Mesenteric Blood Flow as Influenced by Progressive Hypercapnia

1956 ◽  
Vol 184 (2) ◽  
pp. 275-281 ◽  
Author(s):  
Eugene W. Brickner ◽  
E. Grant Dowds ◽  
Bruce Willitts ◽  
Ewald E. Selkurt

The influence of hypercapnia on mesenteric blood flow was studied in dogs subjected to progressive increments in CO2 content of inspired air produced by rebreathing from a large spirometer. Oxygen content was maintained above 21 volumes %. Although some animals showed an initial tendency for mesenteric blood flow to decrease and arterial pressure to increase in the range 0–5 volumes % of CO2, the usual hemodynamic change in the range 5–16 volumes % was an increase in mesenteric blood flow resulting from decrease in intestinal vascular resistance, accompanied by a decline in arterial pressure. Portal venous pressure was progressively elevated. Heart rate slowed in association with an increase in pulse pressure. The observations suggest that in higher ranges of hypercapnia, CO2 has a direct dilating action on the mesenteric vasculature.

1993 ◽  
Vol 75 (4) ◽  
pp. 1740-1747 ◽  
Author(s):  
J. Peters ◽  
B. Hecker ◽  
D. Neuser ◽  
W. Schaden

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.


2007 ◽  
Vol 103 (6) ◽  
pp. 2018-2025 ◽  
Author(s):  
D. Fischer ◽  
P. Arbeille ◽  
J. K. Shoemaker ◽  
D. D. O'Leary ◽  
R. L. Hughson

This study tested the hypothesis that cardiovascular and hormonal responses to lower body negative pressure (LBNP) would be altered by 4-h head down bed rest (HDBR) in 11 healthy young men. In post-HDBR testing, three subjects failed to finish the protocol due to presyncopal symptoms, heart rate was increased during LBNP compared with pre-HDBR, mean arterial blood pressure was elevated at 0, −10, and −20 mmHg and reduced at −40 mmHg, central venous pressure (CVP) and cardiac stroke volume were reduced at all levels of LBNP. Plasma concentrations of renin, angiotensin II, and aldosterone were significantly lower after HDBR. Renin and angiotensin II increased in response to LBNP only post-HDBR. There was no effect of HDBR or LBNP on norepinephrine while epinephrine tended to increase at −40 mmHg post-HDBR ( P = 0.07). Total blood volume was not significantly reduced. Splanchnic blood flow taken from ultrasound measurement of the portal vein was higher at each level of LBNP post-compared with pre-HDBR. The gain of the cardiopulmonary baroreflex relating changes in total peripheral resistance to CVP was increased after HDBR, but splanchnic vascular resistance was actually reduced. These results are consistent with our hypothesis and suggest that cardiovascular instability following only 4-h HDBR might be related to altered hormonal and/or neural control of regional vascular resistance. Impaired ability to distribute blood away from the splanchnic region was associated with reduced stroke volume, elevated heart rate, and the inability to protect mean arterial pressure.


1985 ◽  
Vol 249 (1) ◽  
pp. R85-R90
Author(s):  
H. J. Lenz ◽  
L. A. Fisher ◽  
W. W. Vale ◽  
M. R. Brown

Corticotropin-releasing factor (CRF), sauvagine (SVG), and urotensin I (UI) were tested for their effects on superior mesenteric blood flow in conscious dogs. Intravenous (iv) administration of CRF, SVG, and UI induced an immediate rise of mesenteric blood flow that was associated with a decrease in mean arterial pressure and an increase in heart rate. Intracerebroventricular (ICV) injection of SVG and UI, but not CRF, rapidly (within 5 min after injection) elicited a long (90 min) elevation of mesenteric blood flow. Central administration of these peptides induced a delayed rise in heart rate and slightly elevated mean arterial pressure. The finding that CRF given ICV did not increase mesenteric blood flow could not be explained by the release of vasoactive agents such as vasopressin, epinephrine, or norepinephrine. After injection of CRF, SVG, and UI, plasma concentrations of CRF-, SVG-, and UI-like immunoreactivity did not increase as determined by radioimmunoassay. These results indicate that SVG and UI, but not CRF, administered ICV produce a long increase of mesenteric blood flow in conscious dogs. Because iv SVG and UI decrease mean arterial pressure and ICV SVG and UI increase mean arterial pressure and do not cause an increase in SVG- and UI-like immunoreactivity in the peripheral circulation, it is proposed that SVG and UI injected into the third cerebral ventricle act within the central nervous system to increase superior mesenteric blood flow in the dog.


