scholarly journals Role of Nitric Oxide in Regulating Cerebrocortical Oxygen Consumption and Blood Flow during Hypercapnia

1994 ◽  
Vol 14 (3) ◽  
pp. 503-509 ◽  
Author(s):  
Ildiko Horvath ◽  
Norbert T. Sandor ◽  
Zoltan Ruttner ◽  
Alan C. McLaughlin
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Methyl Ester ◽  
Superior Sagittal Sinus ◽  
No Synthase ◽  
Sagittal Sinus ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

The effect of the nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (Paco2 ∼ 60 mm Hg and Paco2 ∼ 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated using the Kety–Schmidt approach and CMRO2 was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. l-NAME treatment did not have a significant effect on either CMRO2 or CBE under normocapnic conditions but inhibited the hypercapnic increase of CMRO2 and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO2 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO2.

Nitric oxide and β-adrenergic agonist-induced bronchial arterial vasodilation

1997 ◽  
Vol 82 (2) ◽  
pp. 686-692 ◽  
Author(s):  
Nirmal B. Charan ◽  
Shane R. Johnson ◽  
S. Lakshminarayan ◽  
William H. Thompson ◽  
Paula Carvalho
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Methyl Ester ◽  
No Synthase ◽  
Ester Hydrochloride ◽  
Methyl Ester Hydrochloride ◽  
Adrenergic Agonist ◽  
Flow Probe ◽  
Cyclic Monophosphate ◽  
Synthase Inhibitor

Charan, Nirmal B., Shane R. Johnson, S. Lakshminarayan, William H. Thompson, and Paula Carvalho. Nitric oxide and β-adrenergic agonist-induced bronchial arterial vasodilation. J. Appl. Physiol. 82(2): 686–692, 1997.—In anesthetized sheep, we measured bronchial blood flow (Q˙br) by an ultrasonic flow probe to investigate the interaction between inhaled nitric oxide (NO; 100 parts/million) given for 5 min and 5 ml of aerosolized isoetharine (1.49 × 10−2 M concentration). NO and isoetharine increased Q˙br from 26.5 ± 6.5 to 39.1 (SE) ± 10.6 and 39.7 ± 10.7 ml/min, respectively ( n = 5). Administration of NO immediately after isoetharine further increasedQ˙br to 57.3 ± 15.1 ml/min. NO synthase inhibitor N ω-nitro-l-arginine methyl ester hydrochloride (l-NAME; 30 mg/kg, in 20 ml saline given iv) decreased Q˙br to 14.6 ± 2.6 ml/min. NO given three times alternately with isoetharine progressively increased Q˙br from 14.6 ± 2.6 to 74.3 ± 17.0 ml/min, suggesting that NO and isoetharine potentiate vasodilator effects of each other. In three other sheep, afterl-NAME, three sequential doses of isoetharine increased Q˙br from 10.2 ± 3.4 to 11.5 ± 5.7, 11.7 ± 4.7, and 13.3 ± 5.7 ml/min, respectively, indicating that effects of isoetharine are predominantly mediated through synthesis of NO. When this was followed by three sequential administrations of NO, Q˙br increased by 146, 172, and 185%, respectively. Thus in the bronchial circulation there seems to be a close interaction between adenosine 3′,5′-cyclic monophosphate- and guanosine 3′,5′-cyclic monophosphate-mediated vasodilatation.

scholarly journals Arteriogenesis and angiogenesis in rat ischemic hindlimb: role of nitric oxide

2001 ◽  
Vol 281 (6) ◽  
pp. H2528-H2538 ◽  
Author(s):  
Pamela G. Lloyd ◽  
Hsiao T. Yang ◽  
Ronald L. Terjung
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Treadmill Exercise ◽  
No Synthase ◽  
Muscle Exercise ◽  
Peripheral Vascular ◽  
Artery Ligation ◽  
Capillary Growth ◽  
Synthase Inhibitor

Nitric oxide (NO) has been implicated in both collateral expansion (arteriogenesis) and capillary growth (angiogenesis). Exercise training increases collateral-dependent blood flow to tissues at risk of ischemia and enhances capillarity in active skeletal muscle. Exercise also acutely elevates NO. Thus we assessed the role of NO in training-induced arteriogenesis and angiogenesis. These studies utilized a rat model of peripheral vascular disease (bilateral femoral artery ligation). Untreated rats (control) and rats treated with the NO synthase inhibitor N ω-nitro-l-arginine methyl ester (l-NAME; 65–70 mg · kg−1 · day−1, via drinking water) were divided into sedentary or exercise-trained subgroups. After ∼3 wk, l-NAME treatment had elevated preexercise mean arterial pressure ∼39–58%, confirming NO synthesis inhibition. The training program (treadmill exercise twice per day, 20–25 m/min, 15% grade, ∼18 days) increased collateral-dependent blood flow to the distal hindlimb, with the greatest increase (∼59%) in the calf ( P < 0.001). This increase was inhibited by l-NAME. In contrast, the training-induced increase in muscle capillarity was not blocked byl-NAME. Thus arteriogenesis and angiogenesis appear to differ in their requirement for NO.

