scholarly journals A novel technique to study the time course of morphological and functional vascular responses to hypertension in conscious rats

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Harald Martin Stauss ◽  
Katie M Leick ◽  
Jason W Burkle ◽  
Diane L Rotella ◽  
Kevin R Rarick ◽  
...  
Keyword(s):  
Time Course ◽  
Vascular Responses ◽  
Conscious Rats ◽  
Novel Technique

Differential effect of taurocholic acid on hepatic arterial resistance vessels and bile flow

1983 ◽  
Vol 244 (4) ◽  
pp. G366-G369 ◽  
Author(s):  
W. W. Lautt ◽  
T. R. Daniels
Keyword(s):  
Hepatic Artery ◽  
Bile Flow ◽  
Time Course ◽  
Parenchymal Cell ◽  
Taurocholic Acid ◽  
Metabolic Effects ◽  
Vascular Effects ◽  
Bile Formation ◽  
Liver Parenchymal Cell ◽  
Vascular Responses

The "hepatic arterial buffer response" hypothesis states that the hepatic artery is not controlled by liver parenchymal cell metabolic activity. Bile salts stimulate liver metabolism (elevate bile formation) and dilate the hepatic artery. The present data show that the vascular and metabolic effects in cats anesthetized with pentobarbital sodium are independent. Low doses of taurocholate (1 microM . min-1 . kg-1) produce metabolic but not vascular responses. At higher doses both the hepatic artery and superior mesenteric artery dilate with equal sensitivity. Taurocholate into the portal vein produced elevated bile flow and hepatic arterial dilation; infusion via the hepatic artery resulted in equal metabolic responses but much greater vascular effects. In addition, the time course of onset and termination of the metabolic and vascular responses supports the conclusion that the effects of taurocholic acid on hepatic bile flow and hepatic arterial flow are independent actions. This adds further support for the hepatic arterial buffer response being controlled by factors other than local hepatic metabolic demands.

Systemic hemodynamics and oxygen transport during pregnancy in chronically instrumented, conscious rats

1992 ◽  
Vol 263 (6) ◽  
pp. H1911-H1918 ◽  
Author(s):  
G. J. Gilson ◽  
M. D. Mosher ◽  
K. P. Conrad
Keyword(s):  
Time Course ◽  
Carbon Dioxide Production ◽  
Respiratory Alkalosis ◽  
Late Gestation ◽  
Control Group ◽  
Peripheral Vascular ◽  
Pregnant Rats ◽  
Conscious Rats ◽  
Content Difference ◽  
Ultimate Purpose

Knowledge about possible alterations in cardiac output (CO), total peripheral vascular resistance (TPVR), and their time course and magnitude of change is conspicuously lacking for the conscious gravid rat. Therefore, we assessed CO using Fick methodology in unrestrained, chronically instrumented, conscious rats. The rats were studied during early (day 7), mid (day 13), or late gestation (day 18) along with nonpregnant control rats matched with respect to age and days postsurgery. Significant differences between pregnant and nonpregnant rats were observed during midgestation, when CO was increased by 26 +/- 12% and TPVR was decreased by 23 +/- 9% in the pregnant animals. These changes were accompanied by a narrowed arterial-mixed venous oxygen content difference (AVD; P < 0.05 vs. nonpregnant). In late gravid rats, CO was higher than nonpregnant values by 49 +/- 8%, and TPVR was lower by 34 +/- 7% (both P < 0.05). Oxygen consumption and carbon dioxide production were significantly increased, and AVD further narrowed when compared with the nonpregnant control group. With the exception of absent chronic respiratory alkalosis in pregnant rats, we conclude that cardiovascular and respiratory changes in conscious, gravid rats and in pregnant women are comparable. We speculate that the ultimate purpose of many of these adaptations is to increase CO so that oxygen delivery and the supply of nutrients to the uteroplacental units are sufficient or more than sufficient to meet oxygen and nutrient demands. At midgestation, the rise in CO seems to anticipate the oxygen needs of the nascent uteroplacental units.

