Spontaneous pressure-flow relationships in renal circulation of conscious dogs

1993 ◽  
Vol 264 (5) ◽  
pp. H1517-H1527 ◽  
Author(s):  
S. Skarlatos ◽  
N. DiPaola ◽  
R. A. Frankel ◽  
R. W. Pomerantz ◽  
P. H. Brand ◽  
...  

Renal pressure-flow (P-F) relationships are usually evaluated by measuring effects of mechanically induced changes in renal arterial pressure (AP) on renal blood flow (RBF). We devised a method allowing evaluation of renal P-F relationships during normal changes in AP occurring spontaneously in a conscious animal rather than during artificially induced changes in AP. In 18 trials in 6 dogs standing at rest, we measured average AP and RBF for each cardiac cycle over periods of approximately 35 min (approximately 3,100 cardiac cycles/trial). AP and RBF values for each cardiac cycle were expressed as percent change (%delta) from the 35-min average (beat-to-beat changes). Slope and angle of each consecutive beat-to-beat P-F change were calculated and collated into one of eight zones representing the possible physiological mechanisms responsible for concurrent, spontaneous changes in RBF and AP. In a predominance of the cardiac cycles (approximately 43%), the spontaneous AP-RBF relationship was consistent with being mediated by arterial baroreflexes (i.e., increases in AP were accompanied by proportionately greater increases in RBF during 44.4% of cardiac cycles in which AP increased, and decreases in AP were accompanied by proportionately greater decreases in RBF during 41.4% of cardiac cycles in which AP decreased). Blockade of autonomic ganglionic transmission with hexamethonium markedly attenuated this pattern. Our results indicate that renal circulation participates in moment-to-moment control of AP via a predominant baroreflex-like pattern.

1993 ◽  
Vol 265 (6) ◽  
pp. H2151-H2159 ◽  
Author(s):  
S. Skarlatos ◽  
P. J. Metting ◽  
S. L. Britton

We have developed a model that permits a quantitative analysis of the contribution of different mechanisms to the spontaneously occurring pressure-flow patterns of a vasculature. In this study we evaluated the spontaneous relationship between arterial pressure (P) and renal blood flow (F) in resting conscious rats during control conditions, autonomic ganglionic blockade (hexamethonium), and nonselective alpha-adrenoreceptor blockade (phentolamine). In a total of 250 trials in 29 rats, we measured the average P and F for each cardiac cycle over 13-min periods (approximately 4,000 cardiac cycles/trial). The P and F values for each cardiac cycle were expressed as percentage change from each 13-min average (beat-to-beat changes). The slope and angle of each consecutive beat-to-beat P-F change were calculated and collated into one of eight zones representing the physiological mechanisms responsible for the concurrent spontaneous changes in P and F. Our results reveal that, in the absence of any chemical or mechanical intervention (control), the renal circulation demonstrated a baroreflex-like P-F pattern approximately 38% of the time. An autoregulatory-like P-F pattern occurred, at the most, 35% of the time. Autonomic ganglionic blockade significantly (P < 0.05) decreased the baroreflex-like pattern and increased the presence of P-F patterns indicative of autoregulation. alpha-Adrenoreceptor blockade resulted in a P-F pattern that was qualitatively similar to that produced by hexamethonium, but with considerably more variability. These results indicate that, in the resting conscious undisturbed state, the autonomic nervous system exerts a tonic influence on the renal circulation that facilitates arterial pressure regulation via a baroreflex-like pattern.


1961 ◽  
Vol 201 (3) ◽  
pp. 495-498 ◽  
Author(s):  
Jimmy B. Langston ◽  
Arthur C. Guyton ◽  
C. C. Hull ◽  
G. G. Armstrong

Previous experiments from this laboratory indicated that normal kidneys may not have significant intrinsic ability to autoregulate their blood flow when renal arterial pressure is varied. However, in these earlier studies, the renal blood flow was less than that generally accepted as normal, and there was a possibility that the renal circulation had not been completely isolated. This could have resulted in extrarenal blood flow during the pressure-flow study. In the present experiments, renal blood flows were in the normal range at all pressure levels. This difference was achieved by rendering the animals areflex prior to the laparotomy. The pressure-flow relationship was studied under these conditions, and the resulting curves were slightly concave to the pressure axis in the lower pressure range, indicating only a mild degree of autoregulation, approximately the same degree as that found in other tissues. However, the renal blood flow still increased rapidly with each increase in perfusion pressure even in the range of so-called autoregulation. It was also shown that all the blood that passed through the perfusion system also passed through the kidney, eliminating the possibility of extrarenal blood flow.


