Vagally and acetylcholine-mediated constriction in small pulmonary vessels of rabbits

1987 ◽  
Vol 63 (4) ◽  
pp. 1601-1609 ◽  
Author(s):  
K. Sada ◽  
M. Shirai ◽  
I. Ninomiya
Keyword(s):  
Nerve Stimulation ◽  
Pulmonary Arteries ◽  
Stimulus Frequency ◽  
Vagal Nerve ◽  
Internal Diameter ◽  
Specific Stimulus ◽  
Pulmonary Vessels ◽  
X Ray ◽  
Branching Points ◽  
Arteries And Veins

Using a new X-ray TV system, we analyzed effects of vagal nerve stimulation (VNS; 1–30 Hz) and intravenous injection of acetylcholine (Ach; 0.3–0.9 microgram) on the internal diameter (ID; 100–1,500 microns) of small pulmonary arteries and veins in anesthetized rabbits. In selective segments of the arteries, ID decreased abruptly and maximally by 50–70% in a specific stimulus frequency to the vagal nerve and a dose of ACh. The vasoconstrictor sites were distributed near the branching points of the arteries, particularly those downstream, and their numbers increased with an increase in the stimulus frequencies and ACh doses. The relative frequencies of occurrences were 15.3% with VNS (30 Hz) and 5.3% with ACh (0.9 microgram). In nonselective segments with VNS, ID decreased frequency dependently by 0, 4, 12, and 26% at 1, 4, 15, and 30 Hz, respectively, and with ACh, decreased dose dependently by 21 and 35% with 0.3 and 0.9 microgram, respectively. The vasoconstriction in response to VNS and ACh was attenuated by atropine, enhanced by eserine, and not affected by phentolamine. That vasoconstriction to VNS was abolished by hexamethonium. No selective constriction was found in veins and the ID was decreased uniformly by 1–2% with VNS and ACh.

Influence of hypoxia and serotonin on small pulmonary vessels

1994 ◽  
Vol 76 (1) ◽  
pp. 56-64 ◽  
Author(s):  
A. al-Tinawi ◽  
G. S. Krenz ◽  
D. A. Rickaby ◽  
J. H. Linehan ◽  
C. A. Dawson
Keyword(s):  
Size Range ◽  
Pulmonary Arteries ◽  
The Other ◽  
Internal Diameter ◽  
Total Response ◽  
Pulmonary Vessels ◽  
X Ray ◽  
Diameter Range ◽  
Maximum Decrease ◽  
Potential Impact

X-ray angiograms obtained from isolated perfused dog lungs were used to measure changes in the internal diameter of small intraparenchymal pulmonary arteries (150–1,600 microns) and veins (200–1,000 microns) in response to hypoxia or intra-arterial serotonin [5-hydroxytryptamine (5-HT)] infusion. The diameter changes in response to the two stimuli were measured over a range of stimulus-induced increases (delta Pa) in the total arteriovenous pressure drop. When the resulting delta Pa was small, all arteries in the diameter range studied constricted in response to either stimuli. The maximum decrease in diameter was approximately 25% with hypoxia and 36% with 5-HT. However, when delta Pa was large, arteries with a control diameter larger than approximately 800 microns distended with hypoxia. On the other hand, 5-HT constricted all the arteries in the size range studied regardless of the resulting magnitude of delta Pa. Hypoxia caused a small (approximately 9%) constriction in all veins in the diameter range studied independent of diameter or the magnitude of delta Pa, whereas in the concentration range studied 5-HT had no significant influence on these veins. An analysis of the potential impact of these vessels on total pulmonary vascular resistance suggested that although vessels in the size range studied contributed significantly to the total response to these two stimuli, vessels smaller than those studied also made a major contribution to the total response.