Hemodynamic responses to leukotriene receptor stimulation in conscious rats

1990 ◽  
Vol 258 (4) ◽  
pp. R1034-R1041
Author(s):  
D. E. Allen ◽  
M. Gellai
Keyword(s):  
Time Course ◽  
Hypotensive Effect ◽  
Hemodynamic Changes ◽  
Vascular Effects ◽  
Conscious Rats ◽  
Intravenous Injections ◽  
Arterial Blood ◽  
Leukotriene Receptor ◽  
Renal Vascular ◽  
Dose Dependent

We evaluated the effects of leukotrienes (LTs) C4 and D4 on systemic and renal hemodynamics in conscious rats. Intravenous injections of LTC4 or LTD4 (0.5-10 micrograms/kg) caused dose-dependent decreases in cardiac output (CO), renal blood flow (RBF), and heart rate (HR). Flow alterations were accompanied by increased systemic and renal vascular resistances (SVR and RVR) and mean arterial blood pressure (MAP). No secondary hypotensive effect was observed. The HR response was biphasic, with tachycardia replacing the initial brief bradycardia. The changes in RBF and CO were not concurrent; the maximum RBF decrease (47.6 +/- 9.5%, P less than 0.05) occurred when CO was down only by 9.1 +/- 3.6% (P less than 0.05) and RBF had fully recovered in 3-4 min, while CO was still down by 26.3 +/- 3.5% (P less than 0.001). Hematocrit (HCT) increased after the injection of 5 and 10 micrograms/kg doses of LTC4 or LTD4, and its time course of recovery to basal level (30-60 min) paralleled that of CO. Sustained intravenous infusion of the selective LT receptor antagonist, SK&F 104353, dose-dependently inhibited the immediate hemodynamic changes after LTD4 injections. SK&F 104353 also attenuated the increase in vascular permeability and the prolonged decrease in CO, suggesting that the observed cardiac and vascular effects of LTs were mediated by stimulation of LT receptors.

A method to evaluate dynamic cerebral pressure-flow relationships in the conscious rat

2021 ◽  
Vol 131 (4) ◽  
pp. 1361-1369
Author(s):  
Debra Fong ◽  
Kelly Gradon ◽  
Carolyn J. Barrett ◽  
Sarah-Jane Guild ◽  
Yu Chieh Tzeng ◽  
...  
Keyword(s):  
Vena Cava ◽  
Vasoactive Agents ◽  
Conscious Rat ◽  
Pressure Flow ◽  
Conscious Rats ◽  
Novel Technique

We present a novel technique to overcome the use of vasoactive agents when studying cerebrovascular dynamics in the conscious rat. Our method of vena cava occlusion to reduce BP was associated with decreased iCBF and no change in iCVR. In contrast, comparable BP falls with intravenous SNP increased iCBF and reduced iCVR. Thus, the dynamic cerebral pressure-flow relationship shows a narrower, less level autoregulatory plateau than conventionally thought. We confirm our method allows repeatable assessment of cerebrovascular dynamics in conscious rats.

Effect of Endothelin on the Function of the Isolated Perfused Working Rat Heart

1990 ◽  
Vol 79 (3) ◽  
pp. 221-226 ◽  
Author(s):  
J. D. Firth ◽  
A. F. C. Roberts ◽  
A. E. G. Raine
Keyword(s):  
Cardiac Output ◽  
Rat Heart ◽  
Time Course ◽  
Calcium Entry ◽  
Calcium Entry Blockers ◽  
High Concentration ◽  
Vascular Responses ◽  
Coronary Vasoconstriction ◽  
Working Rat Heart ◽  
Sustained Increase

1. The effect of endothelin on the performance of the isolated perfused working rat heart has been examined. 2. A low concentration of endothelin (60 pmol/l) produced a gradual but sustained increase in cardiac output; coronary vascular resistance was unaffected. 3. A high concentration of endothelin (600 pmol/l) produced a rapid increase in cardiac output, followed by a marked fall in cardiac output as progressive, severe coronary vasoconstriction developed. 4. The coronary vasoconstriction induced by endothelin (600 pmol/l) was partially blocked by nicardipine (0.5 pmol/l) 5. In the presence of either nicardipine (0.5 μmol/l) or verapamil (0.2 μmol/l), the increment in cardiac output induced by endothelin (600 pmol/l) was greater than that induced by the addition of the same concentration of endothelin to hearts which had not been exposed to calcium-entry blockers. 6. The effect of endothelin on myocardial contractility has a different time course, concentration dependence and response to calcium-entry blockade than the effect on the coronary vasculature. This suggests that different mechanisms are involved in the generation of the myocardial and vascular responses to endothelin.

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