Acanthopanax senticosus Induces Vasorelaxation via Endothelial Nitric Oxide-Dependent and -Independent Pathways

Planta Medica ◽  
2019 ◽  
Vol 85 (13) ◽  
pp. 1080-1087 ◽  
Author(s):  
Yayoi Shiokawa ◽  
Shino Miyauchi-Wakuda ◽  
Satomi Kagota ◽  
Kana Maruyama-Fumoto ◽  
Shizuo Yamada ◽  
...  

AbstractAlthough Acanthopanax senticosus root extract (ASRE), a functional food used in Japan, improves peripheral blood circulation and exerts vasorelaxant effects in rats under healthy conditions, the underlying mechanisms currently remain unclear. Therefore, we investigated the mechanisms responsible for ASRE-induced relaxation in isolated thoracic aortas using organ bath techniques and examined whether ASRE affects systemic and peripheral circulation using a photoplethysmographic tail-cuff system and noncontact laser tissue blood flow meter in Wistar rats. Similar to acetylcholine (ACh), ASRE induced dose-dependent relaxation in aortas pre-contracted with phenylephrine; however, in contrast to ACh, ASRE-induced relaxation was partially inhibited by treatments with antagonists of nitric oxide (NO) synthase and soluble guanylyl cyclase as well as by endothelium removal. Contractile responses to phenylephrine or potassium chloride were observed in the presence of ASRE. The oral administration of ASRE (900 mg/kg/d for 1 wk) decreased systolic blood pressure in rats 3 h after the treatment and did not affect heart rate, tail blood flow, mass, or velocity; this decreasing effect was not observed on day 2. A 1-wk treatment with ASRE did not affect vasorelaxation in response to ASRE. These results demonstrate that ASRE induces vasorelaxation via endothelial NO production and an NO-independent pathway in rats. Based on these findings, positive impacts of ASRE on blood pressure and peripheral blood circulation cannot be expected under healthy conditions as the systemic effects of ASRE are temporary. Instead, caution is needed to prevent the occurrence of side effects (i.e., orthostatic dizziness) at the beginning of ASRE dosing.

2018 ◽  
pp. 15-21
Author(s):  
Igor Isupov ◽  
Rimma Zatrudina

Methods of pulse oximetry and photoplethysmography are widely used in clinical medicine and practice of biomedical research outside the clinic. The advantages of the method are high efficiency of preparation for the diagnostic procedure, non-invasive, complete safety for health. The method provides the possibility of unlimited long - term monitoring of the dynamics of saturation and desaturation of hemoglobin. In combination with the above, subject to the qualitative registration of photoplethysmograms, the method allows the calculation and analysis of a number of indicators of peripheral blood circulation: the total pulse blood flow to the study region, the tone of arterial vessels of different diameters, the state of capillary blood flow. Most modern foreign models of pulse oximeters are integrated devices that provide measurement of a very limited set of physiological parameters: the percentage of hemoglobin oxygen saturation and pulse rate. The range of pulse oximeters containing the interface with the personal computer and providing operational calculation of indicators of peripheral photoplethysmograms is small. Such devices have a fairlyhigh cost and are not portable. The development of domestic integrated electronic devices is extremely relevant, allowing along with obtaining information about blood oxygenation to perform continuous monitoring of peripheral blood circulation. The authors developed an electronic module that provides long-term registration of photoplethysmograms in the infrared and red areas of the light spectrum. The electronic module is made exclusively with the use of domestic active radio elements – discrete semiconductor devices and integrated circuits. The device was developed in full compliance with the import substitution policy pursued by the President and the Government of the Russian Federation. The advantage of the device is the "open architecture" of the electronic circuit, which provides four analog signals suitable for further digitization. The signals contain information about pulsating and non-pulsating components of the optical density of biological tissue in the infrared and red ranges of the spectrum. The device has an electronic filter of mains interference. Tests of the device demonstrated high quality of photoplethysmograms. This makes it possible tosuccessfullyuse the device for studies of hemoglobin oxygenation and peripheral hemodynamics.


