Role of gastric blood flow in impaired defense and repair of aged rat stomachs

1995 ◽  
Vol 269 (5) ◽  
pp. G737-G744 ◽  
Author(s):  
J. E. Gronbech ◽  
E. R. Lacy
Keyword(s):  
Blood Flow ◽  
Mucosal Injury ◽  
Nerve Fibers ◽  
Gastric Blood Flow ◽  
Aged Rats ◽  
Young Rats ◽  
Calcitonin Gene ◽  
Hyperemic Response

To study impaired gastric mucosal tolerance against noxious agents in aged rats, possible factors underlying this observation were compared in anesthetized Fisher 344 young and aged rats. The gastric mucosa was damaged by in situ exposure to 80% ethanol for 30-45 s and by 1 M NaCl for 10 min followed by saline (pH = 1.0) for 60 min in chambered stomachs. The lesion area was significantly larger and epithelial restitution was significantly slower in aged than in young rats after both types of injury. Changes in gastric blood flow were monitored by laser-Doppler velocimetry. Young, but not aged, rats showed a marked increase in gastric blood flow in response to 1 M NaCl, acid challenge, and 640 microM capsaicin for 60 min. Young rats showed a higher density of calcitonin gene-related peptide (CGRP)-staining nerve fibers around submucosal blood vessels and higher mucosal release of prostaglandin E2 and leukotriene C4 than did aged rats. These data suggest that impaired mucosal defense and reduced restitution in aged rats is related to lack of hyperemic response caused by mucosal injury and H+ back-diffusion, which is probably due to decreased density of CGRP-staining nerve fibers and prostaglandin biosynthetic capacity in the mucosa.

scholarly journals Role of convective O2 delivery in determiningV˙o 2 on-kinetics in canine muscle contracting at peak V˙o 2

2000 ◽  
Vol 89 (4) ◽  
pp. 1293-1301 ◽  
Author(s):  
Bruno Grassi ◽  
Michael C. Hogan ◽  
Kevin M. Kelley ◽  
William G. Aschenbach ◽  
Jason J. Hamann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Muscle Fatigue ◽  
Oxidative Metabolism ◽  
Muscle Blood Flow ◽  
Content Difference ◽  
O2 Delivery ◽  
Gastrocnemius Muscles

A previous study (Grassi B, Gladden LB, Samaja M, Stary CM, and Hogan MC, J Appl Physiol 85: 1394–1403, 1998) showed that convective O2 delivery to muscle did not limit O2 uptake (V˙o 2) on-kinetics during transitions from rest to contractions at ∼60% of peakV˙o 2. The present study aimed to determine whether this finding is also true for transitions involving contractions of higher metabolic intensities.V˙o 2 on-kinetics were determined in isolated canine gastrocnemius muscles in situ ( n = 5) during transitions from rest to 4 min of electrically stimulated isometric tetanic contractions corresponding to the muscle peakV˙o 2. Two conditions were compared: 1) spontaneous adjustment of muscle blood flow (Q˙) (Control) and 2) pump-perfused Q˙, adjusted ∼15–30 s before contractions at a constant level corresponding to the steady-state value during contractions in Control (Fast O2 Delivery). In Fast O2 Delivery, adenosine was infused intra-arterially. Q˙ was measured continuously in the popliteal vein; arterial and popliteal venous O2 contents were measured at rest and at 5- to 7-s intervals during the transition. Muscle V˙o 2 was determined as Q˙times the arteriovenous blood O2 content difference. The time to reach 63% of the V˙o 2 difference between resting baseline and steady-state values during contractions was 24.9 ± 1.6 (SE) s in Control and 18.5 ± 1.8 s in Fast O2 Delivery ( P < 0.05). FasterV˙o 2 on-kinetics in Fast O2Delivery was associated with an ∼30% reduction in the calculated O2 deficit and with less muscle fatigue. During transitions involving contractions at peak V˙o 2, convective O2 delivery to muscle, together with an inertia of oxidative metabolism, contributes in determining theV˙o 2 on-kinetics.