1991 ◽  
Vol 261 (6) ◽  
pp. H1836-H1841 ◽  
Author(s):  
J. G. Kennedy ◽  
M. J. Breslow ◽  
J. R. Tobin ◽  
R. J. Traystman

To determine the relative role of nicotinic and muscarinic mechanisms in splanchnic nerve stimulation (NS)-induced adrenal catecholamine secretion and medullary vasodilation, 12 pentobarbital-anesthetized dogs were subjected to three identical stimulations. The first NS was performed before drug administration and served as a control. The second NS was performed after administration of either the muscarinic antagonist, atropine 0.5 mg/kg (group 1), or the nicotinic antagonist, hexamethonium 20 mg/kg (group 2). The third NS was performed after administration of both drugs. NS in the absence of drug resulted in 4-fold and greater than 200-fold increases in medullary blood flow (Q, measured with radiolabeled microspheres) and catecholamine secretion (assayed by high-pressure liquid chromatography), respectively. Atropine, when administered alone (group 1), had no effect on these responses. Subsequent administration of hexamethonium to group 1 animals resulted in complete blockade of NS-induced changes in medullary Q and secretion. Hexamethonium alone (group 2) reduced the catecholamine response to NS by 95% but had no effect on the medullary Q response. Addition of atropine further attenuated the increase in catecholamine secretion induced by NS and completely blocked the medullary Q increase. These data suggest the presence of redundant mechanisms to increase medullary Q during NS. One mechanism likely involves neurally released acetylcholine-stimulating vascular muscarinic receptors, whereas the second requires either chromaffin cell degranulation or nicotinic ganglionic transmission.


Cephalalgia ◽  
2005 ◽  
Vol 25 (5) ◽  
pp. 344-352 ◽  
Author(s):  
LH Lassen ◽  
B Sperling ◽  
AR Andersen ◽  
J Olesen

The aim of this study was to estimate the effect of Nitric Oxide synthase (NOS)-inhibition (L-NMMA) on the diameter of the middle cerebral artery (MCA) and on regional cerebral blood flow (rCBF). Furthermore, to assess the effect of L-NMMA on acetazolamide induced increases in MCA blood velocity (Vmean) and rCBF. In an open crossover design 12 healthy subjects attended the laboratory twice. The first day 6 mg/kg L-LNMMA i.v. over 15 min preceded 1 g acetazolamide iv over 5 min. Eight days later only acetazolamide was given. Vmean in MCA was determined with transcranial Doppler (TCD) and rCBF with Xe-133 inhalation SPECT at baseline, after L-NMMA and 25 and 55 min after acetazolamide infusion. After L-NMMA the decrease in rCBFMCA was 6.8% (± 7.4) ( P < 0.019, n = 12), whereas Vmean was not affected ( P = 0.83, n = 8). The change in MCA diameter was estimated to -1.3% ( P = 0.44, n = 8). L-NMMA did not affect acetazolamide increases in Vmean ( P = 0.67, n = 8) nor rCBF ( P = 0.29, n = 12). The percentage increase of Vmean was 1.5 times that of rCBF ( n = 8). Our data suggest that the basal tone of human cerebral arterioles but not of conduit arteries is NO-dependent. The action of acetazolamide in man is not NO-dependent.


