Effects of vesical and perfusion pressure on perfusate flow, and flow on vesical pressure, in the isolated perfused working pig bladder reveal a potential mechanism for the regulation of detrusor compliance

The purpose of this study was to determine the effect of vasodilation on the distribution of perfusate flow in the isolated guinea pig heart. Hearts were perfused retrogradely through the aorta with oxygenated Krebs-Henseleit buffer solution at 37 degrees C. Regional myocardial flows were measured with 15-micron radioactive microspheres. Each heart was subdivided into 45 pieces (average size 44 mg), and heterogeneity of flow was quantified as the relative dispersion (standard deviation/mean). Under control conditions at a perfusion pressure of 46 mmHg (60 cm water), the relative dispersion of left ventricular (LV) flow was 30 +/- 2% (n = 8). Vasodilation was induced via infusion of dipyridamole (10(-5) M). When flow was held constant at the resting value, relative flow dispersion increased to 43 +/- 6% (n = 8). When perfusion pressure was held constant and flow allowed to increase, relative dispersion fell to 20 +/- 5% (n = 5). Heterogeneity for the heart as a whole was higher than for the left ventricle but followed the same pattern with vasodilation. In a separate series of hearts (n = 5) equipped with LV balloons but without microsphere flow measurements, vasodilation at constant flow decreased LV pressure development, dP/dt, and O2 consumption. Vasodilation at constant pressure increased O2 consumption, but did not increase LV pressure or dP/dt. We conclude that vasodilation in this preparation will increase flow heterogeneity during constant-flow perfusion but decrease heterogeneity during constant-pressure perfusion. Furthermore, increased flow heterogeneity can compromise ventricular function.

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Attenuated pressure natriuresis in the early phases of two-kidney Goldblatt hypertension

AJP Renal Physiology ◽

10.1152/ajprenal.1984.246.5.f691 ◽

1984 ◽

Vol 246 (5) ◽

pp. F691-F699

Author(s):

S. G. Rostand ◽

K. A. Kirk

Keyword(s):

Blood Pressure ◽

Sodium Excretion ◽

Adrenal Glands ◽

Perfusion Pressure ◽

Hypertensive Rats ◽

Excretory Function ◽

Perfusate Flow ◽

Pressure Natriuresis ◽

Early Phases ◽

Intact Rats

We studied the effect of changing perfusion pressure on the excretory function of isolated perfused nonclipped kidneys from the two-kidney Goldblatt hypertensive rat ( GHR ). Kidneys were studied from newly hypertensive rats about 8 days after contralateral renal artery clipping [blood pressure (BP) 138 +/- 4.3 mmHg] and before onset of hypertension 3 days following surgery (BP 111 +/- 1.9 mmHg). In addition, nonclipped kidneys from adrenalectomized Goldblatt rats were also examined approximately 9 days following surgery (BP 114 +/- 4.7 mmHg). Kidneys from sham-operated rats served as controls. We noted no differences in GFR in kidneys from newly hypertensive rats and sham controls above a perfusion pressure of 120 mmHg. In response to increasing perfusing pressure, perfusate flow and fractional sodium excretion were significantly lower in newly hypertensive rats than in sham-operated controls. No differences in glomerular filtration rate, perfusate flow, or sodium excretion were noted in kidneys from sham-operated rats or Goldblatt rats 3 days following surgery. After clipping, adrenalectomized (ADX) Goldblatt rats had less of a rise in blood pressure than did rats with intact adrenal glands. No attenuation of natriuresis was noted in the ADX-clipped group in response to increasing perfusion pressure. Isolated perfused kidneys from ADX rats had greater sodium excretion at all levels of pressure than kidneys from rats with intact adrenal glands. Deoxycorticosterone acetate replacement returned sodium excretion to that approaching intact rats. We conclude that nonclipped kidneys of newly hypertensive Goldblatt rats exhibit blunted pressure natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

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Angiotensinogen's role in ANG formation, renin release, and renal hemodynamics in isolated perfused kidney

AJP Renal Physiology ◽

10.1152/ajprenal.1989.256.4.f719 ◽

1989 ◽

Vol 256 (4) ◽

pp. F719-F727 ◽

Cited By ~ 1

Author(s):

J. Misumi ◽

J. Gardes ◽

M. F. Gonzalez ◽

P. Corvol ◽

J. Menard

Keyword(s):

Perfusion Pressure ◽

Renin Angiotensin System ◽

Renal Hemodynamics ◽

Renin Release ◽

Ang Ii ◽

Angiotensin I ◽

Angiotensin System ◽

Perfusate Flow ◽

Free Plasma

Isolated perfused rat kidneys were used to investigate the effects of the addition of pure angiotensinogen or renin-free plasma to the perfusate on angiotensin I (ANG I) and angiotensin II (ANG II) generation, renal hemodynamics, and renin release. When no angiotensinogen or plasma is added, a very small amount of angiotensinogen is initially detected in the perfusate. Whereas renin secreted by the kidney accumulates in the perfusate, angiotensinogen disappears during the perfusion and immunoreactive ANG II cannot be detected. The addition of angiotensinogen reactivates the renin-angiotensin system. ANG I, [des-Asp1] ANG I, ANG II, and [des-Asp1] ANG II are progressively generated in the perfusate. At a constant perfusion pressure, as well as at a variable perfusion pressure, a progressive fall in renal perfusate flow is observed that is significantly correlated to the level of immunoreactive ANG II. ANG II significantly blunts the rise in renin, and renin release in the perfusate is negatively correlated to immunoreactive ANG II levels. Comparison of the ANG I and ANG II levels in in vitro incubated perfusates and circulated perfusates shows that in plasma-injected perfusates the level of immunoreactive ANG II is dependent on both the production of ANG I and its conversion to ANG II by renal and perfusate converting-enzyme activity, and on ANG I and ANG II degradation by the kidney and the perfusate.

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Microvascular features that suggest effectors of blood-flow regulation in the brain: Evidence by SEM of corrosion casts of intracerebral vessels

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100158923 ◽

1990 ◽

Vol 48 (3) ◽

pp. 274-275

Author(s):

Enrico D.F. Motti ◽

Hans-Georg Imhof ◽

Gazi M. Yasargil

Keyword(s):

Blood Flow ◽

Perfusion Pressure ◽

Corrosion Casts ◽

Cerebral Microcirculation ◽

Pial Arteries ◽

Random Occurrence ◽

Brain Arteries ◽

Homogeneous Network ◽

The Brain

Physiologists have devoted most attention in the cerebrovascular tree to the arterial side of the circulation which has been subdivided in three levels: 1) major brain arteries which keep microcirculation constant despite changes in perfusion pressure; 2) pial arteries supposed to be effectors regulating microcirculation; 3) intracerebral arteries supposed to be deprived of active cerebral blood flow regulating devices.The morphological search for microvascular effectors in the cerebrovascular bed has been elusive. The opaque substance of the brain confines in vivo investigation to the superficial pial arteries. Most morphologists had to limit their observation to the random occurrence of a favorable site in the practically two-dimensional thickness of diaphanized histological sections. It is then not surprising most investigators of the cerebral microcirculation refer to an homogeneous network of microvessels interposed between arterioles and venules.We have taken advantage of the excellent depth of focus afforded by the scanning electron microscope (SEM) to investigate corrosion casts obtained injecting a range of experimental animals with a modified Batson's acrylic mixture.

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Emotional Impact Feedback Changes How We Remember Negative Autobiographical Experiences

Experimental Psychology (formerly Zeitschrift für Experimentelle Psychologie) ◽

10.1027/1618-3169/a000042 ◽

2010 ◽

Vol 57 (5) ◽

pp. 354-359 ◽

Cited By ~ 10

Author(s):

Melanie K. T. Takarangi ◽

Deryn Strange

Keyword(s):

Well Being ◽

The Other ◽

Personal Perspective ◽

Emotional Impact ◽

Potential Mechanism ◽

Negative Experiences ◽

Negative Memory ◽

The Relationship ◽

Negative Memories ◽

Over Time

When people are told that their negative memories are worse than other people’s, do they later remember those events differently? We asked participants to recall a recent negative memory then, 24 h later, we gave some participants feedback about the emotional impact of their event – stating it was more or less negative compared to other people’s experiences. One week later, participants recalled the event again. We predicted that if feedback affected how participants remembered their negative experiences, their ratings of the memory’s characteristics should change over time. That is, when participants are told that their negative event is extremely negative, their memories should be more vivid, recollected strongly, and remembered from a personal perspective, compared to participants in the other conditions. Our results provide support for this hypothesis. We suggest that external feedback might be a potential mechanism in the relationship between negative memories and psychological well-being.

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