1982 ◽  
Vol 242 (6) ◽  
pp. G596-G602
Author(s):  
P. R. Kvietys ◽  
J. M. McLendon ◽  
G. B. Bulkley ◽  
M. A. Perry ◽  
D. N. Granger

The purpose of the present study was to characterize the intrinsic mechanisms involved in the regulation of blood flow and oxygenation in the totally isolated, perfused canine pancreas. Arterial pressure, venous outflow pressure, blood flow, arteriovenous oxygen difference, and capillary filtration coefficient were measured during graded arterial pressure reductions and venous pressure elevation. Reductions in arterial pressure caused pancreatic blood flow and vascular resistance to decrease, whereas venous pressure elevation resulted in a decreased blood flow and increased vascular resistance. The reductions in blood flow produced by arterial and venous pressure alterations were associated with increases in oxygen extraction and capillary filtration coefficient. During the same pressure perturbations, oxygen uptake remained constant between blood flows of 40-100 ml.min-1.100 g-1, yet decreased progressively as blood flow was reduced below 40 ml.min-1.100 g-1. Arterial occlusion resulted in a postocclusive reactive hyperemia, the magnitude of which was related to the duration of occlusion. The findings of this study suggest that intrinsic regulation of pancreatic blood flow can be attributed to both metabolic and myogenic mechanisms. Resistance and exchange vessels both appear to play a role in the regulation of oxygen delivery to the pancreatic parenchyma.


2002 ◽  
Vol 282 (1) ◽  
pp. H328-H334 ◽  
Author(s):  
M. Keith Wilkerson ◽  
Patrick N. Colleran ◽  
Michael D. Delp

10.1152/ajpheart.00727.2001.—The purpose of this study was to test the hypothesis that regional brain blood flow and vascular resistance are altered by acute and chronic head-down tail suspension (HDT). Regional cerebral blood flow, arterial pressure, heart rate, and vascular resistance were measured in a group of control rats during normal standing and following 10 min of HDT and in two other groups of rats after 7 and 28 days of HDT. Heart rate was not different among conditions, whereas mean arterial pressure was elevated at 10 min of HDT relative to the other conditions. Total brain blood flow was reduced from that during standing by 48, 24, and 27% following 10 min and 7 and 28 days of HDT, respectively. Regional blood flows to all cerebral tissues and the eyes were reduced with 10 min of HDT and remained lower in the eye, olfactory bulbs, left and right cerebrum, thalamic region, and the midbrain with 7 and 28 days of HDT. Total brain vascular resistance was 116, 44, and 38% greater following 10 min and 7 and 28 days of HDT, respectively, relative to that during control standing. Vascular resistance was elevated in all cerebral regions with 10 min of HDT and remained higher than control levels in most brain regions. These results demonstrate that HDT results in chronic elevations in total and regional cerebral vascular resistance, and this may be the underlying stimulus for the HDT-induced smooth muscle hypertrophy of cerebral resistance arteries.


1997 ◽  
Vol 272 (2) ◽  
pp. H894-H903 ◽  
Author(s):  
W. N. Henley ◽  
F. Vladic

Three experiments were conducted in unanesthetized rats made hypothyroid (Hypo) or maintained as euthyroid controls (Eu) to examine general cardiovascular responsiveness [experiment I (Exp I)]; responsiveness to a serotonin (5-HT2) agonist, dl-2,5-dimethoxy-4-iodoamphetamine [DOI intracerebroventricularly; experiment II (Exp II)]; or responsiveness to a 5-HT(1A) agonist dl-8-hydroxydipropyl-aminotetralin hydrobromide [8-OH-DPAT intracerebroventricularly; experiment III (Exp III)]. In Exp I, intravenous infusions of phenylephrine and nitroprusside provided little evidence that findings in Exp II and III were caused by generalized impairment in cardiovascular responsiveness in Hypo. In Exp II and III, Eu and Hypo were given either intra-arterial atropine or vehicle. Atropine significantly elevated heart rate (Exp II and III) and mean arterial pressure (Exp II) in Eu only. When compared with Eu, Hypo had a reduced pressor response (5.2 vs. 20.1%), an attenuated pulse pressure response (19.3 vs. 35.4%), and a more robust bradycardia (-17.7 vs. -7.0%) in response to DOI. These differences were atropine sensitive. In Exp III, Hypo had larger decrements in mean arterial pressure (-9.0 vs. -5.1%), heart rate ( -13.9 vs. - 7.7%), and body temperature (-4.5 vs. -2.7%) in response to 8-OH-DPAT in comparison to Eu. Parasympathetic involvement in the differential responses to 8-OH-DPAT was less clear than with DOI. Deranged autonomic control in hypothyroidism may be caused, in part, by changes in central serotonergic activity.


2007 ◽  
Vol 22 (4) ◽  
pp. 291-298 ◽  
Author(s):  
Marco Aurelio Marangoni ◽  
Alex Hausch ◽  
Pedro Thadeu Galvão Vianna ◽  
José Reinaldo Cerqueira Braz ◽  
Rosa Marlene Viero ◽  
...  

