drop in carotid artery blood pressure.

Effects of khellin on coronary blood flow and related metabolic functions

1959 ◽  
Vol 196 (2) ◽  
pp. 391-393 ◽  
Author(s):  
Richard L. Farrand ◽  
Steven M. Horvath
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Blood Flow ◽  
Control Period ◽  
Systemic Arterial Pressure ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Fick Principle ◽  
Metabolic Functions ◽  
Pulmonary Arterial

Khellin, a drug employed as a coronary dilator, was tested to determine its effects on the cardiovascular system of the dog. Ten mongrel dogs were anesthetized with Nembutal and, after control observations were made, given an intravenous administration of 1 mg/kg body weight of khellin. Coronary blood flow and cardiac output samples were drawn during the control period and at 10, 40 and 80 minutes after administration of the drug Cardiac output was calculated by the direct Fick principle and coronary blood flow by the nitrous oxide method. There was a significant (5%) increase in the arterial oxygen content during the 10- and 40-minute intervals, but no change was observed at 80 minutes. An increase in arterial-mixed venous oxygen difference occurred at 40 and 80 minutes. No change in systemic arterial pressure or cardiac output was noted at any time. Coronary blood flow had decreased slightly at 80 minutes. A significant decrease in carbon dioxide content of the arterial, pulmonary arterial and coronary sinus blood was observed, possibly as a consequence of hyperventilation. Khellin appeared to alter the metabolism of the myocardial and splanchnic tissues.

scholarly journals Effect of Fast Ascent, Acclimatization and Re-Exposure To 5050 m On Cerebral Autoregulation in Unacclimatized Lowlanders. A Prospective Cohort Study.

2021 ◽  
Author(s):  
Laura C. Graf ◽  
Sara E. Hartmann ◽  
Mona Lichtblau ◽  
Lara Muralt ◽  
Patrick R. Bader ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Autoregulation ◽  
Real Life ◽  
Percentage Change ◽  
Sit To Stand ◽  
Arterial Blood ◽  
Autoregulation Index ◽  
Change In Mean ◽  
Peak Blood

Abstract ABSTRACT Cerebral autoregulation (CA) is impaired during acute high-altitude (HA) exposure and effects of acclimatization and re-exposure on CA are unknown. In 18 healthy lowlanders (11 women), we hypothesized that the cerebral autoregulation index (ARI) assessed by the percentage change in middle cerebral artery peak blood flow velocity (Δ%MCAv)/percentage change in mean arterial blood pressure (Δ%MAP) induced by a sit-to-stand maneuver, is i) reduced on Day1 at 5050m compared to 520m, ii) is improved after 6 days at 5050m, and iii) is less impaired during re-exposure to 5050m after 7 days at 520m compared to Cycle1. Participants spent 4-8h/day at 5050m and slept at 2900m similar to real-life working shifts. High/low ARI indicate impaired/intact CA, respectively. With the sit-to-stand at 520m, mean(95%CI) in ΔMAP and ΔMCAv were -26%(-41 to -10) and -13%(-19 to -7); mean±SE in ARI was 0.58±0.63Δ%/Δ%, respectively. On Day1 at 5050m, ARI worsened compared to 520m (3.29±0.70Δ%/Δ%), but improved with acclimatization (1.44±0.65Δ%/Δ%, P<0.05 for both). ARI was less affected during re-exposure to 5050m (1.22±0.70Δ%/Δ%, P<0.05 acute altitude-induced change between sojourns). This study showed that CA i) is impaired during acute HA exposure, ii) improves with acclimatization and iii) is ameliorated during re-exposure to HA a week later.

Renal Response to Nonshocking Hemorrhage: the Role of Intrarenal Shunts

1958 ◽  
Vol 193 (2) ◽  
pp. 360-364 ◽  
Author(s):  
Allan V. N. Goodyer ◽  
Louis R. Mattie ◽  
Allen Chetrick
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Body Weight ◽  
Arterial Pressure ◽  
The Body ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Renal Innervation ◽  
Aortic Obstruction

In anesthetized dogs, bleeding (1.5–3% of the body weight) was allowed while renal arterial pressure was maintained at constant levels by graded changes of mechanical aortic obstruction. The renal hematocrit decreased, (as measured with I131 albumin and acid hematin, and as compared to the blood hematocrit), primarily as a result of an increased renal plasma volume. These changes are correlated with previously identified alterations of sodium excretion, all independent of renal innervation or arterial blood pressure. It is proposed that hemorrhage may involve an intrarenal redistribution of blood flow favoring diversion of plasma to cell-poor capillaries or to lymphatic spaces.

