Supersensitivity of the Isolated Rat Heart after Chemical Sympathectomy with 6-Hydroxydopamine

1971 ◽  
Vol 49 (1) ◽  
pp. 36-44 ◽  
Author(s):  
R. A. Nadeau ◽  
J. De Champlain ◽  
G. M. Tremblay
Keyword(s):  
Nerve Fibers ◽  
Isolated Rat Heart ◽  
Adrenergic Nerve ◽  
Noradrenaline Content ◽  
Chronotropic Response ◽  
Endogenous Noradrenaline ◽  
6 Hydroxydopamine ◽  
Perfused Hearts ◽  
Supersensitivity To Noradrenaline ◽  
Isolated Rat

Presynaptic supersensitivity was demonstrated in isolated rat atria and perfused hearts 2 h after an intravenous injection of 6-hydroxydopamine (6-OH-DA), 100 mg/kg. This coincided with a maximum depletion of cardiac endogenous noradrenaline, a disappearance of the fluorescence of terminal adrenergic nerve fibers in the atrial myocardium, and an abolished chronotropic response to tyramine. The chronotropic response to dopamine was also significantly diminished. Maximal supersensitivity to the chronotropic effect of noradrenaline was observed 72 h after the injection of 6-OH-DA. Two weeks after the administration of 6-OH-DA, supersensitivity to noradrenaline was less marked, and the response to tyramine was restored. These changes corresponded to an increasing noradrenaline content in the heart and to the reappearance of histofluorescent fibers in the atria.

Degeneration and Regrowth of Adrenergic Nerve Fibers in the Rat Peripheral Tissues after 6-Hydroxydopamine

1971 ◽  
Vol 49 (4) ◽  
pp. 345-355 ◽  
Author(s):  
J. de Champlain
Keyword(s):  
Ganglion Cells ◽  
Adrenergic Innervation ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
High Dose ◽  
Rat Tissues ◽  
Peripheral Tissues ◽  
Endogenous Noradrenaline ◽  
6 Hydroxydopamine ◽  
Noradrenaline Levels

Histofluorescent and biochemical changes in the adrenergic nervous system were followed up in rat tissues after one single intravenous injection of a high dose of 100 mg/kg of 6-hydroxydopamine (6-OH-DA). This treatment results in the rapid disappearance of terminal and preterminal fibers in the iris, atria, and small arteries of rats, whereas endogenous noradrenaline pools of the heart are 95% depleted. The capacity of the adrenergic nerve to take up and accumulate tritiated noradrenaline is reduced proportionally to the reduction in endogenous noradrenaline levels. These changes are compatible with the concept of a complete sympathectomy induced by the specific toxic action of 6-OH-DA on the adrenergic fibers. This sympathectomy is not permanent, however, and numerous bundles of preterminal fibers start to grow in the iris and atria within 4 to 5 days following injection. Progressively, in the following weeks, these fibers distribute over the whole organ and give birth to terminal fibers which form a new adrenergic plexus in these tissues. A completely normal innervation is restored 2 to 3 months after administration of 6-OH-DA. The endogenous noradrenaline levels rise progressively in parallel to the development of the new plexus of fibers. Since a complete regeneration of the adrenergic innervation can be demonstrated in the weeks following injection of 6-OH-DA, it appears that this compound can selectively destroy the adrenergic terminal and preterminal fibers without causing a degeneration of the adrenergic ganglion cells.

Origins of endogenous noradrenaline overflow during reperfusion of the ischaemic rat heart

1988 ◽  
Vol 74 (3) ◽  
pp. 269-274 ◽  
Author(s):  
A. M. Dart ◽  
R. A. Riemersma
Keyword(s):  
Extracellular Space ◽  
Rat Heart ◽  
Fold Increase ◽  
Isolated Rat Heart ◽  
Significant Rise ◽  
Endogenous Noradrenaline ◽  
Substrate Deprivation ◽  
Space Marker ◽  
Isolated Rat ◽  
Ischaemic Episode

1. Reperfusion of the globally ischaemic isolated rat heart is associated with an enhanced overflow of endogenous noradrenaline (NA) after ischaemic periods of 20, 40 or 60 min but not of 10 min. 2. Reperfusion NA overflow, after 40 min of ischaemia, is suppressed by desipramine and increased when ischaemia follows a period of substrate deprivation. 3. Reperfusion after 40 min of ischaemia is associated with a significant rise in NA concentration despite a simultaneous 20-fold increase in flow. This increase in concentration is abolished by treatment with desipramine or if ischaemia follows a period of substrate deprivation. 4. Reperfusion NA overflow correlates with the reperfusion overflow of an extracellular space marker infused before the ischaemic episode. 5. These results suggest that ischaemia is heterogeneous and that NA is released into regions of particularly profound ischaemia from which it is subsequently eluted during reperfusion.

