Ectopic jejunal pacemakers after jejunal transection and their relationship to transit

1995 ◽  
Vol 268 (6) ◽  
pp. G959-G967
Author(s):  
J. J. Cullen ◽  
J. C. Eagon ◽  
F. S. Hould ◽  
R. B. Hanson ◽  
K. A. Kelly

The hypothesis was that orally moving pacesetter potentials distal to a site of jejunal transection and anastomosis would slow transit through jejunum containing them and that reoperation with excision of bowel containing these pacesetter potentials would restore transit to the control. In six conscious dogs with jejunal serosal electrodes for recording myoelectric activity and a jejunal perfusion/aspiration catheter for measuring transit, jejunal pacesetter potential frequency decreased distal to a midjejunal transection and anastomosis from 18.7 +/- 0.3 (SE) cycles/min (cpm) proximal to the site to 14.4 +/- 0.6 cpm distal to the site (P < 0.05). In addition, orally propagating pacesetter potentials occurred > 25% of the time in a 37 +/- 7 cm length of bowel distal to the site during fasting and after feeding. Transit through the segment with the orally moving pacesetter potentials was slowed during feeding (half time before and after transection, 7.7 +/- 1.1 and 13 +/- 2.0 min, respectively, P < 0.05). Resection of the segment with the abnormal pacesetter potentials shortened the length of bowel containing them to 24 +/- 2 cm (P > 0.05) and restored transit to the control. In conclusion, orally moving pacesetter potentials distal to a canine jejunal transection and anastomosis slowed transit through the segment of bowel containing them. Resection of the segment restored transit to the control.

1972 ◽  
Vol 70 (4) ◽  
pp. 736-740 ◽  
Author(s):  
T. Suzuki ◽  
R. Higashi ◽  
T. Hirose ◽  
H. Ikeda ◽  
K. Tamura

ABSTRACT Conscious dogs were infused intravenously with ethanol in doses of 0.7 and 1.0 g/kg. The adrenal venous blood samples were collected before and after the infusion of ethanol and analysed for 17-hydroxycorticosteroids (17-OHCS). After the infusion of 0.7 g/kg (subanaesthetic dose) of ethanol the adrenal 17-OHCS secretion rate showed either a slight increase or no change. After the infusion of 1.0 g/kg (anaesthetic dose) of ethanol the adrenal 17-OHCS secretion rate increased markedly and reached 1.21±0.15 (mean±sem) μg/kg/min, while it was 0.09±0.023 μg/kg/min before the infusion.


1993 ◽  
Vol 264 (4) ◽  
pp. H1259-H1268 ◽  
Author(s):  
N. Uemura ◽  
D. E. Vatner ◽  
Y. T. Shen ◽  
J. Wang ◽  
S. F. Vatner

The goal of this study was to determine whether enhanced vascular responsiveness during the development of perinephritic hypertension is selective or nonspecific. The effects of graded infusions of norepinephrine (NE), phenylephrine (PE), angiotensin II (ANG II), and vasopressin (VP) were examined on mean arterial pressure, total peripheral resistance (TPR), and aortic pressure-diameter relationships in conscious dogs. NE increased TPR significantly greater (P < 0.01) in hypertension than normotension, as did PE infusion, whereas ANG II and VP increased TPR similarly before and after hypertension. Analysis of aortic pressure-diameter relationships also demonstrated significant (P < 0.05) shifts in response to NE and PE, but not ANG II and VP, during the development of hypertension. In normotensive dogs, low doses of ANG II infusion also enhanced the vasoconstrictor response not only to NE and PE but also to VP. In contrast to what was observed in hypertension, in the presence of ANG II infusion after ganglionic blockade, enhanced responses to PE and NE were no longer observed. The alpha 1-adrenergic receptor density in membrane preparations from aortic tissue, as determined by [3H]prazosin binding, was higher (P < 0.05) in hypertensive dogs than control dogs. Thus the vascular responsiveness in the aorta and resistance vessels is enhanced to alpha 1-adrenergic stimulation, but not to all vasoconstrictors, during developing perinephritic hypertension. The mechanism appears to involve increased alpha 1-adrenergic receptor density.


1990 ◽  
Vol 68 (1) ◽  
pp. 341-347 ◽  
Author(s):  
M. P. Barrowcliffe ◽  
G. D. Zanelli ◽  
D. Ellison ◽  
J. G. Jones