Effect of furosemide on thoracic duct lymph flow in the dog

1980 ◽  
Vol 238 (5) ◽  
pp. F363-F371 ◽  
Author(s):  
C. McCaffrey ◽  
M. Levy
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Thoracic Duct ◽  
Interstitial Fluid ◽  
Lymph Flow ◽  
Splanchnic Blood Flow ◽  
Thoracic Duct Lymph ◽  
Plasma Sodium ◽  
Duct Lymph ◽  
Anesthetized Dogs

Furosemide 20 mg/kg was given intravenously to 12 anesthetized dogs with clamped renal pedicles. Thoracic duct lymph flow (TDLF) increased promptly by 38% (P less than 0.05), an increment that lasted 80 min. Because in 6 of 12 dogs there was a transient increase in splanchnic blood flow, in separate groups splanchnic blood flow was either markedly constricted or markedly increased by intravenous isoproterenol. Thoracic duct lymph flow increased by 95 and 90%, respectively, following furosemid despite no further change in splanchnic blood flow. Furosemide had no effect on blood pressure, lymph protein, or plasma sodium. In four chronic caval dogs, TDLF was increased by 400%, yet furosemide produced a further increment in lymph flow of 30% (P less than 0.05). Infusion of a 25% albumin solution to contract the interstitial fluid did not abolish the furosemide effect, but a 10% mannitol solution did. Furosemide increased TDLF even after the infusion of papaverine reduced blood pressure to 60 mmHg. We conclude that furosemide increases TDLF by acting directly on splanchnic capillaries to allow increased filtration of fluid in the absence of increased splanchnic blood flow or capillary hydrostatic pressure.

scholarly journals Modulation of Myocardial Oxygen Delivery in Response to Isovolemic Hemodilution

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Blake R. Simon ◽  
Hana E. Baker ◽  
Conner C. Earl ◽  
Adam G. Goodwill ◽  
Sam Luebbe ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Oxygen Delivery ◽  
Venous Blood ◽  
Blood Gases ◽  
Arterial Oxygen ◽  
Neural Pathways ◽  
Isovolemic Hemodilution ◽  
Arterial Oxygen Content ◽  
Arterial Blood

Background and Hypothesis: Prior studies have established that progressive increases in coronary blood flow are sufficient to maintain myocardial oxygen delivery in response to reductions in arterial oxygenation. However, the precise mechanisms responsible for anemic coronary vasodilation remain poorly understood. This investigation tested the hypothesis that autonomic neural pathways contribute to the maintenance of myocardial oxygen delivery in response to graded reductions in arterial hematocrit.  Experimental Design: Experiments were conducted in open-chest anesthetized swine while assessing coronary blood flow and coronary arterial and venous blood gases in response to progressive hemodilution. Isovolemic hemodilution was achieved via simultaneous removal of 250mL of arterial blood and addition of 250mL of a synthetic plasma expander (Hespan) in swine that received either vehicle or a combination of atropine (0.5mg/kg) and propranolol (1mg/kg) (Atro/Pro).  Results: Relative to vehicle control swine, treatment with Atro/Pro increased heart rate by ~50±4 beats/min and arterial pressure by ~10±1 mmHg.  However, Atro/Pro did not significantly alter increases in coronary blood flow in response to isovolemic hemodilution (hematocrits ranging from ~35±1% to ~15±1%). Coronary venous PO2, an index of myocardial oxygenation, was also unchanged by hemodilution in both vehicle and Atro/Pro treated swine.   Conclusion and Potential Impact: These data suggest that autonomic neural pathways do not play a significant role in the maintenance of myocardial oxygen delivery in response to graded reduction in arterial oxygen content. Understanding of how myocardial oxygen supply is ultimately sensed and regulated in response to reductions in tissue oxygenation remains elusive.  

Adrenal blood flow and secretory relationships during hypoxia in anesthetized dogs

1989 ◽  
Vol 257 (5) ◽  
pp. H1458-H1465 ◽  
Author(s):  
M. J. Breslow ◽  
T. D. Ball ◽  
C. F. Miller ◽  
H. Raff ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Oxygen Content ◽  
Adrenocorticotropic Hormone ◽  
Secretory Activity ◽  
Catecholamine Secretion ◽  
Arterial Oxygen ◽  
Vascular Effects ◽  
Arterial Oxygen Content ◽  
Anesthetized Dogs

To evaluate whether hypoxia-induced increases in adrenal cortical (CQ) and medullary (MQ) blood flow (radiolabeled microspheres) occur secondary to hypoxia-induced secretory activity, pentobarbital-anesthetized ventilated dogs were pretreated with dexamethasone (DEX) to prevent adrenocorticotropic hormone (ACTH) and corticosteroid secretory changes or underwent unilateral adrenal denervation to prevent adrenal catecholamine secretory responses. In nonsurgically stressed dogs, DEX completely prevented increases in ACTH or corticosteroid levels during reduction of arterial oxygen content to 8 vol% but had no effect on hypoxia-induced doubling of CQ. In dogs in which adrenal oxygen consumption (VO2) was measured, DEX reduced VO2 by 50% without altering CQ. Unilateral adrenal denervation prevented hypoxia-induced increases in adrenal catecholamine secretion and MQ but had no effect on the CQ response. These results suggest that hypoxia-induced medullary vasodilation is associated with adrenal catecholamine secretory activity but that increases in CQ occur independent of secretory activity and likely represent direct vascular effects of hypoxia.