2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 132-132
Author(s):  
Zully E Contreras-Correa ◽  
Riley D Messman ◽  
Hector Sanchez-Rodriguez ◽  
Caleb O Lemley

Abstract The objectives were to examine melatonin mediated changes in temporal uterine blood flow (UBF) and vaginal temperatures (VT) in 54 Brangus heifers (Fall, n = 29; Summer, n = 25) during compromised pregnancy. At d160 of gestation, heifers were assigned to 1 of 4 groups consisting of adequately fed (ADQ-CON; 100% NRC; n=13), global nutrient restricted (RES-CON; 60% NRC; n = 13), and ADQ or RES supplemented with 20 mg of melatonin (ADQ-MEL, n = 13; RES-MEL, n = 15). In the morning (0500h) and afternoon (1300h) of d220 of gestation, temperature dataloggers (Onset Computer Corporation) attached to progesterone-free CIDRs were used to record VT, while UBF was determined via Doppler ultrasonography. Data were analyzed using repeated measures of ANOVA (SAS). Significant differences were found in UBF and VT between Fall and Summer groups (P&lt; 0.05), therefore seasons were individually analyzed. In Fall, a nutrition by treatment interaction was significant, where the RES-CON heifers exhibited reduced total UBF compared to ADQ-CON (5.67±0.68 vs. 7.97±0.54 L/min; P = 0.012). In Summer, there was not a main effect of nutrition (P = 0.390); nevertheless, the MEL heifers exhibited increased total UBF compared to the CON counterparts (8.16±0.73 vs. 6.00±0.70 L/min; P = 0.048). Moreover, there was a nutrition by treatment by time interaction in VT for Fall and Summer heifers (P &lt; 0.0001). In Fall, all groups had decreased VT in the morning compared to the afternoon (P &lt; 0.0001). Whereas, in Summer, VT increased for ADQ-CON, RES-CON, and ADQ-MEL from morning to afternoon (P &lt; 0.0001), while the RES-MEL remained constant throughout the day (P = 0.649). Furthermore, during the afternoon RES-MEL heifers exhibited decreased VT compared to ADQ-CON (38.91±0.09 vs. 39.26±0.09°C, respectively; P=0.039). In summary, nutrient restriction and melatonin supplementation altered UBF in a season dependent manner. Additionally, with the VT differences observed in Summer, future studies should evaluate the potential of melatonin supplementation for mitigating heat stress in farm animals.


2011 ◽  
Vol 110 (1) ◽  
pp. 188-198 ◽  
Author(s):  
Rebecca R. Vanderpool ◽  
Ah Ram Kim ◽  
Robert Molthen ◽  
Naomi C. Chesler

Hypoxic pulmonary hypertension (HPH) is initially a disease of the small pulmonary arteries. Its severity is usually quantified by pulmonary vascular resistance (PVR). Acute Rho kinase inhibition has been found to reduce PVR toward control values in animal models, suggesting that persistent pulmonary vasoconstriction is the dominant mechanism for increased PVR. However, HPH may also cause proximal arterial changes, which are relevant to right ventricular (RV) afterload. RV afterload can be quantified by pulmonary vascular impedance, which is obtained via spectral analysis of pulsatile pressure-flow relationships. To determine the effects of HPH independent of persistent pulmonary vasoconstriction in proximal and distal arteries, we quantified pulsatile pressure-flow relationships before and after acute Rho kinase inhibition and measured pulmonary arterial structure with microcomputed tomography. In control lungs, Rho kinase inhibition decreased 0 Hz impedance (Z0), which is equivalent to PVR, from 2.1 ± 0.4 to 1.5 ± 0.2 mmHg·min·ml−1 ( P < 0.05) and tended to increase characteristic impedance (ZC) from 0.21 ± 0.01 to 0.22 ± 0.01 mmHg·min·ml−1. In HPH lungs, Rho kinase inhibition decreased Z0 ( P < 0.05) without affecting ZC. Microcomputed tomography measurements performed on lungs after acute Rho kinase inhibition demonstrated that HPH significantly decreased the unstressed diameter of the main pulmonary artery (760 ± 60 vs. 650 ± 80 μm; P < 0.05), decreased right pulmonary artery compliance, and reduced the frequency of arteries of diameter 50–100 μm (both P < 0.05). These results demonstrate that acute Rho kinase inhibition reverses many but not all HPH-induced changes in distal pulmonary arteries but does not affect HPH-induced changes in the conduit arteries that impact RV afterload.