To examine how molecular charge affects the transfer of molecules across the alveolar-capillary barrier, we prepared the following dextrans of equivalent molecular size (mol wt 10,000) but varying molecular charge: neutral dextran, cationic DEAE dextran, and anionic dextran sulfate. These were labeled with 99mTc. The lungs of three groups of anesthetized rabbits were insufflated with dextran aerosols, with six rabbits receiving each type, and the half-time pulmonary clearance (t1/2) was measured. Control t1/2's (95% confidence limits) were 95 (74-120), 227 (192-268), and 291 (246-345) min for neutral, cationic, and anionic dextrans, respectively. One week later, when the same animals were restudied 4 h after 3 micrograms/kg iv endotoxin, t1/2's were 102 (75-139), 167 (149-187), and 126 (102-154) min, respectively. After 30 min during this repeat study, animals were ventilated with 20 breaths of cigarette smoke, which acutely increased the clearance rate to 34 (26-46), 25 (20-31), and 13 (7-24) min, respectively. Mean carboxyhemoglobin levels were not significantly different in the three groups: 13.6, 12.7, and 11.1%, respectively. These results demonstrated that neutral dextrans showed the same clearance rate before and after endotoxin, whereas the charged dextrans had a significantly faster clearance after endotoxin. After smoke exposure the anionic dextran left the lung more rapidly than the neutral dextran. Thus molecular charge affects solute transfer across the alveolar-capillary barrier in both normal and injured lungs, and an effect of endotoxin on the lung can be detected with charged dextrans but not with neutral dextran.


1982 ◽  
Vol 52 (3) ◽  
pp. 705-709 ◽  
Author(s):  
B. R. Walker ◽  
N. F. Voelkel ◽  
J. T. Reeves

Recent studies have shown that vasodilator prostaglandins are continually produced by the isolated rat lung. We postulated that these vasodilators may contribute to maintenance of normal low pulmonary arterial pressure. Pulmonary pressure and cardiac output were measured in conscious dogs prior to and 30 to 60 min following administration of meclofenamate (2 mg/kg iv, followed by infusion at 2 mg . kg-1 . h-1) or the structurally dissimilar inhibitor RO–20–5720 (1 mg/kg iv, followed by infusion at 1 mg . kg-1 . h-1). The animals were also made hypoxic with inhalation of 10% O2 before and after inhibition. Time-control experiments were conducted in which only the saline vehicle was administered. Meclofenamate or RO–20–5720 caused an increase in mean pulmonary arterial pressure and total pulmonary resistance. Cardiac output and systemic pressure were unaffected. The mild hypoxic pulmonary pressor response observed was not affected by meclofenamate. Animals breathing 30% O2 to offset Denver's altitude also demonstrated increased pulmonary pressure and resistance when given meclofenamate. It is concluded that endogenous vasodilator prostaglandins may contribute to normal, low vascular tone in the pulmonary circulation.


1980 ◽  
Vol 239 (4) ◽  
pp. H545-H545 ◽  
Author(s):  
Raymond C. Koehler ◽  
Brian W. McDonald ◽  
John A. Krasney

The modulating effect of CO2 on the circulatory response to hypoxia in chronically instrumented conscious dogs was examined over a wide range of arterial partial pressure of O2 [PaO2 (from 80 to 25 Torr)] during a 41-min rebreathing period at three CO2 levels: hypocapnia (from PaCO2 of 32 to 18 Torr), eucapnia (32 Torr), and mild hypercapnia (40 Torr). Eucapnic and hypercapnic hypoxic responses were also measured after sinoaortic denervation (SAD) to assess the arterial chemoreceptor and baroreceptor reflex contributions. Elevating PaCO2 attenuated the tachycardia during hypoxia and produced progressively greater systemic, renal, and splanchnic vasoconstriction before but not after SAD. Vagal block converted the rises in renal and splanchnic flows observed during hypocapnic hypoxia to declines. The increase in left ventricular dP/d tmax was not affected by varying PaCO2 either before or after SAD. Coronary flow increased an additional onefold during hypoxia when PaCO2 was elevated both before and after SAD, but the tension-time indices did not differ significantly. These results indicate that: a) cardiopulmonary vagal afferents effectively counteract chemoreflex-induced vasoconstriction during hypocapnic hypoxia; b) chemoreflex vasoconstriction predominates in the renal and splanchnic beds when PaCO2 is elevated; c) the sinoaortic reflexes restrain the heart rate, but not the contractility response to hypoxia when PaCO2 is increased; and d) the augmented coronary vasodilation produced by CO2 is probably mediated by local CO2-hypoxic interactions.


1986 ◽  
Vol 250 (5) ◽  
pp. H892-H897 ◽  
Author(s):  
M. A. Young ◽  
S. F. Vatner

We studied, in conscious dogs, the effects of removal of endothelium on the responses of iliac artery diameter and iliac blood flow to intra-arterial infusions of adrenergic agonists. With endothelium intact, iliac diameter increased with intra-arterial infusion of nitroglycerin (4.7 +/- 0.4%), acetylcholine (4.2 +/- 0.6%), and epinephrine (4.5 +/- 1.3%), and decreased with norepinephrine (-7.5 +/- 1.7%), phenylephrine (-6.6 +/- 1.0%), and B-HT 920 (-2.1 +/- 0.6%). One- to-five days following removal of endothelium with a balloon-tipped catheter, base-line iliac diameter was unchanged, and still increased with nitroglycerin (4.6 +/- 0.5%), but not with acetyl-choline, and epinephrine actually decreased diameter (-3.5 +/- 1.3%). Removal of the endothelium also enhanced the constriction observed with norepinephrine (-12.5 +/- 2.0%) and phenylephrine (-11.4 +/- 1.6%), but not with B-HT 920 (-1.8 +/- 0.5%). The changes in arterial pressure, iliac blood flow, iliac vascular resistance, and heart rate induced by any of the agonists did not differ before and after removal of the endothelium. These results indicate that the endothelium mediates the dilation in response to epinephrine and also serves an important role in protecting against alpha 1-adrenergic vasoconstriction of large iliac arteries.


