Nitric oxide modulates regional blood flow differences in the fetal gastrointestinal tract

1996 ◽  
Vol 271 (4) ◽  
pp. G598-G604 ◽  
Author(s):  
W. Q. Fan ◽  
J. J. Smolich ◽  
J. Wild ◽  
V. Y. Yu ◽  
A. M. Walker
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Blood Flow ◽  
Small Intestine ◽  
Vascular Resistance ◽  
Oxygen Delivery ◽  
Intestinal Blood Flow ◽  
Flow Reduction ◽  
Blood Flows ◽  
Blood Flow Reduction

We studied the role of endogenous nitric oxide (NO) in the regulation of gastrointestinal (GI) circulation in 11 chronically instrumented and unanesthetized late-gestation fetal sheep. Systemic and GI blood flows were measured by the radiolabeled microsphere technique. Mean arterial pressure (MAP), heart rate, blood flows, oxygen delivery, and vascular resistance were determined before and after infusion of the specific NO synthase inhibitor, N omega-nitro-L-arginine (L-NNA), to cumulative doses of 10 and 25 mg/kg. At both L-NNA doses, MAP increased, and combined ventricular output and heart rate decreased. GI blood flow and oxygen delivery decreased and vascular resistance increased for the stomach, all segments of the small intestine, and proximal colon and cecum but were unchanged in the middle and distal colon and rectum. Because blood flow reduction in the small intestine was pronounced (from 176 to 107 ml.min-1.100 g-1, P < 0.001) and blood flow in the large intestine was unchanged, distribution of intestinal blood flow became more uniform. Overall, blood flow reduction was proportionally greater in GI circulation than in the remainder of fetal circulation. In three additional animals we established that L-NNA reduced blood flow to the mucosal-submucosal layer (P < 0.02) but not to the muscularis serosa of the small intestine. In the same animals, L-arginine (250 mg/kg) restored systemic hemodynamics and partially restored small intestinal blood flow. Our results suggest that NO is an important differential regulator of vascular tone in the developing GI circulation.

scholarly journals Vasodilator tone in the llama fetus: the role of nitric oxide during normoxemia and hypoxemia

2005 ◽  
Vol 289 (3) ◽  
pp. R776-R783 ◽  
Author(s):  
Emilia M. Sanhueza ◽  
Raquel A. Riquelme ◽  
Emilio A. Herrera ◽  
Dino A. Giussani ◽  
Carlos E. Blanco ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Control Group ◽  
Blood Flows ◽  
Vasoconstrictor Effect ◽  
Vascular Beds ◽  
Oxide Synthase

The fetal llama responds to hypoxemia, with a marked peripheral vasoconstriction but, unlike the sheep, with little or no increase in cerebral blood flow. We tested the hypothesis that the role of nitric oxide (NO) may be increased during hypoxemia in this species, to counterbalance a strong vasoconstrictor effect. Ten fetal llamas were operated under general anesthesia. Mean arterial pressure (MAP), heart rate, cardiac output, total vascular resistance, blood flows, and vascular resistances in cerebral, carotid and femoral vascular beds were determined. Two groups were studied, one with nitric oxide synthase (NOS) blocker NG-nitro-l-arginine methyl ester (l-NAME), and the other with 0.9% NaCl (control group), during normoxemia, hypoxemia, and recovery. During normoxemia, l-NAME produced an increase in fetal MAP and a rapid bradycardia. Cerebral, carotid, and femoral vascular resistance increased and blood flow decreased to carotid and femoral beds, while cerebral blood flow did not change significantly. However, during hypoxemia cerebral and carotid vascular resistance fell by 44% from its value in normoxemia after l-NAME, although femoral vascular resistance progressively increased and remained high during recovery. We conclude that in the llama fetus: 1) NO has an important role in maintaining a vasodilator tone during both normoxemia and hypoxemia in cerebral and femoral vascular beds and 2) during hypoxemia, NOS blockade unmasked the action of other vasodilator agents that contribute, with nitric oxide, to preserving blood flow and oxygen delivery to the tissues.

Intestinal tissue PO2 and microvascular responses during glucose exposure

1980 ◽  
Vol 238 (2) ◽  
pp. H164-H171 ◽  
Author(s):  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Small Intestine ◽  
Normal Distribution ◽  
Vascular Resistance ◽  
Intestinal Blood Flow ◽  
Rat Small Intestine ◽  
Intestinal Tissue ◽  
Tissue Po2 ◽  
In Series ◽  
Glucose Exposure

The microvessels responsible for the major decrease in intestinal vascular resistance during the presence of glucose were defined. In addition, the normal distribution of tissue PO2 in the various layers of the intestinal tissue was measured at rest and during glucose exposure to determine if part of the absorptive hyperemia mechanism is related to a decrease in tissue PO2. In the rat small intestine, exposure of the mucosa only to glucose concentrations of 25--500 mg/100 causes a 20--25% dilation of all submucosal vessels in series with the mucosal vessels and mucosal arterioles. Total intestinal blood flow increased to 200-210% of control at all glucose concentrations. The tissue and perivascular PO2 in the villus apex decreased from 14.8 +/- 1.2 (SE) mmHg at rest to 6--8 mmHg during glucose exposure; the PO2 in the muscle and submucosal layers tended to slightly increase above a normal of 26.4 +/- 1.6 mmHg during glucose exposure. The data indicate virtually all intestinal arterioles are equally involved in absorptive hyperemia. The dilation of mucosal vessels may be related to a decrease in tissue PO2, but submucosal vessels dilate even though PO2 is slightly increased.

