Effects of Intraabdominanlly Insufflated Carbon Dioxide and Elevated Intraabdominal Pressure on Splanchnic Circulation 

1998 ◽  
Vol 89 (2) ◽  
pp. 475-482 ◽  
Author(s):  
Manfred Blobner ◽  
Ralph Bogdanski ◽  
Eberhard Kochs ◽  
Julia Henke ◽  
Alexander Findeis ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Splanchnic Circulation ◽  
Arterial Blood Flow ◽  
Intraabdominal Pressure ◽  
Arterial Blood ◽  
Baseline Values ◽  
Air Insufflation

Background Intraabdominally insufflated carbon dioxide (CO2) during laparoscopy may have a specific effect on splanchnic circulation that may be unrelated to the effects of increased intraabdominal pressure alone. Therefore, the influences of insufflation with CO2 versus air on splanchnic circulation were compared. Methods Pigs were chronically instrumented for continuous recording of mesenteric artery, portal venous, inferior vena cava, and pulmonary arterial blood flow and portal venous pressure. After induction of anesthesia, CO2 or air was insufflated in 14 and 10 pigs, respectively. With the pigs in the supine position, intraabdominal pressure was increased in steps of 4 mmHg up to 24 mmHg by graded gas insufflation. Results During air insufflation, mesenteric artery vascular resistance was unchanged, whereas mesenteric arterial blood flow decreased with increasing intraabdominal pressure. Shortly after CO2 insufflation to an intraabdominal pressure of 4 mmHg, mean arterial pressure, mesenteric arterial blood flow, and mesenteric arterial vascular resistance were increased by 21%, 12% and 9%, respectively. Subsequently, with the onset of CO2 resorption in the third minute, mean arterial pressure declined to baseline values and mesenteric arterial vascular resistance declined to 85% of baseline values, whereas mesenteric arterial blood flow continued to increase to a maximum of 24% higher than baseline values. At steady-state conditions during CO2 insufflation, mesenteric arterial blood flow was increased up to an intraabdominal pressure 16 mmHg but decreased at higher intraabdominal pressures. Conclusions In contrast to air insufflation, intraabdominal insufflation of CO2 resulted in a moderate splanchnic hyperemia at an intraabdominal pressure < or = 12 mmHg. At higher intraabdominal pressure values, pressure-induced changes became more important than the type of gas used.

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

Pulmonary blood flow, pressure and resistance following tetraethylammonium and aminophylline

1961 ◽  
Vol 200 (2) ◽  
pp. 287-291 ◽  
Author(s):  
M. Harasawa ◽  
S. Rodbard
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Arterial Blood Flow ◽  
Tetraethylammonium Chloride ◽  
Blood Flows ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Flow Pressure

The effects of tetraethylammonium chloride (TEAC) and aminophylline on the pulmonary vascular resistance were studied in thoracotomized dogs. Pulmonary arterial blood flow and pressure, and systemic blood pressure were measured simultaneously. Both drugs showed marked hypotensive effects on the systemic vessels. In every instance pulmonary arterial pressures and blood flows were reduced by TEAC given via the pulmonary artery and increased by aminophylline. However, the calculated pulmonary vascular resistance remained essentially unchanged in all experiments. These data challenge the concept that the pulmonary vessels respond to these drugs by active vasodilatation

Intraabdominal Carbon Dioxide Insufflation in the Pregnant Ewe

1996 ◽  
Vol 85 (6) ◽  
pp. 1395-1402. ◽  
Author(s):  
Antonio M. Cruz ◽  
Lucy C. Southerland ◽  
Tanya Duke ◽  
Hugh G. G. Townsend ◽  
James G. Ferguson ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Intraabdominal Pressure ◽  
Control Group ◽  
Uterine Blood Flow ◽  
Carbon Dioxide Insufflation ◽  
Carbon Dioxide Pneumoperitoneum ◽  
Arterial Blood ◽  
End Tidal Carbon Dioxide ◽  
End Tidal

Background Laparoscopic surgical procedures are being performed in pregnant women with increasing frequency. Maternal-fetal physiologic changes occurring during intraabdominal carbon dioxide insufflation are poorly understood, and maternal-fetal safety is of concern during carbon dioxide pneumoperitoneum. A previous pilot study using end-tidal carbon dioxide-guided ventilation resulted in maternal and fetal acidosis and tachycardia during carbon dioxide pneumoperitoneum. Using serial arterial PCO2 to guide ventilation, this study was designed to evaluate maternal-fetal cardiopulmonary status, uterine blood flow, and the intraamniotic pressure effects of intraabdominal carbon dioxide insufflation in singleton pregnant ewes between 120 and 135 days of gestation. Methods In a prospective randomized cross-over study, nine ewes were to receive either abdominal insufflation with carbon dioxide to an intraabdominal pressure of 15 mmHg (n = 9; insufflation group) or receive no insufflation (n = 9; control group). Anesthesia was induced with thiopental and maintained with end-tidal halothane (1 to 1.5 minimum alveolar concentration/100% oxygen). Mechanical ventilation was guided by serial maternal arterial blood gas analysis to maintain PaCO2 between 35 and 40 mmHg. Data from insufflated animals were collected during insufflation (60 min) and after desufflation (30 min). Control group data were collected and matched to similar time intervals for 90 min. Ewes were allowed to recover, and after a rest period (48 h) they were entered in the cross-over study. Results During insufflation there was a significant increase (P < 0.05) in maternal PaCO2 to end-tidal carbon dioxide gradient and minute ventilation, with concomitant decreases in maternal end-tidal carbon dioxide and PaO2. Intraamniotic pressure increased significantly during insufflation. No significant changes were observed in maternal hemodynamic variables, fetal variables, or in uterine blood flow during the study. There were no fetal deaths or preterm labor in any of the animals during the experiment. Conclusions During the 1-h insufflation, a marked increase in PaCO2-to-end-tidal carbon dioxide gradient was observed, suggesting that capnography may be an inadequate guide to ventilation during carbon dioxide pneumoperitoneum in the pregnant patient. No other significant circulatory changes were observed.

