Role of NO mechanism in cardiovascular effects of diaspirin cross-linked hemoglobin in anesthetized rats

1995 ◽  
Vol 269 (4) ◽  
pp. H1379-H1388 ◽  
Author(s):  
A. C. Sharma ◽  
G. Singh ◽  
A. Gulati
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Mechanism Of Action ◽  
Cardiovascular Effects ◽  
Hemodynamic Effects ◽  
Systemic Hemodynamic ◽  
Cardiovascular Actions ◽  
Anesthetized Rats ◽  
Nos Inhibitor

The role of nitric oxide (NO) in the cardiovascular actions of diaspirin cross-linked hemoglobin (DCLHb) was studied in anesthetized rats. The regional circulatory and systemic hemodynamic effects of DCLHb (400 mg/kg iv) were studied using a radioactive microsphere technique in control (untreated) and L-arginine (a NO precursor) pretreated rats. DCLHb produced a significant increase in blood pressure (75%), cardiac output (42%), stroke volume (36%), and total peripheral resistance (45%), without affecting heart rate, when administered to control rats. L-Arginine pretreatment significantly attenuated DCLHb-induced systemic hemodynamic effects. DCLHb-induced increase in blood flow to the skin and spleen was completely blocked, and that to the heart was partially blocked, by L-arginine pretreatment, suggesting that cardiovascular actions induced by DCLHb could be antagonized by the NO precursor L-arginine. The NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) produced significant increases in regional vascular resistance, leading to a decrease in blood flow to all the organs except the heart, where an increase in blood flow and a decrease in vascular resistance was observed. DCLHb, when administered in L-NAME-pretreated rats, accentuated the decrease in blood flow to the gastrointestinal system, spleen, mesentery and pancreas, skin, and musculoskeletal system. These studies provide evidence that the NO precursor L-arginine can attenuate the effects of DCLHb and that DCLHb can potentiate the effect of the NOS inhibitor L-NAME. The role of NO in the mechanism of action of DCLHb was further studied by estimating plasma guanosine 3',5'-cyclic monophosphate (cGMP) in control, DCLHb-treated, L-NAME-treated, and L-NAME followed by DCLHb-treated rats. DCLHb and L-NAME significantly decreased the concentration of circulating cGMP in blood plasma. L-NAME pretreatment potentiated DCLHb-induced decrease in cGMP levels. Because the formation of cGMP is stimulated by NO, these studies provide additional evidence for the involvement of NO in the mechanism of action of DCLHb. It is concluded that NO plays an important role in the cardiovascular effects of DCLHb.

The role of oxidative stress in the cardiovascular actions of particulate air pollution

2014 ◽  
Vol 42 (4) ◽  
pp. 1006-1011 ◽  
Author(s):  
Mark R. Miller
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Diesel Exhaust ◽  
Vascular Function ◽  
Cardiovascular Effects ◽  
Increase Blood Pressure ◽  
Potential Mechanism ◽  
Particulate Air Pollution ◽  
Cardiovascular Actions

Air pollution has been estimated to be responsible for several millions of deaths worldwide per year, the majority of which have been attributed to cardiovascular causes. The particulate matter in air pollution has been shown impair vascular function, increase blood pressure, promote thrombosis and impair fibrinolysis, accelerate the development of atherosclerosis, increase the extent of myocardial ischaemia, and increase susceptibility to myocardial infarction. The pathways underlying these effects are complex and poorly understood; however, particulate-induced oxidative stress repeatedly emerges as a potential mechanism in all of these detrimental cardiovascular actions. The present mini-review will use diesel exhaust as an example of a pollutant rich in combustion-derived nanoparticles, to describe the potential by which oxidative stress could drive the cardiovascular effects of air pollution.

Protective role of NO in the regional hemodynamic changes during acute endotoxemia in rats

1994 ◽  
Vol 266 (4) ◽  
pp. H1558-H1564 ◽  
Author(s):  
M. F. Mulder ◽  
A. A. van Lambalgen ◽  
E. Huisman ◽  
J. J. Visser ◽  
G. C. van den Bos ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Saline Group ◽  
Protective Role ◽  
Organ Blood Flow ◽  
Organ Perfusion ◽  
Hemodynamic Changes ◽  
Systemic Blood