Differential effects of l-NAME on rat venular hydraulic conductivity

2000 ◽  
Vol 279 (4) ◽  
pp. H2017-H2023 ◽  
Author(s):  
Rolando E. Rumbaut ◽  
Jianjie Wang ◽  
Virginia H. Huxley
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Methyl Ester ◽  
Hydraulic Conductivity ◽  
No Synthase ◽  
Vascular Effects ◽  
Nos Inhibitors ◽  
Before And After ◽  
Nos Inhibitor

The role of nitric oxide (NO) in microvascular permeability remains unclear because both increases and decreases in permeability by NO synthase (NOS) inhibitors have been reported. We sought to determine whether blood-borne constituents modify venular permeability responses to the NOS inhibitor N G-nitro-l-arginine methyl ester (l-NAME). We assessed hydraulic conductivity ( L p) of pipette-perfused rat mesenteric venules before and after exposure to 10−4 M l-NAME. In the absence of blood-borne constituents, l-NAME reduced L p by nearly 50% (from a median of 2.4 × 10−7cm · s−1 · cmH2O−1, n = 17, P < 0.001). The reduction in L p by l-NAME was inhibited by a 10-fold molar excess of l-arginine but notd-arginine ( n = 6). In a separate group of venules, blood flow was allowed to resume during exposure tol-NAME. In vessels perfused by blood duringl-NAME exposure, L p increased by 78% (from 1.4 × 10−7cm · s−1 · cmH2O−1, n = 10, P < 0.01). N G-nitro-d-arginine methyl ester did not affect L p in either of the two groups. These data imply that NO has direct vascular effects on permeability that are opposed by secondary changes in permeability mediated by blood-borne constituents.

Role of Nitric Oxide in the Development of Thermal Hyperesthesia Induced by Sciatic Nerve Constriction Injury in the Rat 

1995 ◽  
Vol 82 (5) ◽  
pp. 1266-1273 ◽  
Author(s):  
Tatsuo Yamamoto ◽  
Naohito Shimoyama
Keyword(s):  
Nitric Oxide ◽  
Sciatic Nerve ◽  
Nerve Injury ◽  
Afferent Input ◽  
No Synthase ◽  
Aspartate Receptor ◽  
No Synthase Inhibitor ◽  
Nociceptive Information ◽  
Synthase Inhibitor

Background Nitric oxide (NO) has been shown to be involved in mediating nociceptive information transmission in the spinal cord. It is known that the N-methyl-D-aspartate receptor plays an important role in the development of the spinal facilitation evoked by a protracted small afferent input and that this effect is mediated at least in part by NO. Recently, it has been found that N-methyl-D-aspartate receptor-mediated spinal facilitation is crucial in the development of thermal hyperesthesia evoked by a nerve constriction injury. In the current study, we investigated the role of NO in the development of thermal hyperesthesia after a nerve constriction injury. Methods The Bennett and Xie model (four loose chromic gut ligations around the rat sciatic nerve) was used to examine the development of thermal hyperesthesia. An NO synthase inhibitor (N omega-nitro-L-arginine or N omega-nitro-L-arginine methyl ester hydrochloride), rat hemoglobin, or L-arginine was administered intrathecally 10 min before the nerve injury (pretreatment study) or 15 min after the nerve injury (posttreatment study). Results Pretreatment but not posttreatment administration of NO synthase inhibitor significantly delayed the development of thermal hyperesthesia. The effect of NO synthase inhibitor was reversed by the coadministration of L-arginine but not by the coadministration of D-arginine. Pretreatment with rat hemoglobin also delayed the development of thermal hyperesthesia. L-Arginine itself had no effect on the development of thermal hyperesthesia. Conclusions NO may play an important role in the development of N-methyl-D-aspartate receptor-mediated spinal facilitation after a nerve constriction injury.

Disruption of renal peritubular blood flow in lipopolysaccharide-induced renal failure: role of nitric oxide and caspases

2005 ◽  
Vol 289 (6) ◽  
pp. F1324-F1332 ◽  
Author(s):  
Manish M. Tiwari ◽  
Robert W. Brock ◽  
Judit K. Megyesi ◽  
Gur P. Kaushal ◽  
Philip R. Mayeux
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Blood Flow ◽  
Saline Group ◽  
No Production ◽  
Capillary Perfusion ◽  
Peritubular Capillary ◽  
Synthase Inhibitor ◽  
Peritubular Capillary Perfusion

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.

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