scholarly journals Galanin is localized in sympathetic neurons of the dog liver

1997 ◽  
Vol 273 (6) ◽  
pp. E1194-E1202 ◽  
Author(s):  
Thomas O. Mundinger ◽  
C. Bruce Verchere ◽  
Denis G. Baskin ◽  
Michael R. Boyle ◽  
Stephan Kowalyk ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Sympathetic Neurons ◽  
Sympathetic Nerves ◽  
Liver Parenchyma ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
Adrenergic Nerve Terminals ◽  
6 Hydroxydopamine ◽  
Hepatic Nerves ◽  
Dog Liver

Stimulation of canine hepatic nerves releases the neuropeptide galanin from the liver; therefore, galanin may be a sympathetic neurotransmitter in the dog liver. To test this hypothesis, we used immunocytochemistry to determine if galanin is localized in hepatic sympathetic nerves and we used hepatic sympathetic denervation to verify such localization. Liver sections from dogs were immunostained for both galanin and the sympathetic enzyme marker tyrosine hydroxylase (TH). Galanin-like immunoreactivity (GALIR) was colocalized with TH in many axons of nerve trunks as well as individual nerve fibers located both in the stroma of hepatic blood vessels and in the liver parenchyma. Neither galanin- nor TH-positive cell bodies were observed. Intraportal 6-hydroxydopamine (6-OHDA) infusion, a treatment that selectively destroys hepatic adrenergic nerve terminals, abolished the GALIR staining in parenchymal neurons but only moderately diminished the GALIR staining in the nerve fibers around blood vessels. To confirm that 6-OHDA pretreatment proportionally depleted galanin and norepinephrine in the liver, we measured both the liver content and the hepatic nerve-stimulated spillover of galanin and norepinephrine from the liver. Pretreatment with 6-OHDA reduced the content and spillover of both galanin and norepinephrine by >90%. Together, these results indicate that galanin in dog liver is primarily colocalized with norepinephrine in sympathetic nerves and may therefore function as a hepatic sympathetic neurotransmitter.

ATP-sensitive potassium channels regulate stimulated ANF secretion in isolated rat heart

1996 ◽  
Vol 271 (6) ◽  
pp. H2339-H2345 ◽  
Author(s):  
T. Xu ◽  
J. H. Jiao ◽  
R. A. Pence ◽  
A. J. Baertschi
Keyword(s):  
Potassium Channels ◽  
Potassium Channel ◽  
Rat Heart ◽  
Atrial Natriuretic Factor ◽  
Left Atrial ◽  
Channel Blocker ◽  
Acute Hypoxia ◽  
Isolated Rat Heart ◽  
Perfused Hearts ◽  
Isolated Rat

Perfused hearts (n = 127) were exposed to acute hypoxia (10% O2 for 12 or 20 min) or left atrial stretch (increase in atrial pressure) in the presence or absence of 100 mumol/l ATP-sensitive potassium channel blocker (tolbutamide) or openers (pinacidil and diazoxide). Hypoxia alone elicited a prolonged atrial natriuretic factor (ANF) release, peaking at 74% over baseline (P < 0.01); with tolbutamide, ANF secretion peaked at 132% over baseline (P < 0.01). Pinacidil and diazoxide abolished the ANF response to hypoxia (P < 0.01). Atrial stretch alone (1 mmHg) transiently (2 min) increased ANF by 56% (P < 0.05); with tolbutamide, ANF increased transiently by 124% and showed a prolonged increase of 52% (P < 0.05). With tolbutamide, graded stretch (0.5-2.3 mmHg) induced a bell-shaped transient (2-min) increase of ANF release [-3% at 0.5 mmHg, 124% (P < 0.05) at 1.0 mmHg, 80% (P < 0.05) at 1.48 mmHg, and 14% at 2.22 mmHg] and a saturating prolonged ANF response. Tolbutamide increased the ANF response nonsignificantly at lower doses (30 mumol/l) and had no effect at 1 mumol/l. Pinacidil abolished the stretch-induced ANF release. These results suggest that ATP-sensitive potassium channels are extremely potent modulators of stimulated ANF secretion.