Effect of orthotopic transplantation of liver on systemic and splanchnic hemodynamics in conscious rat

1995 ◽  
Vol 269 (1) ◽  
pp. G153-G159 ◽  
Author(s):  
L. V. Kuznetsova ◽  
D. Zhao ◽  
A. M. Wheatley
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Portal Pressure ◽  
Peripheral Resistance ◽  
Vena Cava ◽  
Cardiovascular Effects ◽  
Suture Technique ◽  
Arterial Blood Flow ◽  
Conscious Rat ◽  
Arterial Blood

The long-term cardiovascular effects of orthotopic liver transplantation (OLT) were studied in conscious Lewis rats with a radioactive microsphere technique. Three months after OLT with an all-suture technique for graft revascularization (s-OLT), all hemodynamic parameters were similar to control. OLT with "cuffs" fitted to the portal vein and infrahepatic inferior vena cava (c-OLT) led to prominent hemodynamic disturbances including 1) hyperkinetic circulation with increased cardiac index (CI; 22%; P < 0.05) and decreased mean arterial pressure (15%; P < 0.05) and total peripheral resistance (TPR; 28%; P < 0.05); 2) a slight increase in portal pressure (11.8 +/- 0.9 vs. 9.3 +/- 1.7 mmHg in control) and marked portal-systemic shunting (51 +/- 11 vs. 0.05 +/- 0.04% in control; P < 0.05); 3) increased hepatic arterial blood flow (0.49 +/- 0.06 vs. 0.27 +/- 0.04 ml.min-1.g liver wt-1; P < 0.05); 4) splanchnic vasodilation with vascular resistance significantly (P < 0.05) lower in the liver, stomach, and large intestine; and 5) increased blood flow and decreased vascular resistance in the kidneys and heart. Ganglionic blockade with chlorisondamine (5 mg/kg body wt iv) indicated that the increase in CI seen in the c-OLT rats was probably sympathetically mediated, whereas the increase in renal blood flow was a reflection of the increase in CI. After ganglionic blocker administration, TPR and regional vascular resistances decreased to approximately the same extent in the control and c-OLT groups, indicating that vascular sympathetic tone was unchanged in the c-OLT rats.(ABSTRACT TRUNCATED AT 250 WORDS)

L-arginine augments nitric oxide production and mesenteric blood flow in ovine endotoxemia

1996 ◽  
Vol 271 (4) ◽  
pp. H1296-H1301
Author(s):  
K. G. Allman ◽  
A. P. Stoddart ◽  
M. M. Kennedy ◽  
J. D. Young
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Nitric Oxide Production ◽  
Mesenteric Blood Flow ◽  
Oxide Production ◽  
Arterial Blood ◽  
Nitrate Concentrations

We studied the effects of administrating the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the nitric oxide precursor, L-arginine, on hemodynamic variables and serum nitrate concentrations in an anesthetized ovine model of endotoxemia to assess the effects on regional visceral blood flow and to determine whether L-arginine availability limits nitric oxide production. Animals received Escherichia coli endotoxin (2 micrograms/kg) followed 2 h later by L-NAME (25 mg/kg), L-arginine (0.575 g/kg), or saline administered over 1 h followed by an infusion of the same dose over 8 h (n = 6 per group). Renal and mesenteric blood flow were measured by placement of electromagnetic flow probes, and serum nitrate concentrations were determined using vanadium III chloride or nitrate reductase reduction to nitric oxide or nitrite, respectively. The results showed L-NAME significantly increased systemic vascular resistance (P < 0.01), decreased serum nitrate concentrations (P < 0.05), and caused a transient reduction in mesenteric blood flow (P < 0.05). L-Arginine caused a reduction in systemic vascular resistance (P < 0.01), increased mesenteric blood flow (P < 0.001) and conductance (P < 0.05). There were no significant changes in renal arterial blood flow in either group. We conclude that the availability of L-arginine limits nitric oxide production in endotoxemia and, furthermore, that L-arginine administration in this model causes significant mesenteric vasodilatation. L-NAME administration had only limited effect on visceral blood flow despite a marked increase in systemic vascular resistance and a reduction in nitric oxide production.