2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Fei Xue ◽  
Caichu Xia ◽  
Guoliang Li ◽  
Baocheng Jin ◽  
Yongwang He ◽  
...  

The effects of tunnel blast excavation on the lining structures of adjacent tunnels are comprehensively studied for the Xinling highway tunnel project. First, the LS-DYNA software is applied to obtain the characteristics of vibration velocities and dynamic stresses at different positions of the tunnel liner. The results indicate that the maximum peak particle velocity (PPV) is located on the haunch of the lining facing the blasting source and that the PPV and peak tensile stress decrease with the increase in the surrounding rock grade. Second, a site test on blasting vibration is conducted to verify the simulation results. By using regression analysis of the measured vibration data, the calculation method of maximum charge per delay for optimizing blasting excavation under different surrounding rock grades is obtained. Finally, based on the statistical relationship between crack alteration and PPV on the lining before and after blasting, the safety thresholds of PPV for different portions of the tunnel are determined. The recommended safety threshold of PPV is 10 cm/s for intact lining and for B-grade and V-grade linings of the surrounding rock tunnel. However, if the lining crack grade falls between 1A and B, then the recommended safety thresholds of PPV for the III-grade and IV-grade surrounding rock tunnel are 5 cm/s and 6 cm/s, respectively. The threshold PPV proposed in this study has been successfully applied to restrict blast-induced damage during new tunnel excavation of the Xinling tunnel project.


1978 ◽  
Vol 234 (2) ◽  
pp. H152-H156
Author(s):  
G. S. Geis ◽  
G. Barratt ◽  
R. D. Wurster

Resting cardiovascular parameters and the responses to bilateral carotid occlusions (BCO) were monitored in pentobarbital-anesthetized and conscious dogs before and after placing lesions in the dorsolateral funiculi at C7-C8 and after spinal transections at C7. Pre- and postlesion blood pressure (BP) and heart rate (HR) responses to exercise were also monitored. The lesions significantly attenuated the responses to BCO and decreased resting BP in anesthetized dogs. Yet neither resting HR in anesthetized or conscious dogs nor the resting BP in conscious dogs was affected by the lesions. Subsequent spinal transections significantly decreased resting HR and BP and the responses to BCO but did not affect the BP response to BCO in anesthetized dogs as compared with corresponding postlesion parameters. BP responses to exercise were significantly attenuated by the lesions, but HR responses were not affected. Since stimulation and BP studies indicated that the descending pressor pathway had been ablated, the data suggest that the pathway mediates BP and HR responses to BCO in pentobarbital-anesthetized and conscious dogs. It does not maintain resting HR in anesthetized or conscious animals, and the resting BP in conscious dogs. This pathway is important for BP responses to exercise but is not necessary for HR responses. Finally, other spinal pathways are involved in cardiovascular control.


1984 ◽  
Vol 247 (6) ◽  
pp. F881-F887 ◽  
Author(s):  
L. C. Gregory ◽  
I. A. Reid

Previous studies have shown that the inhibition of renin secretion by vasopressin (AVP) in conscious dogs is related to vasoconstrictor activity and may be a reflex response mediated by the renal nerves. The aim of the present experiments was to determine whether the suppression of plasma renin activity (PRA) by AVP is blocked by renal denervation. AVP and, for comparison, angiotensin II (ANG II) were infused intravenously for 45 min in seven conscious dogs before and after bilateral renal denervation. Before denervation, AVP infusion at 0.2 and 1.0 ng X kg-1 X min-1 suppressed PRA from 7.4 +/- 1.1 to 4.7 +/- 1.0 (P less than 0.01) and from 7.9 +/- 1.8 to 3.8 +/- 0.8 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. ANG II infusion at 5.0 and 10.0 ng X kg-1 X min-1 decreased PRA from 7.5 +/- 2.3 to 2.5 +/- 0.7 (P less than 0.01) and from 6.0 +/- 1.1 to 1.8 +/- 0.4 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. One to three weeks following renal denervation, PRA had decreased from 6.7 +/- 1.3 to 2.9 +/- 0.5 ng X ml-1 X 3 h-1 (P less than 0.01), and renal norepinephrine was undetectable. After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)


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