2020 ◽  
Vol 30 (3) ◽  
pp. 270-279
Author(s):  
Stepan Vadzyuk ◽  
◽  
Liudmyla Horban ◽  
Ihor Papinko ◽  
Olena Kulianda ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Taner Ciftci ◽  
Ali Bestemi Kepekci ◽  
Hatice Pınar Yavasca ◽  
Hayrettin Daskaya ◽  
Volkan İnal

Obesity has a significant effect on the cephalic spread of a spinal block (SB) due to a reduction in cerebrospinal fluid (CSF). SB is controlled by the tissue blood flow in addition to the CSF. Some positions and techniques of surgery used can cause changes in hemodynamics. We investigated effects of hemodynamic changes that may occur during Transurethral prostate resection (TUR-P) and lithotomy position (LP) at the SB level in obese versus nonobese individuals. Sixty patients who had undergone TUR-P operation under spinal anesthesia were divided into a nonobese (BMI<25 kg/m2, Group N) or obese (BMI≥30 kg/m2, Group O) group. SB assessments were recorded afterthe LP. SB at 6 and 120 min and the peak SB level were compared between two groups. Hemodynamics were recorded after LP. Peak and 6 min SB levels were similar between the groups, while 120 min SB levels were significantly higher for Group O (P<0.05). Blood pressure (BP) after the LP was significantly higher for Group N (P<0.05). LP and TUR-P increased the BP in Group N when compared to Group O. The increase in hemodynamics enhances the blood flow in the spinal cord and may form similar SB levels in nonobese patients to those in obese patients. However, SB time may be longer in obese patients.


2005 ◽  
Vol 289 (6) ◽  
pp. F1324-F1332 ◽  
Author(s):  
Manish M. Tiwari ◽  
Robert W. Brock ◽  
Judit K. Megyesi ◽  
Gur P. Kaushal ◽  
Philip R. Mayeux

Acute renal failure (ARF) is a frequent and serious complication of endotoxemia caused by lipopolysaccharide (LPS) and contributes significantly to mortality. The present studies were undertaken to examine the roles of nitric oxide (NO) and caspase activation on renal peritubular blood flow and apoptosis in a murine model of LPS-induced ARF. Male C57BL/6 mice treated with LPS ( Escherichia coli) at a dose of 10 mg/kg developed ARF at 18 h. Renal failure was associated with a significant decrease in peritubular capillary perfusion. Vessels with no flow increased from 7 ± 3% in the saline group to 30 ± 4% in the LPS group ( P < 0.01). Both the inducible NO synthase inhibitor l- N6-1-iminoethyl-lysine (l-NIL) and the nonselective caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone (Z-VAD) prevented renal failure and reversed perfusion deficits. Renal failure was also associated with an increase in renal caspase-3 activity and an increase in renal apoptosis. Both l-NIL and Z-VAD prevented these changes. LPS caused an increase in NO production that was blocked by l-NIL but not by Z-VAD. Taken together, these data suggest NO-mediated activation of renal caspases and the resulting disruption in peritubular blood flow are an important mechanism of LPS-induced ARF.


1996 ◽  
Vol 7 (12) ◽  
pp. 2694-2699
Author(s):  
M C Ortíz ◽  
L A Fortepiani ◽  
C Martínez ◽  
N M Atucha ◽  
J García-Estañ

Recent work indicates that nitric oxide (NO) plays an important role in the systemic and renal alterations of liver cirrhosis. This study used aminoguanidine (AG), a preferential inhibitor of inducible nitric oxide synthase (iNOS), to evaluate the role of this NOS isoform in the systemic and renal alterations of an experimental model of liver cirrhosis with ascites (carbon tetrachloride/ phenobarbital). Experiments have been performed in anesthetized cirrhotic rats and their respective control rats prepared for clearance studies. Administration of AG (10 to 100 mg/kg, iv) elevated dose-dependent mean arterial pressure (MAP, in mm Hg) in the cirrhotic rats from a basal level of 79.3 +/- 3.6 to 115.0 +/- 4.7, whereas in the control animals, MAP increased only with the highest dose of the inhibitor (from 121.8 +/- 3.6 to 133.3 +/- 1.4). In the cirrhotic group, AG also significantly increased sodium and water excretion, whereas these effects were very modest in the control group. Plasma concentration of nitrates+nitrites, measured as an index of NO production, were significantly increased in the cirrhotic animals in the basal period and decreased with AG to levels not significantly different from the control animals. Similar experiments performed with the nonspecific NOS inhibitor N omega-nitro-L-arginine (NNA) also demonstrated an increased pressor sensitivity of the cirrhotic rats, but the arterial hypotension was completely corrected. These results, in an experimental model of liver cirrhosis with ascites, show that AG exerts a beneficial effect as a result of inhibition of NO production, increasing blood pressure and improving the reduced excretory function. Because NNA, but not AG, completely normalized the arterial hypotension, it is suggested that the constitutive NOS isoform is also contributing in an important degree. It is concluded that the activation of both inducible and constitutive NOS isoforms plays an important role in the lower systemic blood pressure and associated abnormalities that characterize liver cirrhosis.