scholarly journals Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

2014 ◽  
Vol 35 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Christopher K Willie ◽  
Philip N Ainslie ◽  
Ivan Drvis ◽  
David B MacLeod ◽  
Anthony R Bain ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Delivery ◽  
Blood Gases ◽  
Arterial Oxygen ◽  
Breath Hold ◽  
Cerebral Oxygen ◽  
Arterial Oxygen Content ◽  
Arterial Blood ◽  
End Tidal ◽  
The Brain

The roles of involuntary breathing movements (IBMs) and cerebral oxygen delivery in the tolerance to extreme hypoxemia displayed by elite breath-hold divers are unknown. Cerebral blood flow (CBF), arterial blood gases (ABGs), and cardiorespiratory metrics were measured during maximum dry apneas in elite breath-hold divers ( n=17). To isolate the effects of apnea and IBM from the concurrent changes on ABG, end-tidal forcing (‘clamp’) was then used to replicate an identical temporal pattern of decreasing arterial PO2 (PaO2) and increasing arterial PCO2 (PaCO2) while breathing. End-apnea PaO2 ranged from 23  to 37 mm Hg (30±7 mm Hg). Elevation in mean arterial pressure was greater during apnea than during clamp reaching +54±24% versus 34±26%, respectively; however, CBF increased similarly between apnea and clamp (93.6±28% and 83.4±38%, respectively). This latter observation indicates that during the overall apnea period IBM per se do not augment CBF and that the brain remains sufficiently protected against hypertension. Termination of apnea was not determined by reduced cerebral oxygen delivery; despite 40% to 50% reductions in arterial oxygen content, oxygen delivery was maintained by commensurately increased CBF.

Effect of Histamine on Regional Cerebral Blood Flow in Man

Cephalalgia ◽  
1982 ◽  
Vol 2 (1) ◽  
pp. 15-18 ◽  
Author(s):  
Annette Æbelholt Krabbe ◽  
Jes Olesen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Resting State ◽  
Regional Cerebral Blood Flow ◽  
Regional Distribution ◽  
Regional Cerebral Blood ◽  
Arterial Blood ◽  
Significant Change ◽  
Change In Mean

Regional cerebral blood flow (rCBF) was measured using the intra-arterial 133Xe technique in 35 or 256 areas of a hemisphere. In seven patients rCBF was measured in the resting state and following intracarotid (i.c.) infusion of histamine 10–50 μg/min. In four patients histamine was infused intravenously in a dose of 25–40 μg/min. Histamine caused no significant change in mean arterial blood pressure or arterial PCO2. There was no significant change in mean hemispheric blood flow during i.v. or i.c. histamine infusion. No change in the regional distribution of hemispheric blood flow was observed. Experimental histamine headache is most likely of extracranial origin.

Fetal cerebral and peripheral circulatory responses to hypoxia after nitric oxide synthase inhibition

2001 ◽  
Vol 281 (2) ◽  
pp. R381-R390 ◽  
Author(s):  
Andrew P. Harris ◽  
Sabah Helou ◽  
Christine A. Gleason ◽  
Richard J. Traystman ◽  
Raymond C. Koehler
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Treated Group ◽  
Arterial Oxygen ◽  
Control Group ◽  
Fetal Sheep ◽  
Arterial Oxygen Content ◽  
Arterial Blood ◽  
Nos Inhibitor ◽  
Oxide Synthase

The increase in cerebral blood flow (CBF) during hypoxia in fetal sheep at 0.6 gestation is less than the increase at 0.9 gestation when normalized for differences in baseline CBF and oxygen consumption. Nitric oxide (NO) synthase (NOS) catalytic activity increases threefold during this period of development. We tested the hypothesis that administration of the NOS inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) decreases the CBF response to systemic hypoxia selectively at 0.9 gestation. We also tested whether any peripheral vasoconstriction during hypoxia is potentiated byl-NAME at 0.9 gestation. Administration ofl-NAME increased arterial blood pressure and decreased microsphere-determined CBF during normoxia in fetal sheep at both 0.6 and 0.9 gestation. With subsequent reduction of arterial oxygen content by ∼50%, the percent increase in forebrain CBF in a control group (57 ± 11%; ± SE) and l-NAME-treated group (51 ± 6%) was similar at 0.6 gestation. Likewise, at 0.9 gestation, the increase in CBF was similar in control (90 ± 25%) andl-NAME (80 ± 28%) groups. At 0.9 gestation,l-NAME treatment attenuated the increase in coronary blood flow and increased gastrointestinal vascular resistance during hypoxia. We conclude that NO exerts a basal vasodilatory influence in brain as early as 0.6 gestation in fetal sheep but is not an important mechanism for hypoxic vasodilation in brain at either 0.6 or 0.9 gestation. Thus the developmental increase in NOS catalytic capacity does not appear to be responsible for developmental increases in the CBF response to hypoxia during this period. In contrast, NO modulates the vascular response to hypoxia in heart and gastrointestinal tract.

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