Inhaled nitric oxide: diameter response patterns in feline small pulmonary arteries and veins

1996 ◽  
Vol 270 (3) ◽  
pp. H974-H980 ◽  
Author(s):  
M. Shirai ◽  
A. Shimouchi ◽  
A. T. Kawaguchi ◽  
K. Sunagawa ◽  
I. Ninomiya
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Arteries ◽  
Internal Diameter ◽  
Response Patterns ◽  
Television System ◽  
X Ray ◽  
Small Vessels ◽  
Pulmonary Vasoconstriction ◽  
Arteries And Veins

Using an X-ray television system on the in vivo cat lung, we directly measured internal diameter (ID) changes in the small pulmonary arteries and veins (100-1,100 microns ID) in response to 5, 15, and 40 ppm nitric oxide (NO) inhalations. We also measured to what extent 40 ppm NO inhalation can attenuate large ID constrictions at the different serial segments of the small vessels due to unilobar anoxic (0% O2) exposure. Under normoxic conditions, 5-40 ppm NO inhalations significantly increased the ID of both arteries and veins less than approximately 900 microns dose dependently but caused no significant, or only slight, ID increases in the vessels larger than this, if any at all. The ID increase in the serially connected arteries was nonuniform (4-18, 8-28, and 7-35% with 5, 15, and 40 ppm NO inhalations, respectively), whereas that for the veins was relatively uniform (4-9, 6-17, and 7-18% with 5, 15, and 40 ppm NO, respectively). The maximum ID increase occurred in the 200- to 500- and 200- to 700-microns arteries in response to 5-15 and 40 ppm NO, respectively. Unilobar anoxic exposure significantly decreased the ID of the 100- to 700-microns arteries and veins, but not the ID of the other-sized vessels. The ID decrease in the serially connected arteries was nonuniform (13-29%) but relatively uniform in the veins (8-12%). The maximum ID decrease occurred in the 200- to 300-microns arteries. However, adding 40 ppm NO to the lobe completely eradicated the ID decreases at all segments of the arteries and veins and, instead, caused significant ID increase (11-21%) in the arteries and (10-12%) in the veins. The data indicate that, according to dosage, 5-40 ppm NO inhalations cause selective dilation of approximately 100- to 900-microns pulmonary arteries and veins, particularly the 200- to 700-microns arteries. During anoxic exposure, the vasodilator effect of NO is preserved and can completely reverse the marked pulmonary vasoconstriction.

Potent vasodilator responses to human urotensin-II in human pulmonary and abdominal resistance arteries

2001 ◽  
Vol 280 (2) ◽  
pp. H925-H928 ◽  
Author(s):  
Alison Stirrat ◽  
Marie Gallagher ◽  
Stephen A. Douglas ◽  
Eliot H. Ohlstein ◽  
Colin Berry ◽  
...  
Keyword(s):  
Sodium Nitroprusside ◽  
Vascular Function ◽  
Pulmonary Arteries ◽  
Systemic Resistance ◽  
Internal Diameter ◽  
Urotensin Ii ◽  
Resistance Arteries ◽  
Pulmonary Vessels ◽  
Potent Vasodilator ◽  
Abdominal Arteries

The peptide human urotensin-II (hUT-II) and its receptor have recently been cloned. The vascular function of this peptide in humans, however, has yet to be determined. Vasoconstrictor and vasodilator responses to hUT-II were investigated in human small muscular pulmonary arteries [∼170 μm internal diameter (ID)] and human abdominal resistance arteries (∼200 μm ID). Vasodilator responses were investigated in endothelin-1 (3 nM) precontracted vessels and, in the small pulmonary vessels, compared with the known vasodilators adrenomedullin, sodium nitroprusside, and acetylcholine. In human small pulmonary arteries, hUT-II did not induce vasoconstriction but was a potent vasodilator [−log M concentration causing 50% of the maximum vasodilator effect (pIC50) 10.4 ± 0.5; percentage of reduction in tone ( E max) 81 ± 8% (vs. 23 ± 11% in time controls), n = 5]. The order of potency for vasodilation was human urotensin-II = adrenomedullin (pIC50 10.1 ± 0.4, n = 6) > sodium nitroprusside (pIC50 7.4 ± 0.2, n = 6) = acetylcholine (pIC50 6.8 ± 0.3, n = 6). In human abdominal arteries, hUT-II did not induce vasoconstriction but was a potent vasodilator [pIC50 10.3 ± 0.7; E max96 ± 8% (vs. 43 ± 16% in time controls), n = 4]. This is the first report that hUT-II is a potent vasodilator but not a vasoconstrictor of human small pulmonary arteries and systemic resistance arteries.