2000 ◽  
Vol 88 (4) ◽  
pp. 1381-1389 ◽  
Author(s):  
Ivan T. Demchenko ◽  
Albert E. Boso ◽  
Thomas J. O'Neill ◽  
Peter B. Bennett ◽  
Claude A. Piantadosi

We have tested the hypothesis that cerebral nitric oxide (NO) production is involved in hyperbaric O2 (HBO2) neurotoxicity. Regional cerebral blood flow (rCBF) and electroencephalogram (EEG) were measured in anesthetized rats during O2 exposure to 1, 3, 4, and 5 ATA with or without administration of the NO synthase inhibitor ( N ω-nitro-l-arginine methyl ester), l-arginine, NO donors, or the N-methyl-d-aspartate receptor inhibitor MK-801. After 30 min of O2 exposure at 3 and 4 ATA, rCBF decreased by 26–39% and by 37–43%, respectively, and was sustained for 75 min. At 5 ATA, rCBF decreased over 30 min in the substantia nigra by one-third but, thereafter, gradually returned to preexposure levels, preceding the onset of EEG spiking activity. Rats pretreated with N ω-nitro-l-arginine methyl ester and exposed to HBO2 at 5 ATA maintained a low rCBF. MK-801 did not alter the cerebrovascular responses to HBO2at 5 ATA but prevented the EEG spikes. NO donors increased rCBF in control rats but were ineffective during HBO2 exposures. The data provide evidence that relative lack of NO activity contributes to decreased rCBF under HBO2, but, as exposure time is prolonged, NO production increases and augments rCBF in anticipation of neuronal excitation.


2019 ◽  
Vol 5 (4) ◽  
pp. 76-102 ◽  
Author(s):  
A. Volobuev ◽  
P. Romanchuk

Modern rational pharmacotherapy allows being provided with a balance of efficacy and safety in clinical geriatrics, which is especially important in patients with neurovascular degeneration, including in the presence of severe forms of vascular comorbidity, requiring multi–component therapy, under the condition of active multidisciplinary and interdepartmental impact. Dementia in its origin is mixed and it is extremely difficult to divide into parts its primary degenerative or vascular component. The differentiated approach is determined by the heterogeneity of the pathological process, which common is the relationship of cerebral vascular damages with the development of the brain symptoms damage. The problem of nosological independence of Alzheimer’s disease is the subject of discussion for patients of older age groups (especially in people 65 years and older). The genesis of mnestic–intellectual disorders is due not so much to primary–degenerative as vascular changes, especially at the level of the microcirculatory canal. The modern problem of neurodegeneration has a neurophysiological, biophysical, gerontological, geriatric and strategic practical orientation since the diagnosis of the cause of the disease determines the choice of adequate treatment. Due to a large number of pathogenetical mechanisms, there is no single and standardized method of treatment for vascular dementia and Alzheimer’s disease. In any case, prevention of the development and progression of vascular dementia and Alzheimer’s disease should take into account the etiological mechanisms of its occurrence, because it will vary in patients with failures of small vessels, occlusive damages of the main arteries of the head or an embolism of cardiogenic origin. In patients with failures of small vessels, the main direction of therapy should be the normalization of blood pressure, which leads to improved cognitive functions. At the same time, excessive lowering of blood pressure can provoke an increase in mnestic-intellectual disorders, possibly caused by a secondary decrease in cerebral blood flow due to a violation of autoregulation. Biophysics of blood circulation in Alzheimer’s disease is characterized by disorders of laminar blood flow and cerebral hypoperfusion. As a result, failure intracellular metabolism, there is a cascade of changes in neurons associated with the processes of excitotoxicity and oxidant stress, which in turn stimulates amyloidogenesis. Experimental and 25-year observations have shown that the long–existing state of hypoperfusion leads to hippocampal disorders. This process is accompanied by memory impairment, structural changes in the capillaries in the hippocampus, impaired glucose and protein metabolism, β–amyloid deposition, activation of glial tissue, the death of hippocampal neurons.


1984 ◽  
Vol 51 (5) ◽  
pp. 219-224 ◽  
Author(s):  
Elizabeth Dean

Ten control and ten diabetic subjects were first given a baseline session of no temperature biofeedback, and then were exposed to four 40-minute temperature biofeedback sessions over consecutive days. As the result of feedback training, peripheral skin temperatures increased on the training (right) hands of both groups, and this occurred to a greater extent in the diabetic group. Concomitant temperature increases occurred also in the left hands of both groups. Neither group produced any significant changes in heart rate, respiration rate, or systolic blood pressure with the exception of a significant decrease in diastolic blood pressure for the diabetic group. No difference in diastolic blood pressure was observed, however, when the diabetics were compared with the control group. The results would suggest further evaluation of temperature biofeedback training is warranted in a diabetic population as a potential means of increasing peripheral blood flow in the extremities.


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