The role of NO during the first hour of endotoxemia is still controversial. To evaluate whether NO is protective or detrimental to the regulation of systemic blood pressure, cardiac output (CO), and organ perfusion in rats during acute endotoxemia, we have studied the effects of inhibition of NO synthesis. Thirty minutes after 0.1 mg NG-nitro-L-arginine (L-NNA; group L, n = 7, partial inhibition), 1 mg L-NNA (group H, n = 6, complete inhibition), or saline (group E, n = 7) intravenous infusion, anesthetized volume-loaded rats were infused with endotoxin Escherichia coli O127:B8 (8 mg.kg-1 x h-1) from time (t) = 0 to 60 min. Organ blood flow was measured with radioactive microspheres. In group H, at time 0, CO was lower than in group E (by -29%; P < 0.05), and systemic vascular resistance (SVR) was higher than in groups E and L (by 72 and 51%, respectively; P < 0.05). Perfusion of the pancreas, stomach, intestines, and kidney was lower (P < 0.05) and corresponding organ vascular resistance (OVR) higher (P < 0.05) in group H than in groups E and L (except kidney in group L). At t = 60 min, in groups H and L, CO was lower (by -45 and -26%, respectively; P < 0.05) and SVR was higher (by 112 and 54%, respectively; P < 0.05) than in group E. In group L only blood flow to the heart, pancreas, intestines, and kidney was significantly lower than in group E, and corresponding OVR was higher.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Characterization and cardiovascular actions of endothelin-1 and endothelin-3 from the American alligator

2002 ◽  
Vol 282 (2) ◽  
pp. R594-R602 ◽  
Author(s):  
Björn Platzack ◽  
Yuqi Wang ◽  
Dane Crossley ◽  
Valentine Lance ◽  
James W. Hicks ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Biological Activities ◽  
Systemic Blood Pressure ◽  
Second Phase ◽  
Systemic Blood ◽  
Cardiovascular Actions ◽  
Dose Dependent Decrease ◽  
Alligator Mississipiensis ◽  
Dose Dependent

The structures and biological activities of the isoforms of endothelin (ET) in a reptile are unknown. ET-3, whose primary structure is identical to human ET-3 except for the substitution Phe4 → Tyr, and a peptide identical to human ET-1 were isolated from an extract of the lung of the alligator, Alligator mississipiensis. Bolus intravenous injections of alligator ET-3 (10, 30, and 100 pmol/kg) into anesthetized alligators produced dose-dependent decreases in systemic blood pressure (Psys) and systemic vascular resistance (Rsys) without change in heart rate (HR), systemic blood flow (Qsys), pulmonary pressure (Ppul), pulmonary vascular resistance (Rpul), or pulmonary blood flow (Qpul). At a dose of 300 pmol/kg, the initial vasodilatation was followed by an increase in Rsys and decreases in Qsys and Ppul. The response to intravenous human/alligator ET-1 (10, 30, 100, and 300 pmol/kg) was biphasic at all doses with initial decreases in Psys and Rsys being followed by sustained increases in these parameters. In the pulmonary circulation, ET-1 produced a dose-dependent decrease in Qpul and an increase in Rpul during the first phase of the response but no significant change during the second phase. There was no change in HR in response to ET-1. The vasodilatator action of arginine, but not ET-1, was attenuated by N ω-nitro-l-arginine methyl ester, indicating that the effect of the peptide is probably not mediated through increased synthesis of nitric oxide. The data demonstrate that the structure of the ET isoforms has been strongly conserved during the evolution of vertebrates but that cardiovascular actions differ significantly between the alligator and mammals, especially in the magnitude and duration of the hypotensive response.

Regulation of hepatic blood flow during resuscitation from hemorrhagic shock: role of NO and endothelins

1997 ◽  
Vol 272 (6) ◽  
pp. H2736-H2745 ◽  
Author(s):  
B. H. Pannen ◽  
M. Bauer ◽  
G. F. Noldge-Schomburg ◽  
J. X. Zhang ◽  
J. L. Robotham ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Receptor Antagonist ◽  
Hepatic Blood Flow ◽  
Vehicle Group ◽  
Venous Flow ◽  
Systemic Hemodynamic ◽  
Eta Receptor ◽  
Eta Receptor Antagonist

We determined the role of nitric oxide (NO) and endothelins (ETs) in the regulation of hepatic blood flow during resuscitation from hemorrhagic shock (HS) in anesthetized rats. Volume resuscitation restored systemic hemodynamics and increased hepatic arterial and portal venous flow above baseline in the vehicle group. Presence of N omega-nitro-L-arginine methyl ester (L-NAME, 1 mg/kg) during resuscitation increased systemic vascular resistance (SVR) above baseline, prevented the restoration of hepatic arterial flow, and abolished portal hyperemia. Although the ETA+B-receptor antagonist bosentan (10 mg/kg) did not alter the systemic hemodynamic response, it abolished the hepatic arterial and portal hyperemia. The ETA-receptor antagonist BQ-610 (150 micrograms/kg) reduced SVR below baseline, allowed hepatic arterial hyperemia to occur, and further enhanced the portal venous hyperemia. This indicates that 1) NO reduces SVR and acts to preserve hepatic blood flow during resuscitation from HS; 2) ETA-receptor-mediated vasoconstriction counteracts the systemic and portal hemodynamic effects of NO; and 3) simultaneous ETB-receptor stimulation enhances blood flow to the liver and may serve to modulate the ETA-receptor-mediated vasoconstrictive effects of ETs.