X-ray TV system for measuring microcirculation in small pulmonary vessels

1985 ◽  
Vol 59 (3) ◽  
pp. 1013-1018 ◽  
Author(s):  
K. Sada ◽  
M. Shirai ◽  
I. Ninomiya
Keyword(s):  
Flow Velocity ◽  
Volume Flow ◽  
Internal Diameter ◽  
Local Circulation ◽  
Cross Sectional ◽  
Pulmonary Vessels ◽  
X Ray ◽  
Transit Times ◽  
Time Required ◽  
Processing Device

We developed a new system that consists of 1) a specially designed X-ray apparatus, 2) an X-ray-sensitive 1-in. Vidicon camera, and 3) a digital image-processing device. The picture element is approximately 20 micron in size, and the time required for one frame is 1/30 s. Using this system, we measured the internal diameter (ID), the cross-sectional area, flow velocity, volume flow, and transit time of small pulmonary vessels of approximately 100–500 micron at control and with serotonin in anesthetized cats. Flow velocity and volume flow from large [458 +/- 22 (SE) micron] to small (340 +/- 32 micron) arteries were 5.4 +/- 0.4 cm/s and 0.53 +/- 0.06 ml/min, respectively. Transit times of the contrast medium from large to small arteries (Ta) and to large veins (Tv) were 0.68 +/- 0.04 and 3.71 +/- 0.25 s, respectively. Serotonin injection (20–30 micrograms/kg iv) decreased ID, flow velocity, and volume flow of arteries by 8–48, 32, and 76%, respectively, whereas Ta and Tv increased by 91 and 69%, respectively. The system can provide useful information regarding the local circulation in the lung.

Effects of regional alveolar hypoxia and hypercapnia on small pulmonary vessels in cats

1986 ◽  
Vol 61 (2) ◽  
pp. 440-448 ◽  
Author(s):  
M. Shirai ◽  
K. Sada ◽  
I. Ninomiya
Keyword(s):  
Flow Velocity ◽  
Volume Flow ◽  
The Other ◽  
Internal Diameter ◽  
Lung Region ◽  
Pulmonary Vessels ◽  
Small Arteries ◽  
X Ray ◽  
Other Hand ◽  
Alveolar Hypoxia

Using an X-ray TV system, we analyzed responses in the internal diameter (ID), flow velocity, and volume flow in small pulmonary vessels (100–600 microns ID) during unilobar hypoxia and hypercapnia in cats. In the hypoxic and hypercapnic lobes, the ID reduced in proportion to the degree of hypoxia and hypercapnia, respectively. The ID reduction was larger in the arteries than in the veins for a given stimulus. In the arteries, the ID reduced nonuniformly in the series-arranged vessels in response to both stimuli. The percentage ID reduction was maximal in the arteries of 200–300 microns ID, in which it was 21, 26, 28, and 36% with 5% O2, 0% O2, 5% CO2, and 10% CO2 inhalations, respectively. On the other hand, in the veins, uniform ID reduction occurred for a given stimulus. In the contralateral normoxic lobe, the ID did not change significantly. In both hypoxic and hypercapnic lobes, the flow velocity and volume flow of the small arteries decreased, with 5% O2, by 18 and 40%, respectively, and, with 5% CO2, by 23 and 50%, respectively. In contrast, in the normoxic lobe, they increased significantly during 5% O2 and 5% CO2 inhalations. We concluded that regional alveolar hypoxia and hypercapnia induced a local vasoconstriction particularly in the small arteries of 200–300 microns ID and decreased the flow velocity and volume flow in the same lung region.