scholarly journals Role Of Cgrp In Sensitization Of Dura Mater

2001 ◽  
Vol 1 ◽  
pp. 20-20
Author(s):  
K. Messlinger
Keyword(s):  
Dura Mater ◽  
Trigeminal Nerve ◽  
Plasma Levels ◽  
Nerve Fibers ◽  
Considerable Proportion ◽  
Trigeminovascular System ◽  
Dura Mater Encephali ◽  
Related Peptide ◽  
Calcitonin Gene

The mammalian dura mater encephali is richly supplied by trigeminal nerve fibers, a considerable proportion of which contains calcitonin gene-related peptide (CGRP). As plasma levels of CGRP are increased in some forms of headaches, the question is in which way CGRP is involved in nociceptive mechanisms within the peripheral and the central trigeminovascular system.

Gastroprotective and vasodilatory effects of epidermal growth factor: the role of sensory afferent neurons

2001 ◽  
Vol 280 (5) ◽  
pp. G897-G903 ◽  
Author(s):  
Yoji Matsumoto ◽  
Kohki Kanamoto ◽  
Keishi Kawakubo ◽  
Hitoshi Aomi ◽  
Takayuki Matsumoto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Mucosal Injury ◽  
Protective Role ◽  
Sensory Nerves ◽  
Afferent Neurons ◽  
Gastric Mucosal Lesions ◽  
Calcitonin Gene ◽  
Epidermal Growth

Epidermal growth factor (EGF) has been shown to exert gastric hyperemic and gastroprotective effects via capsaicin-sensitive afferent neurons, including the release of calcitonin gene-related peptide (CGRP). We examined the protective and vasodilatory effects of EGF on the gastric mucosa and its interaction with sensory nerves, CGRP, and nitric oxide (NO) in anesthetized rats. Intragastric EGF (10 or 30 μg) significantly reduced gastric mucosal lesions induced by intragastric 60% ethanol (50.6% by 10 μg EGF and 70.0% by 30 μg EGF). The protective effect of EGF was significantly inhibited by pretreatment with capsaicin desensitization, human CGRP1 antagonist hCGRP-(8–37), or N ω-nitro-l-arginine methyl ester (l-NAME). Intravital microscopy showed that topically applied EGF (10–1,000 μg/ml) dilated the gastric mucosal arterioles dose dependently and that this vasodilatory effect was significantly inhibited by equivalent pretreatments. These findings suggest that EGF plays a protective role against ethanol-induced gastric mucosal injury, possibly by dilating the gastric mucosal arterioles via capsaicin-sensitive afferent neurons involving CGRP and NO mechanisms.

Intracoronary adenosine enhances myocardial reactive hyperemia after brief coronary occlusion

1985 ◽  
Vol 248 (6) ◽  
pp. H812-H817
Author(s):  
D. Saito ◽  
T. Hyodo ◽  
K. Takeda ◽  
Y. Abe ◽  
H. Tani ◽  
...  
Keyword(s):  
Blood Flow ◽  
Left Atrium ◽  
Coronary Occlusion ◽  
Reactive Hyperemia ◽  
Control Level ◽  
Direct Effects ◽  
Intracoronary Infusion ◽  
Hyperemic Flow ◽  
Hyperemic Response

Adenosine is a prime candidate for the role of mediator between myocardial metabolic state and coronary blood flow. However, there are few reports concerning the direct effects of exogenously added adenosine on coronary autoregulation. The present investigation in the open-chest dog studied the effects of a threshold dose of intracoronary adenosine infusion on reactive hyperemia following brief coronary occlusions. The infused dose did not increase nonocclusive flow by greater than 10%. Adenosine enhanced total hyperemic flow at all occlusions tested (5, 10, 15, 20, and 30 s). Aminophylline pretreatment reduced reactive hyperemia below the control level even in the presence of an intracoronary infusion of adenosine. Adenosine injected into the left atrium and intracoronarily infused papaverine did not affect hyperemic response to 5- and 15-s coronary occlusions. The results suggest that a minimum dose of exogenously added adenosine enhances myocardial reactive hyperemia, possibly by potentiating the effects of endogenous adenosine released during ischemia.

Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons

2007 ◽  
Vol 293 (1) ◽  
pp. E96-E101 ◽  
Author(s):  
Satoshi Fujita ◽  
MaryAnn Bohland ◽  
Graciela Sanchez-Watts ◽  
Alan G. Watts ◽  
Casey M. Donovan
Keyword(s):  
Portal Vein ◽  
Sensory Neurons ◽  
Jugular Vein ◽  
Immunohistochemical Analysis ◽  
Nerve Fibers ◽  
Similar Response ◽  
Primary Sensory Neurons ◽  
Calcitonin Gene ◽  
Epinephrine Concentration

To elucidate the type of spinal afferent involved in hypoglycemic detection at the portal vein, we considered the potential role of capsaicin-sensitive primary sensory neurons. Specifically, we examined the effect of capsaicin-induced ablation of portal vein afferents on the sympathoadrenal response to hypoglycemia. Under anesthesia, the portal vein was isolated in rats and either capsaicin (CAP) or the vehicle (CON) solution applied topically. During the same surgery, the carotid artery (sampling) and jugular vein (infusion) were cannulated. One week later, all animals underwent a hyperinsulinemic hypoglycemic clamp, with glucose (variable) and insulin (25 mU·kg−1·min−1) infused via the jugular vein. Systemic hypoglycemia (2.76 ± 0.05 mM) was induced by minute 75 and sustained until minute 105. By design, no significant differences were observed in arterial glucose or insulin concentrations between groups. When hypoglycemia was induced in CON, the plasma epinephrine concentration increased from 0.67 ± 0.05 nM at basal to 36.15 ± 2.32 nM by minute 105. Compared with CON, CAP animals demonstrated an 80% suppression in epinephrine levels by minute 105, 7.11 ± 0.55 nM ( P < 0.001). A similar response to hypoglycemia was observed for norepinephrine, with CAP values suppressed by 48% compared with CON. Immunohistochemical analysis of the portal vein revealed an 85% decrease in the number of calcitonin gene-related peptide-reactive nerve fibers following capsaicin-induced ablation. That the suppression in the sympathoadrenal response was comparable to our previous findings for total denervation of the portal vein indicates that hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons.

scholarly journals Role of CO2 in the cerebral hyperemic response to incremental normoxic and hyperoxic exercise

2016 ◽  
Vol 120 (8) ◽  
pp. 843-854 ◽  
Author(s):  
K. J. Smith ◽  
K. W. Wildfong ◽  
R. L. Hoiland ◽  
M. Harper ◽  
N. C. Lewis ◽  
...  
Keyword(s):  
Blood Flow ◽  
Posterior Cerebral Artery ◽  
Submaximal Exercise ◽  
Maximum Workload ◽  
Exercise Induced ◽  
End Tidal ◽  
Induced Changes ◽  
Isocapnic Hyperpnea ◽  
Hyperemic Response

Cerebral blood flow (CBF) is temporally related to exercise-induced changes in partial pressure of end-tidal carbon dioxide (PetCO2); hyperoxia is known to enhance this relationship. We examined the hypothesis that preventing PetCO2 from rising (isocapnia) during submaximal exercise with and without hyperoxia [end-tidal Po2 (PetO2) = 300 mmHg] would attenuate the increases in CBF. Additionally, we aimed to identify the magnitude that breathing, per se, influences the CBF response to normoxic and hyperoxic exercise. In 14 participants, CBF (intra- and extracranial) measurements were measured during exercise [20, 40, 60, and 80% of maximum workload (Wmax)] and during rest while ventilation (V̇e) was volitionally increased to mimic volumes achieved during exercise (isocapnic hyperpnea). While V̇e was uncontrolled during poikilocapnic exercise, during isocapnic exercise and isocapnic hyperpnea, V̇e was increased to prevent PetCO2 from rising above resting values (∼40 mmHg). Although PetCO2 differed by 2 ± 3 mmHg during normoxic poikilocapnic and isocapnic exercise, except for a greater poikilocapnic compared with isocapnic increase in blood velocity in the posterior cerebral artery at 60% Wmax, the between condition increases in intracranial (∼12-15%) and extracranial (15–20%) blood flow were similar at each workload. The poikilocapnic hyperoxic increases in both intra- and extracranial blood-flow (∼17–29%) were greater compared with poikilocapnic normoxia (∼8–20%) at intensities >40% Wmax ( P < 0.01). During both normoxic and hyperoxic conditions, isocapnia normalized both the intracranial and extracranial blood-flow differences. Isocapnic hyperpnea did not alter CBF. Our findings demonstrate a differential effect of PetCO2 on CBF during exercise influenced by the prevailing PetO2.