Vasodilation induced by endothelin: role of EDRF and prostanoids in rat hindquarters

1990 ◽  
Vol 259 (6) ◽  
pp. H1835-H1841 ◽  
Author(s):  
E. H. Ohlstein ◽  
L. Vickery ◽  
C. Sauermelch ◽  
R. N. Willette
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Microvascular Perfusion ◽  
Hemodynamic Effects ◽  
Hemodynamic Responses ◽  
Pithed Rats ◽  
Dose Dependent

Hemodynamic responses to endothelin (ET-1) were studied in hindquarters of anesthetized rats and also in isolated buffer-perfused hindquarters of pithed rats. ET-1 (10-100 pmol ia) produced brief dose-related increases in hindquarter blood flow. Acetylcholine (ACh. 0.3-1 micrograms ia) produced similar vasodilator responses. Hemodynamic responses elicited by either ET-1 or ACh were not significantly altered by pretreatment with indomethacin. ET-1 produced dose-dependent increases in skeletal muscle microvascular perfusion, whereas ET-1 had no effect on cutaneous microvascular perfusion, suggesting that vasodilation in the skeletal muscle of the hindlimb contributes to the increase in hindquarter blood flow induced by ET-1. Hemodynamic effects of ET-1 and ACh were studied in the isolated in situ buffer-perfused hindquarters of pithed rats. ET-1 (0.01-300 pmol ia) produced only dose-dependent increases in hindquarter perfusion pressure under basal conditions or when the vascular preparation was precontracted with methoxamine. ET-1 induced vasorelaxation was not observed. ACh (3 microgram ia) produced a 64% reduction in hindquarter perfusion pressure; indicative of endothelium-dependent relaxation. ET-3 (0.1-300 pmol) produced only dose-dependent increases in hindquarter perfusion pressure. When hemodynamic effects of ET-1 were studied under conditions of constant pressure, results were similar to those obtained under constant flow. This study demonstrates that in the rat hindquarters endothelium-derived relaxing factors and prostanoids do not appear to be mediators of endothelin-induced vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin in the hemodynamic response to chronic nephron obstruction

1983 ◽  
Vol 245 (1) ◽  
pp. F75-F82
Author(s):  
P. K. Carmines ◽  
G. A. Tanner
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Salt Intake ◽  
Hemodynamic Response ◽  
Local Factor ◽  
High Salt Intake ◽  
The Difference ◽  
Glomerular Hemodynamics ◽  
Captopril Treatment

Microsphere techniques were employed to investigate the role of intrarenal angiotensin generation in producing the arteriolar constriction associated with 24-h tubular obstruction in rats. In each animal, glomerular blood flow (GBF) and nephron vascular resistance were determined for normal and oil-blocked superficial cortical nephrons. In 17 control rats, GBF of normal and blocked nephrons averaged 226 +/- 12 and 130 +/- 9 nl/min, respectively (P less than 0.001). Captopril treatment in five rats (10 mg/kg orally) improved GBF to blocked nephrons to 252 +/- 31 nl/min. Saralasin treatment in six rats (10 micrograms . kg-1 . min-1 i.v.) lessened the difference between GBF of normal and obstructed nephrons. In six rats subjected to a high salt intake and deoxycorticosterone injections, GBF to obstructed nephrons was improved to 181 +/- 21 nl/min. Since both pharmacologic interruption of angiotensin activity and renin suppression were associated with improved GBF of blocked nephrons, these observations support a role for angiotensin as a local factor controlling glomerular hemodynamics of chronically obstructed nephrons.

Effect of orthotopic transplantation of liver on systemic and splanchnic hemodynamics in conscious rat

1995 ◽  
Vol 269 (1) ◽  
pp. G153-G159 ◽  
Author(s):  
L. V. Kuznetsova ◽  
D. Zhao ◽  
A. M. Wheatley
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Portal Pressure ◽  
Peripheral Resistance ◽  
Vena Cava ◽  
Cardiovascular Effects ◽  
Suture Technique ◽  
Arterial Blood Flow ◽  
Conscious Rat ◽  
Arterial Blood