Endothelium-dependent relaxations to adenosine in juvenile rabbit pulmonary arteries and veins

1994 ◽  
Vol 266 (5) ◽  
pp. H2001-H2006 ◽  
Author(s):  
R. H. Steinhorn ◽  
F. C. Morin ◽  
D. G. Van Wylen ◽  
S. F. Gugino ◽  
E. C. Giese ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Adenosine Receptor ◽  
Receptor Agonist ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Response Curves ◽  
Pulmonary Vessels ◽  
Oxide Synthase ◽  
Arteries And Veins

We studied the actions of adenosine and its analogues 5'-(N-ethylcarboxamido)-adenosine (NECA) and N6-cyclohexyladenosine (CHA) in pulmonary vessels isolated from juvenile rabbits. Pulmonary arteries relaxed in a concentration-dependent fashion to all three compounds. Pretreatment with the methylxanthine 8-p-sulfophenyltheophylline shifted the concentration-response curves to adenosine and NECA rightward, indicating that the vasodilator effects were mediated by the adenosine receptor. The order of potency of adenosine compounds was NECA > adenosine > CHA, indicating that the A2-receptor mediates relaxations to adenosine in rabbit pulmonary arteries. Endothelium rubbing attenuated relaxations to adenosine at concentrations of < or = 3 x 10(-7) M and to all NECA concentrations. Inhibition of nitric oxide synthase with NG-nitro-L-arginine (L-NNA) similarly attenuated relaxations at concentrations of < or = 3 x 10(-7) M for adenosine and < or = 3 x 10(-8) M for NECA. With the use of the same methods, a substantial endothelial contribution was additionally observed in pulmonary veins to the vasodilator effects of NECA. We conclude that adenosine, and the more specific A2-receptor agonist NECA, dilate pulmonary arteries and veins isolated from young rabbits via a mechanism that is partially dependent on endothelium-derived nitric oxide.

Calcitonin gene-related peptide vasodilation of human pulmonary vessels

1989 ◽  
Vol 67 (3) ◽  
pp. 1265-1270 ◽  
Author(s):  
D. G. McCormack ◽  
J. C. Mak ◽  
M. O. Coupe ◽  
P. J. Barnes
Keyword(s):  
Pulmonary Arteries ◽  
Calcitonin Gene Related Peptide ◽  
Human Calcitonin ◽  
Organ Bath ◽  
Pulmonary Vessels ◽  
Functional Studies ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Potent Vasodilator ◽  
Arteries And Veins

Human calcitonin gene-related peptide (CGRP) is localized to sensory neurons in pulmonary vessels and is a potent vasodilator. We have characterized the effects of CGRP in human pulmonary vessels and localized the receptors for this peptide by autoradiography. Fresh human lung tissue was obtained from eight patients undergoing surgery and small (200–400 microns ID) pulmonary arteries and veins were dissected free of surrounding connective and pulmonary tissue. Pairs of vessels were studied and in one of each pair the endothelium was left intact and from the other of each pair the endothelium was removed by gentle abrasion. For functional studies arteries (n = 9) and veins (n = 9) were suspended in an organ bath, precontracted with 1 microM prostaglandin F2 alpha. CGRP (10 pM to 10 microM) was added in a cumulative manner. CGRP caused a dose-dependent relaxation of endothelium intact human pulmonary arteries and veins with log EC50 values of -8.01 +/- 0.35 and -8.70 +/- 0.40, respectively (not significant). Removal of the endothelium did not diminish the vasodilator potency of CGRP in either vessel. For autoradiographic studies, cryostat sections of the small human pulmonary vessels with or without endothelium were used. 125I-CGRP densely labeled CGRP receptors on vascular smooth muscle and endothelial removal did not have any effect on grain density. We concluded that CGRP is a potent vasodilator of human pulmonary arteries and veins that is not dependent on an intact endothelium. These functional studies correlate with the distribution of CGRP receptors as localized by autoradiography.