Persistent fetal pulmonary hypoperfusion after acute hypoxia

1987 ◽  
Vol 253 (4) ◽  
pp. H941-H948 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso ◽  
R. B. Wilkening ◽  
G. Meschia
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Blood Flow ◽  
Acute Hypoxia ◽  
Arterial Blood Flow ◽  
Adrenergic Blockade ◽  
Flow Transducer ◽  
Arterial Blood ◽  
Pulmonary Arterial

To determine the effects of duration of hypoxia on fetal pulmonary blood flow and vasoreactivity, we studied the response of the fetal pulmonary vascular bed before, during, and after prolonged (2-h) and more brief (30-min) exposures to acute hypoxia in 19 chronically instrumented unanesthetized fetal lambs. Left pulmonary arterial blood flow was measured by an electromagnetic flow transducer. Fetal PO2 was lowered by delivering 10-12% O2 to the ewe. During 2-h periods of hypoxia left pulmonary arterial blood flow decreased, and main pulmonary arterial and pulmonary vascular resistance increased. The increase in pulmonary vascular resistance was sustained throughout the 2-h period of hypoxia. After the return of the ewe to room air breathing, pulmonary vascular resistance remained elevated for at least 1 h despite the rapid correction of hypoxemia and in the absence of acidemia. In contrast, after 30 min of hypoxia, left pulmonary arterial blood flow, pulmonary arterial pressure, and pulmonary vascular resistance returned to base-line values rapidly with the termination of hypoxia. The persistent pulmonary hypoperfusion after 2 h of hypoxia was attenuated by alpha-adrenergic blockade and was characterized by a blunted vasodilatory response to increases in fetal PO2. When fetal PO2 was elevated during the posthypoxia period in the presence of alpha-blockade, pulmonary blood flow still remained unresponsive to increases in fetal PO2. We conclude that 2-h periods of acute hypoxia can decrease fetal pulmonary vasoreactivity, and we speculate that related mechanisms may contribute to the failure of the normal adaptation of the pulmonary circulation at birth.

Participation of adrenoceptors in liver blood flow regulation in anesthetized dogs

1987 ◽  
Vol 253 (5) ◽  
pp. H1053-H1058
Author(s):  
N. Terada ◽  
S. Koyama ◽  
J. Horiuchi ◽  
T. Takeuchi
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Vascular Resistance ◽  
Adrenergic Receptors ◽  
Liver Blood Flow ◽  
Arterial Blood Flow ◽  
Tissue Blood Flow ◽  
Intact Group ◽  
Arterial Blood

We evaluated involvement of adrenergic receptors in the responses of the hepatic vasculature to reduction either of portal venous flow or hepatic arterial inflow. Portal vein occlusion caused an increase in hepatic arterial blood flow (HAF) and decreases in hepatic arterial pressure (HAP) and hepatic arterial vascular resistance (HAR) in the intact group. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the portal vein produced a greater decrease in HAP as compared with that in the intact group. No significant changes in HAF, HAR, or hepatic tissue blood flow (HTF) occurred after the treatment. These results indicate that the compensatory response of the hepatic arterial vasculature to altered portal blood flow (PVF) is regulated independently of the intrahepatic adrenergic receptors. Hepatic arterial occlusion caused a significant decrease in portal venous pressure, PVF, and HTF. Portal venous vascular resistance (PVR) was reduced slightly, but not significantly. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the hepatic artery produced an opposite effect: to increase PVF and significantly decrease PVR. These results indicate that intrahepatic alpha-adrenoceptors participate in the regulation of portal vascular tone to maintain portal vein pressure at a steady level, when inflow from the hepatic artery is reduced.

Maintenance of hepatic arterial blood flow during hemorrhage is mediated by adenosine

1989 ◽  
Vol 67 (9) ◽  
pp. 1023-1028 ◽  
Author(s):  
W. Wayne Lautt ◽  
Janet E. McQuaker
Keyword(s):  
Blood Flow ◽  
Superior Mesenteric Artery ◽  
Adenosine Receptor ◽  
Mesenteric Artery ◽  
Portal Blood Flow ◽  
Arterial Blood Flow ◽  
Splanchnic Blood Flow ◽  
Receptor Blockade ◽  
Shed Blood ◽  
Arterial Blood

The effect of hemorrhage (1.91 mL/min, 10 mL/kg) on splanchnic blood flow was determined in cats anesthetized with pentobarbital. The hepatic artery (HA) is relatively protected during hemorrhage and does not constrict, whereas the superior mesenteric artery (SMA) undergoes significant vasoconstriction. Adenosine receptor antagonism with 8-phenyltheophylline blocks the dilator response to infused adenosine selectively (does not block responses to isoproterenol). The dilator response to reduced portal blood flow (the HA buffer response) is also antagonized and adenosine receptor blockade converts the HA response to hemorrhage to one similar to that of the SMA. Thus, the protective dilation of the HA during hemorrhage is mediated by adenosine. In contrast, the vasodilation of the HA seen with reinfusion of the shed blood is not altered by adenosine receptor antagonism.Key words: adenosine, hemorrhage, splanchnic blood flow, hepatic blood flow, hepatic arterial buffer response.

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