scholarly journals The role of the endothelium in the hyperemic response to passive leg movement: looking beyond nitric oxide

2020 ◽  
Author(s):  
Joel D. Trinity ◽  
Oh Sung Kwon ◽  
Ryan M. Broxterman ◽  
Jayson R. Gifford ◽  
Andrew C. Kithas ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Vascular Function ◽  
No Synthase ◽  
Ketorolac Tromethamine ◽  
Arterial Infusion ◽  
Healthy Men ◽  
Leg Movement ◽  
Hyperemic Response

Passive leg movement (PLM) evokes a robust and predominantly nitric oxide (NO)-mediated increase in blood flow that declines with age and disease. Consequently, PLM is becoming increasingly accepted as a sensitive assessment of endothelium-mediated vascular function. However, a substantial PLM-induced hyperemic response is still evoked despite NO synthase (NOS) inhibition. Therefore, in 9 young healthy men (25±4 yrs), this investigation aimed to determine if the combination of two potent endothelium-dependent vasodilators, specifically prostaglandin (PG) and endothelium-derived hyperpolarizing factor (EDHF), account for the remaining hyperemic response to the two variants of PLM, PLM (60 movements) and single PLM (sPLM, 1 movement) when NOS is inhibited. The leg blood flow (LBF, Doppler ultrasound) response to PLM and sPLM following the intra-arterial infusion of NG-monomethyl L-arginine (L-NMMA), to inhibit NOS, was compared to the combined inhibition of NOS, cyclooxygenase (COX), and cytochrome P450 (CYP450) by L-NMMA, ketorolac tromethamine (KET), and fluconazole (FLUC), respectively. NOS inhibition attenuated the overall LBF (LBFAUC) response to both PLM (control: 456±194, L-NMMA: 168±127 ml, p<0.01) and sPLM (control: 185±171, L-NMMA: 62±31 ml, p=0.03). The combined inhibition of NOS, COX, and CYP450 (i.e. L-NMMA+KET+FLUC) did not further attenuate the hyperemic responses to PLM (LBFAUC: 271±97 ml, p>0.05) or sPLM (LBFAUC: 72±45 ml, p>0.05). Therefore, PG and EDHF do not collectively contribute to the non-NOS-derived NO-mediated, endothelium-dependent, hyperemic response to either PLM or sPLM in healthy young men. These findings add to the mounting evidence and understanding of the vasodilatory pathways assessed by the PLM and sPLM vascular function tests.

Inhibition of vascular ATP-sensitive K+channels does not affect reactive hyperemia in human forearm

2003 ◽  
Vol 284 (2) ◽  
pp. H711-H718 ◽  
Author(s):  
H. M. Omar Farouque ◽  
Ian T. Meredith
Keyword(s):  
Blood Flow ◽  
Adaptive Response ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Channel Inhibition ◽  
Human Forearm ◽  
Hyperemic Response

The extent to which ATP-sensitive K+ channels contribute to reactive hyperemia in humans is unresolved. We examined the role of ATP-sensitive K+channels in regulating reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects had forearm blood flow measured with venous occlusion plethysmography. Reactive hyperemia could be reproducibly induced ( n = 9). The contribution of vascular ATP-sensitive K+ channels to reactive hyperemia was determined by measuring forearm blood flow before and during brachial artery infusion of glibenclamide, an ATP-sensitive K+ channel inhibitor ( n = 12). To document ATP-sensitive K+ channel inhibition with glibenclamide, coinfusion with diazoxide, an ATP-sensitive K+ channel opener, was undertaken ( n = 10). Glibenclamide did not significantly alter resting forearm blood flow or the initial and sustained phases of reactive hyperemia. However, glibenclamide attenuated the hyperemic response induced by diazoxide. These data suggest that ATP-sensitive K+ channels do not play an important role in controlling forearm reactive hyperemia and that other mechanisms are active in this adaptive response.

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