Activation by Phoneutria nigriventer spider venom of autonomic nerve fibers in the isolated rat heart

1998 ◽  
Vol 363 (2-3) ◽  
pp. 139-146 ◽  
Author(s):  
Soraia K.P Costa ◽  
Stephen Hyslop ◽  
Luciana P Nathan ◽  
Angelina Zanesco ◽  
Susan D Brain ◽  
...  
Keyword(s):  
Rat Heart ◽  
Nerve Fibers ◽  
Isolated Rat Heart ◽  
Spider Venom ◽  
Autonomic Nerve ◽  
Phoneutria Nigriventer ◽  
Isolated Rat

Effect of fasting on glucose and palmitate metabolism of perfused rat heart

1963 ◽  
Vol 205 (6) ◽  
pp. 1203-1208 ◽  
Author(s):  
Lionel H. Opie ◽  
John R. Evans ◽  
Joseph C. Shipp
Keyword(s):  
Rat Heart ◽  
Glucose Oxidation ◽  
Isolated Rat Heart ◽  
Perfused Rat Heart ◽  
Glucose Carbon ◽  
Ad Libitum ◽  
Perfused Hearts ◽  
Palmitate Metabolism ◽  
Isolated Rat ◽  
Pyruvate Ratio

The metabolism of glucose U-C14, 5 mm, and palmitate 1-C14, 0.75 mm (complexed to 0.5% albumin), was studied in isolated perfused hearts taken from three groups of rats: fed ad libitum, fasted overnight, or fasted 4 days. The changes in glucose metabolism associated with fasting were: decreased glucose uptake, decreased C14O2 formation, decreased lactate/pyruvate ratio, and decreased incorporation of glucose carbon into glycogen. In contrast, the uptake of palmitate and incorporation of label into C14O2 and tissue fatty acids were similar in the three groups. When the perfusate contained both glucose and palmitate, glucose oxidation was reduced in both fed and fasted states, but palmitate oxidation was virtually unaltered. It is concluded that the nutritional state of the donor rat markedly affects glucose but not palmitate metabolism of the isolated rat heart, and that palmitate is preferentially oxidized in both fed and fasted states. The possible mechanisms involved are discussed.

Early in reperfusion, leukocytes alter perfused coronary capillarity and vascular resistance

1989 ◽  
Vol 256 (4) ◽  
pp. H982-H989 ◽  
Author(s):  
J. M. Reynolds ◽  
P. F. McDonagh
Keyword(s):  
Vascular Resistance ◽  
Ischemia Reperfusion ◽  
Capillary Density ◽  
Isolated Rat Heart ◽  
Microvascular Perfusion ◽  
Coronary Vascular Resistance ◽  
No Reflow ◽  
Before And After ◽  
Perfused Hearts ◽  
Isolated Rat

Myocardial no-reflow is a critical consequence of myocardial ischemia-reperfusion (I/R). Recent studies indicate that formed blood elements (e.g., leukocytes and platelets) contribute greatly to the compromise of myocardial blood flow that occurs after I/R. To assess the contributions of leukocytes and platelets to alterations in microvascular perfusion, we measured total coronary vascular resistance and perfused coronary capillary density before and after a 30-min period of no-flow ischemia in isolated rat hearts perfused with either 1) a Krebs-albumin-red cell solution [K(2)RBC]; 2) diluted whole blood (DWB) with Krebs (1:1); or 3) leukocyte-free DWB (LFB). We found that hearts perfused with K(2)RBC before ischemia demonstrated a significant decrease in perfused capillarity (-25%, P less than 0.05) after 25 min of reperfusion. Hearts perfused with LFB before ischemia exhibited a similar decrease in perfused capillarity (-33%, P less than 0.05) during reperfusion. However, in the DWB-perfused hearts, there was a 62% decrease in perfused capillarity (-62%, P less than 0.01) during reperfusion. Moreover, during reperfusion, total coronary vascular resistance was elevated significantly (+76%, P less than 0.01) in the DWB-perfused hearts but not in either the K(2)RBC or LFB groups. These results indicate that 1) platelets do not play a major role in alterations of microvascular perfusion after ischemia; 2) leukocytes are not requisite for the development of microvascular no-reflow early in reperfusion but their presence further exacerbates this deleterious effect; and 3) a relationship exists between perfused capillarity and vascular resistance in the isolated rat heart after global ischemia.

Effect of Hydrogen Sulfide on Reactions of Isolated Rat Heart under Volume Load and Ischemia-Reperfusion

2013 ◽  
Vol 4 (3) ◽  
pp. 201-212
Author(s):  
Tetyana V Shimanskaya ◽  
Yulia V. Goshovska ