Amelioration of arterial pressure lability: an unmissable target for diabetes management

2017 ◽  
Vol 40 (7) ◽  
pp. 629-631
Author(s):  
Atsushi Tanaka ◽  
Koichi Node
Keyword(s):  
Arterial Pressure ◽  
Diabetes Management ◽  
Arterial Pressure Lability

Central and peripheral mechanisms of arterial pressure lability following baroreceptor denervation

1987 ◽  
Vol 65 (8) ◽  
pp. 1615-1618 ◽  
Author(s):  
R. H. Alper ◽  
H. J. Jacob ◽  
M. J. Brody
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Humoral Factors ◽  
Neural Transmission ◽  
Sympathetic Transmission ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine ◽  
Alpha Adrenergic Agonist ◽  
Arterial Pressure Lability

Deafferentation of sinoaortic baroreceptors produces a marked increase in the lability of arterial pressure that is sustained chronically. Studies reviewed in this paper were designed to determine the mechanisms responsible for generating arterial pressure lability. Pharmacological interruption of the humoral vasopressin and angiotensin systems failed to alter arterial pressure lability. In contrast, blockade of sympathetic nervous system transmission at both ganglionic and alpha-adrenergic receptor levels significantly attenuated lability. A similar effect was observed with the peripheral neurotoxin, 6-hydroxydopamine. After blockade of sympathetic transmission, a further reduction in lability was produced by blocking the renin–angiotensin or vasopressin systems. The dissociation of the level of arterial pressure from lability was achieved with parachloroamphetamine which raised arterial pressure but reduced lability. A substantial peripheral contribution to lability was obtained in experiments in which the alpha-adrenergic agonist, phenylephrine, produced a marked increase in lability in both normal and baroreceptor-denervated animals in which humoral and neural transmission were blocked. These data demonstrate that following baroreceptor deafferentation, arterial pressure lability is produced primarily by the sympathetic nervous system and secondarily by circulating humoral factors that appear to act on vascular smooth muscle to induce fluctuations in the level of arterial pressure.

scholarly journals Arterial pressure lability is improved by sodium-glucose cotransporter 2 inhibitor in streptozotocin-induced diabetic rats

2017 ◽  
Vol 40 (7) ◽  
pp. 646-651 ◽  
Author(s):  
Tomoko Yoshikawa ◽  
Takuya Kishi ◽  
Keisuke Shinohara ◽  
Ko Takesue ◽  
Risa Shibata ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Diabetic Rats ◽  
Sodium Glucose Cotransporter ◽  
Arterial Pressure Lability

EFFECTS OF ARTERIAL PRESSURE LABILITY ON THE FUNCTION AND STRUCTURE OF LARGE ARTERIES IN RATS

1997 ◽  
Vol 11 (S1) ◽  
pp. 94s-94s
Author(s):  
Y Bézie ◽  
P Challande ◽  
E Glaser ◽  
B Lucet ◽  
M Safar ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Large Arteries ◽  
Arterial Pressure Lability

Regulation of arterial pressure lability in rats with chronic sinoaortic deafferentation

1987 ◽  
Vol 253 (2) ◽  
pp. H466-H474 ◽  
Author(s):  
R. H. Alper ◽  
H. J. Jacob ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Adrenergic Receptors ◽  
Sympathetic Nerves ◽  
Adrenergic Blockade ◽  
Pressure Regulation ◽  
Arterial Pressure Variability ◽  
Sympathetic Nervous ◽  
Arterial Pressure Lability ◽  
Arterial Pressure Regulation ◽  
Intact Rats

After chronic (2-6 wk) sinoaortic deafferentation (SAD), rats exhibit slight increases in mean arterial pressure (MAP) and heart rate and marked increases in arterial pressure lability. Neither antagonists of humoral vasoconstrictors angiotensin and vasopressin nor acute hypophysectomy altered MAP or lability after chronic SAD. Ganglionic blockade produced hypotension and significantly reduced lability in SAD rats but decreased MAP and increased lability in normal rats. Although chlorisondamine reduced lability in rats with SAD to levels observed in similarly treated sham-operated rats, lability was significantly greater in both groups than in saline-treated sham-operated rats. When intact or SAD rats were administered chlorisondamine plus either captopril or a vasopressin antagonist, pressure lability was returned to levels seen in intact untreated animals. Selective antagonism of alpha 1- or alpha 2-adrenergic receptors did not markedly alter lability in SAD rats. Combined alpha-adrenergic blockade reduced lability in SAD rats and increased lability in intact rats, similar to chlorisondamine treatment. These data suggest that chronic SAD establishes arterial pressure variability that is maintained or generated in large part by the sympathetic nervous system through mechanisms dependent on higher central structures or descending efferent sympathetic nerves. The data further suggest that peripheral mechanisms may also be involved in arterial pressure regulation in baroreceptor-deficient rats.

An Algorithm for Assessing Intraoperative Mean Arterial Pressure Lability 

1997 ◽  
Vol 87 (1) ◽  
pp. 156-161 ◽  
Author(s):  
David L. Reich ◽  
Todd K. Osinski ◽  
Carol Bodian ◽  
Marina Krol ◽  
Kaya Sarier ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Fractional Change ◽  
Absolute Value ◽  
Anesthesia Practice ◽  
Precise Data ◽  
Blood Pressure Lability ◽  
Collection Methods ◽  
Arterial Pressure Lability

Background Intraoperative blood pressure lability may be related to risk factors, hypovolemia, light anesthesia, and morbid outcomes, but the measurements of lability in previous studies have been limited by imprecise and infrequent data collection methods. Computerized intraoperative data acquisition systems have provided an opportunity to readdress the issue of intraoperative blood pressure lability with more abundant and precise data. This study sought to derive and validate an algorithm (expert system) to measure mean arterial pressure (MAP) lability. Methods Two hundred thirty-nine computerized anesthesis records were reviewed retrospectively. Three anesthesiologists separately rated MAP as very stable, average, or very labile. The parameters of a computer algorithm that measured the change of median MAP between consecutive 2-min epochs were optimized to achieve the best possible agreement among the anesthesiologists. The algorithm was then validated on 229 additional anesthesia records. Results The proportion of consecutive 2-min epochs in which the absolute value of the fractional change of median MAP exceeded 0.06 (i.e., 6%) correlated strongly with the anesthesiologists' ratings (r = 0.78; P < 0.0001). The optimal sensitivity and specificity of the algorithm for detecting MAP lability were 98% and 59%, respectively. Conclusions One potential application of expert systems to anesthesia practice is a "smart alarm" to detect blood pressure lability. It may also provide a better tool to assess the relation between lability and outcome than has been available previously.

Transient changes in blood pressure during spontaneous deep breaths in rats with sinoaortic deafferentation

1992 ◽  
Vol 72 (3) ◽  
pp. 920-924 ◽  
Author(s):  
B. H. Machado ◽  
H. Mauad ◽  
M. L. Glass
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Context Effects ◽  
Pulmonary Ventilation ◽  
General Pattern ◽  
Arterial Blood ◽  
Moment Control ◽  
Arterial Pressure Lability

Sinoaortic deafferentation (SAD) in rats produces moderate increases in mean arterial pressure (MAP) along with a large augmentation of arterial pressure lability (APL). The mechanisms generating this APL are incompletely understood. To study the possible influence of breathing activity on APL in conscious SAD rats, we simultaneously recorded pulmonary ventilation and arterial blood pressure. The general pattern of pulmonary ventilation was the same in normal, sham-operated, and SAD rats. In all groups single large tidal volumes were regularly interposed in 1- to 2-min periods of shallower breathing. In SAD rats these single large inspirations were consistently accompanied by substantial and abrupt reductions of MAP, whereas this effect was markedly smaller or absent in normal and sham-operated rats. The data reflect the lack of fast moment-to-moment control of arterial pressure normally exerted by the aortic and carotid baroreceptors. In this context, effects of ventilatory changes must be considered along with humoral and neurogenic factors to explain APL after SAD.

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