1988 ◽  
Vol 65 (1) ◽  
pp. 272-282 ◽  
Author(s):  
W. M. Long ◽  
L. D. Yerger ◽  
H. Martinez ◽  
E. Codias ◽  
C. L. Sprung ◽  
...  

Ascaris suum antigen effects on mean airflow resistance (RL) and bronchial arterial blood flow (Qbr) were studied in allergic anesthetized sheep with documented airway responses. Qbr was measured with electromagnetic flow probes, and supplemental O2 prevented antigen-induced hypoxemia. Aerosol challenge with this specific antigen increased RL and Qbr significantly. Cromolyn sodium aerosol pretreatment prevented antigen-induced increases in RL but not in Qbr. Intravenous cromolyn, however, prevented increases in Qbr and RL, suggesting a role for mast cell degranulation in both bronchomotor and bronchovascular responses to antigen. Antigen-induced increases in Qbr were not solely attributable to histamine release. Indomethacin pretreatment attenuated the antigen-induced increase in Qbr, thus suggesting that vasodilator cyclooxygenase products contribute to the vascular response. Antigen challenge significantly decreased Qbr after indomethacin and metiamide pretreatment, which suggests that vasoconstrictor substances released after antigen exposure also modulate Qbr; however, released vasodilators overshadow vasoconstrictor effects. Thus antigen challenge affects Qbr by locally releasing histamine and vasodilator prostaglandins as well as vasoconstrictor substances. These effects were independent of antigen-induced changes in systemic and pulmonary hemodynamics.


2006 ◽  
Vol 34 (02) ◽  
pp. 351-361 ◽  
Author(s):  
Ching-Liang Hsieh ◽  
Qwang-Yuen Chang ◽  
I-hsin Lin ◽  
Jaung-Geng Lin ◽  
Chung-Hsiang Liu ◽  
...  

Electroacupuncture (EA) is widely used to treat disorders of the nervous system, such as stroke. The aim of the present study was to investigate the effect of EA on cerebral blood flow (CBF) in cerebral ischemic rats. We developed an animal model of cerebral ischemia (CI) by occluding the blood flow of both common carotid arteries in Sprague-Dawley (SD) rats; 2 or 15 Hz EA was applied to both Zusanli acupoints. The levels of nitric oxide (NO) in the peripheral blood and amounts of calcitonin gene-related peptide (CGRP) in the cerebral cortex and thalamus were measured. In addition, L-N (G)-nitro arginine methyl ester (L-NAME) was used to measure the changes in CBF induced by EA in rats with and without CI. The results indicated that both 2 and 15 Hz EA increase the mean CBF in rats with and without CI. However, neither 2 nor 15 Hz EA induced changes in levels of NO in peripheral blood or changes in CGRP levels in cerebral cortex and thalamus. In addition, L-NAME did not change the increase in CBF. We concluded that both 2 and 15 Hz EA at both Zusanli acupoints induced the increase of CBF in rats with and without CI. Whether the effect of EA is related to NO or CGRP will be investigated in a future study.


2013 ◽  
Vol 33 (12) ◽  
pp. 1915-1920 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Kohei Sato ◽  
Kazunobu Okazaki ◽  
Tadayoshi Miyamoto ◽  
Ai Hirasawa ◽  
...  

The purpose of the present study was to assess the effect of heat stress-induced changes in systemic circulation on intra- and extracranial blood flows and its distribution. Twelve healthy subjects with a mean age of 22±2 (s.d.) years dressed in a tube-lined suit and rested in a supine position. Cardiac output (Q), internal carotid artery (ICA), external carotid artery (ECA), and vertebral artery (VA) blood flows were measured by ultrasonography before and during whole body heating. Esophageal temperature increased from 37.0±0.2°C to 38.4±0.2°C during whole body heating. Despite an increase in Q (59±31%, P<0.001), ICA and VA decreased to 83±15% ( P=0.001) and 87±8% ( P=0.002), respectively, whereas ECA blood flow gradually increased from 188±72 to 422±189 mL/minute (+135%, P<0.001). These findings indicate that heat stress modified the effect of Q on blood flows at each artery; the increased Q due to heat stress was redistributed to extracranial vascular beds.


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