The long-term cardiovascular effects of orthotopic liver transplantation (OLT) were studied in conscious Lewis rats with a radioactive microsphere technique. Three months after OLT with an all-suture technique for graft revascularization (s-OLT), all hemodynamic parameters were similar to control. OLT with "cuffs" fitted to the portal vein and infrahepatic inferior vena cava (c-OLT) led to prominent hemodynamic disturbances including 1) hyperkinetic circulation with increased cardiac index (CI; 22%; P < 0.05) and decreased mean arterial pressure (15%; P < 0.05) and total peripheral resistance (TPR; 28%; P < 0.05); 2) a slight increase in portal pressure (11.8 +/- 0.9 vs. 9.3 +/- 1.7 mmHg in control) and marked portal-systemic shunting (51 +/- 11 vs. 0.05 +/- 0.04% in control; P < 0.05); 3) increased hepatic arterial blood flow (0.49 +/- 0.06 vs. 0.27 +/- 0.04 ml.min-1.g liver wt-1; P < 0.05); 4) splanchnic vasodilation with vascular resistance significantly (P < 0.05) lower in the liver, stomach, and large intestine; and 5) increased blood flow and decreased vascular resistance in the kidneys and heart. Ganglionic blockade with chlorisondamine (5 mg/kg body wt iv) indicated that the increase in CI seen in the c-OLT rats was probably sympathetically mediated, whereas the increase in renal blood flow was a reflection of the increase in CI. After ganglionic blocker administration, TPR and regional vascular resistances decreased to approximately the same extent in the control and c-OLT groups, indicating that vascular sympathetic tone was unchanged in the c-OLT rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhanced pressor responses to ICV vasopressin after pretreatment with oxytocin

1994 ◽  
Vol 266 (2) ◽  
pp. R592-R598 ◽  
Author(s):  
P. Poulin ◽  
A. Komulainen ◽  
Y. Takahashi ◽  
Q. J. Pittman
Keyword(s):  
Skeletal Muscle ◽  
Cardiovascular Effects ◽  
Intracerebroventricular Injection ◽  
Central Administration ◽  
Cardiovascular Actions ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Dose Dependent ◽  
Higher Doses

The role of oxytocin (OT) in the modulation of arginine vasopressin (AVP)-induced cardiovascular effects within the central nervous system was investigated in urethan-anesthetized rats. Intracerebroventricular injection of AVP (1-10 pmol) produced dose-dependent increases in mean arterial pressure (MAP) and heart rate (HR). These responses were enhanced in rats pretreated 24 h earlier with OT (10 pmol icv). The enhanced cardiovascular effects of AVP in OT-pretreated animals were dose dependent, blocked by the V1 antagonist d(CH2)5Tyr(Me)AVP, not evoked by OT alone, and occurred in the absence of changes in basal (nonstimulated) MAP and HR. In addition, central administration of AVP in OT-pretreated rats, but not in saline-pretreated controls, caused dose-dependent oscillations of the MAP and HR responses and, at higher doses, death of the animals. The enhanced cardiovascular actions of centrally injected AVP in OT-pretreated rats do not appear to be secondary to skeletal muscle contractions or the result of cerebral ischemia. Our data point to an interaction between the central oxytocinergic and vasopressinergic systems in cardiovascular control.

scholarly journals Vasodilator tone in the llama fetus: the role of nitric oxide during normoxemia and hypoxemia

2005 ◽  
Vol 289 (3) ◽  
pp. R776-R783 ◽  
Author(s):  
Emilia M. Sanhueza ◽  
Raquel A. Riquelme ◽  
Emilio A. Herrera ◽  
Dino A. Giussani ◽  
Carlos E. Blanco ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Control Group ◽  
Blood Flows ◽  
Vasoconstrictor Effect ◽  
Vascular Beds ◽  
Oxide Synthase

The fetal llama responds to hypoxemia, with a marked peripheral vasoconstriction but, unlike the sheep, with little or no increase in cerebral blood flow. We tested the hypothesis that the role of nitric oxide (NO) may be increased during hypoxemia in this species, to counterbalance a strong vasoconstrictor effect. Ten fetal llamas were operated under general anesthesia. Mean arterial pressure (MAP), heart rate, cardiac output, total vascular resistance, blood flows, and vascular resistances in cerebral, carotid and femoral vascular beds were determined. Two groups were studied, one with nitric oxide synthase (NOS) blocker NG-nitro-l-arginine methyl ester (l-NAME), and the other with 0.9% NaCl (control group), during normoxemia, hypoxemia, and recovery. During normoxemia, l-NAME produced an increase in fetal MAP and a rapid bradycardia. Cerebral, carotid, and femoral vascular resistance increased and blood flow decreased to carotid and femoral beds, while cerebral blood flow did not change significantly. However, during hypoxemia cerebral and carotid vascular resistance fell by 44% from its value in normoxemia after l-NAME, although femoral vascular resistance progressively increased and remained high during recovery. We conclude that in the llama fetus: 1) NO has an important role in maintaining a vasodilator tone during both normoxemia and hypoxemia in cerebral and femoral vascular beds and 2) during hypoxemia, NOS blockade unmasked the action of other vasodilator agents that contribute, with nitric oxide, to preserving blood flow and oxygen delivery to the tissues.

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