PURPOSE: About 50 % of indications for dialysis in acute renal failure are related to problems originated during the perioperative period. Intraoperative hemodynamic changes lead to renal vasoconstriction and hypoperfusion. Previous studies have not defined the dexmedetomidine renal role in hemorrhage situations. This study evaluated the effect of dexmedetomidine on renal function and histology after acute hemorrhage in rats. METHODS: Covered study with 20 Wistars rats, anesthetized with sodium pentobarbital, 50 mg. kg-1, intraperitoneal, randomized into 2 groups submitted to 30% volemia bleeding: DG - iv dexmedetomidine, 3 µg. kg-1 (10 min) and continuous infusion - 3 µg. kg-1. h-1; CG - pentobarbital. For renal clearance estimative, sodium p-aminohippurate and iothalamate were administered. Studied attributes: heart rate, mean arterial pressure, rectal temperature, hematocrit, iothalamate and p-aminohippurate clearance, filtration fraction, renal blood flow, renal vascular resistance, and histological evaluations of the kidneys. RESULTS: DG showed smaller values of heart rate, mean arterial pressure, and renal vascular resistance, but iothalamate clearance and filtration fraction values were higher. There was similarity in p-aminohippurate clearance and renal blood flow. Both groups had histological changes ischemia-like, but dexmedetomidine determined higher tubular dilatation scores. CONCLUSION: In rats, after acute hemorrhage, dexmedetomidine determined better renal function, but higher tubular dilation scores.


1978 ◽  
Vol 235 (2) ◽  
pp. H157-H161 ◽  
Author(s):  
A. P. Shepherd

In intestine, raising venous pressure (PV) elicits a precapillary vasconstriction that has been ascribed to a myogenic mechanism through which passive stretch elicits active contraction of vascular smooth muscle. A previous report from this laboratory indicated that myogenic responses in the gut were largely dependent on control conditions. The purpose of the present study was to determine whether control blood flow rates or the arterial pulse pressure affects the magnitude of myogenic responses. In isolated perfused canine small bowel arterial hypoxia was used to increase blood flow. Myogenic responses to elevated PV were not significantly different in the normoxic and hypoxic periods, indicating that blood flow per se does not greatly alter myogenic responses. When gut loops were perfused with pulsatile arterial pressure, myogenic responses occurred more than twice as frequently as during nonpulsatile pefusion and they had a greater magnitude. The results are consistent with the observation that vascular smooth muscle is stimulated not only by steady stretch but also by the rate of stretch. The results also suggest that the arterial pressure pulse should be considered in the design and interpretation of future studies of local circulatory control.


1975 ◽  
Vol 228 (2) ◽  
pp. 386-391 ◽  
Author(s):  
LA Hohnke

Arterial blood pressure (ABP) responses to graded hemorrhage and passive head-up tilt were studied in restrained, anesthetized, and unanesthetized iguanas. The ABP fell slowly in response to hemorrhage up to a critical deficit of 35 plus or minus 19% of the estimated blood volume; the rate of ABP fall then increased nearly 40-fold to continued hemorrhage. Increased heart rate and decreased femoral arterial blood flow accompanied progressive hemorrhage. Propranolol (2-3 mug/kg) did not appreciably alter arterial pressure-hemorrhage curves but hemorrhage-induced increases in heart rate were diminished nearly 50%. Atropine had little effect on either the blood pressure or heart rate changes induced by hemorrhage. During passive tilts of 0-90 degrees carotid arterial pressure fell 33% before returning to control levels (2 min). Heart rate increased and femoral arterial blood flow and central venous pressure fell in response to head-up tilts. It is concluded that hemorrhage and passive head-up tilting can induce reflex cardiovascular changes that assist ABP regulation in iguanas.


1985 ◽  
Vol 249 (6) ◽  
pp. G786-G791 ◽  
Author(s):  
D. N. Granger ◽  
S. L. Harper ◽  
R. J. Korthuis ◽  
H. G. Bohlen ◽  
P. R. Kvietys

The intestinal vascular responses to graded reductions in arterial pressure and elevations in venous pressure were measured in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Blood flow and capillary pressure were measured in denervated, autoperfused segments of small intestine. Blood flow, capillary pressure, and total vascular resistance were significantly higher in SHR than WKY at the resting mean arterial pressures. Decrements in arterial pressure led to significant reductions in total vascular resistance in WKY but not in SHR. There was a significant tendency for capillary pressure autoregulation in WKY but not in SHR. Increments in venous pressure did not alter vascular resistance in WKY, yet significantly increased total vascular resistance in SHR. The latter effect was due entirely to a rise in precapillary resistance and is consistent with an enhanced sensitivity of the vasculature to myogenic factors. Intestinal blood flow, measured using 15-micro microspheres, was not significantly different between WKY and SHR in innervated preparations. However, in denervated preparations intestinal blood flow was significantly higher in SHR than WKY, indicating that there is a significant neural component to the increased intestinal vascular resistance in SHR.


Sign in / Sign up

Export Citation Format

Share Document