Regional blood flow in newborn piglets during environmental cold stress

1986 ◽  
Vol 251 (3) ◽  
pp. G308-G313 ◽  
Author(s):  
S. R. Mayfield ◽  
B. S. Stonestreet ◽  
A. M. Brubakk ◽  
P. W. Shaul ◽  
W. Oh
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Small Intestine ◽  
Cold Stress ◽  
Vascular Resistance ◽  
Oxygen Delivery ◽  
Regional Blood Flow ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Newborn Piglets

Regional blood flow, oxygen delivery, and vascular resistance were determined in newborn piglets during a successful homeothermic response to environmental cold stress. Eight 3- to 4-day-old awake piglets were studied in a thermoneutral environment and 30, 45, and 60 min after onset of environmental cold stress. During cold stress, blood flow was significantly increased to skeletal muscle, the thermogenic organ, and decreased to the small intestine (P less than 0.05). Because arterial oxygen content (CaO2) was stable during the study, changes in oxygen delivery (CaO2 X blood flow) paralleled blood flow. Vascular resistance during cold stress was significantly decreased in skeletal muscle and increased in both the adrenals and the small intestine (P less than 0.05). We conclude that, during successful thermogenesis, the redistribution of cardiac output toward the thermogenic organ (skeletal muscle) is associated with a significant decrease in intestinal blood flow and oxygen delivery. This is not a passive process as evidenced by the coincident observation of increased intestinal vascular resistance.

Severe Cerebral Blood Flow Reduction Inhibits Nitric Oxide Synthesis

2002 ◽  
Vol 19 (9) ◽  
pp. 1105-1116 ◽  
Author(s):  
Shinpei Uetsuka ◽  
Hirosuke Fujisawa ◽  
Hiroaki Yasuda ◽  
Hidehiro Shima ◽  
Michiyasu Suzuki
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthesis ◽  
Flow Reduction ◽  
Blood Flow Reduction

alpha-Adrenergic control of oxygen delivery to myocardium during exercise in conscious dogs

1982 ◽  
Vol 242 (5) ◽  
pp. H805-H809 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. Muylaert ◽  
J. L. Pannier
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Oxygen Delivery ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Adrenergic Control

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.

scholarly journals Famotidine prevents canine gastric blood flow reduction by NSAIDs

2005 ◽  
Vol 21 (s2) ◽  
pp. 55-59 ◽  
Author(s):  
J. Hata ◽  
T. Kamada ◽  
N. Manabe ◽  
H. Kusunoki ◽  
D. Kamino ◽  
...  
Keyword(s):  
Blood Flow ◽  
Gastric Blood Flow ◽  
Flow Reduction ◽  
Blood Flow Reduction

Derecruitment of filtration surface area in paraquat-injured isolated dog lungs

1990 ◽  
Vol 68 (4) ◽  
pp. 1581-1589 ◽  
Author(s):  
T. Shibamoto ◽  
J. C. Parker ◽  
A. E. Taylor ◽  
M. I. Townsley
Keyword(s):  
Blood Flow ◽  
Surface Area ◽  
Vascular Resistance ◽  
High Flow ◽  
Base Line ◽  
Flow Rates ◽  
Blood Flows ◽  
Capillary Filtration Coefficient ◽  
Specific Index ◽  
Filtration Surface

The capillary filtration coefficient (Kf,c) is a sensitive and specific index of vascular permeability if surface area remains constant, but derecruitment might affect Kf,c in severely damaged lungs with high vascular resistance. We studied the effect of high and low blood flow rates on Kf,c in papaverine-pretreated blood-perfused isolated dog lungs perfused under zone 3 conditions with and without paraquat (PQ, 10(-2) M). Three Kf,cs were measured successively at hourly intervals for 5 h. These progressed sequentially from isogravimetric blood flow with low vascular pressure (I/L) to high flow with low vascular pressure (H/L) to high flow with high vascular pressure (H/H). The blood flows of H/L and H/H were greater than or equal to 1.5 times that of I/L. There were no significant changes in Kf,c in lungs without paraquat over a 50-fold range of blood flow rates. At 3 h after PQ, I/L-Kf,c was significantly increased and both isogravimetric capillary pressure and total protein reflection coefficient were decreased from base line. At 4 and 5 h, H/L-Kf,c was significantly greater than the corresponding I/L-Kf,c (1.01 +/- 0.22 vs. 0.69 +/- 0.09 and 1.26 +/- 0.19 vs. 0.79 +/- 0.10 ml.min-1.cmH2O-1.100 g-1, respectively) and isogravimetric blood flow decreased to 32.0 and 12.0% of base line, respectively. Pulmonary vascular resistance increased to 12 times base line at 5 h after PQ. We conclude that Kf,c is independent of blood flow in uninjured lungs. However, Kf,c measured at isogravimetric blood flow underestimated the degree of increase in Kf,c in severely damaged and edematous lungs because of a high vascular resistance and derecruitment of filtering surface area.

Regional blood volume distribution during positive and negative airway pressure breathing in supine humans

1993 ◽  
Vol 75 (4) ◽  
pp. 1740-1747 ◽  
Author(s):  
J. Peters ◽  
B. Hecker ◽  
D. Neuser ◽  
W. Schaden
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Airway Pressure ◽  
Left Ventricular ◽  
Whole Body ◽  
Blood Content ◽  
Calf Blood Flow ◽  
Negative Airway Pressure

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10#x2013;12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7#x2013;10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.

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