Nonuniform effects of histamine on small pulmonary vessels in cats

1987 ◽  
Vol 62 (2) ◽  
pp. 451-458 ◽  
Author(s):  
M. Shirai ◽  
K. Sada ◽  
I. Ninomiya
Keyword(s):  
Flow Velocity ◽  
Pulmonary Arteries ◽  
Flow Distribution ◽  
Volume Flow ◽  
Beta Blockade ◽  
Internal Diameter ◽  
Vascular Walls ◽  
Beta Receptors ◽  
Arteries And Veins

In in vivo cat lung, using an X-ray TV system, we analyzed responses in internal diameter (ID), flow velocity, and volume flow of arteries and veins (100–500 microns ID) to histamine (8–15 micrograms/kg iv) under three conditions. With histamine alone, three types of ID response (constriction, dilatation, and no change) occurred in parallel-arranged arteries. Relative frequency and magnitude of constriction were maximum in arteries of 300–400 micron ID, whereas those of dilatation were maximum in arteries of 100–200 micron ID. In veins, relatively uniform constriction occurred. Under H2-blockade, histamine caused greater constriction than that with histamine alone in arteries and veins of 300–500 micron ID. Under beta-blockade, with histamine, ID of all vessels decreased significantly below the ID sizes under the above two conditions, and no dilatation occurred. In two parallel arteries that showed opposite ID changes to histamine, flow velocity increased, but volume flow decreased in a constricted artery while it increased in a dilated one. Those data indicated that, with histamine, qualitatively and quantitatively nonuniform ID response was induced in both parallel- and series-arranged small pulmonary arteries and, in turn, produced heterogeneous flow distribution. Factors to cause the nonuniformity may be partly explained by difference in density of H2- and beta-receptors in vascular walls.

Benefit of vagal nerve stimulation in epilepsia partialis continua: a case report

2006 ◽  
Vol 37 (03) ◽  
Author(s):  
C Bussmann ◽  
HM Meinck ◽  
HH Steiner ◽  
W Broxtermann ◽  
CG Bien ◽  
...  
Keyword(s):  
Case Report ◽  
Nerve Stimulation ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Epilepsia Partialis Continua

Implanted vagus nerve stimulation in 126 patients: surgical technique and complications

2020 ◽  
Vol 99 (7) ◽  
Keyword(s):  
Vagus Nerve ◽  
Vocal Cord ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Pulse Generator ◽  
Operative Procedure ◽  
Intractable Epilepsy ◽  
Vagal Nerve ◽  
University Hospital ◽  
Nerve Stimulator

Introduction: Vagus nerve stimulation is a palliative treatment for patients with refractory epilepsy to reduce the frequency and intensity of seizures. A bipolar helical electrode is placed around the left vagus nerve at the cervical level and is connected to the pulse generator placed in a subcutaneous pocket, most commonly in the subclavian region. Methods: Between March 1998 and October 2019, we performed 196 procedures related to the vagal nerve stimulation at the Neurosurgery Department in Motol University Hospital. Of these, 126 patients were vagal nerve stimulator implantation surgeries for intractable epilepsy. The cases included 69 female and 57 male patients with mean age at the time of the implantation surgery 22±12.4 years (range 2.1−58.4 years). Results: Nine patients (7.1%) were afflicted by complications related to implantation. Surgical complications included postoperative infection in 1.6%, VNS-associated arrhythmias in 1.6%, jugular vein bleeding in 0.8% and vocal cord paresis in 2.4%. One patient with vocal cord palsy also suffered from severe dysphagia. One patient (0.8%) did not tolerate extra stimulation with magnet due to a prolonged spasm in his throat. The extra added benefit of vagus stimulation in one patient was a significant reduction of previously regular severe headaches. Conclusion: Vagus nerve stimulation is an appropriate treatment for patients with drug-resistant epilepsy who are not candidates for focal resective surgery. Implantation of the vagus nerve stimulator is a relatively safe operative procedure.

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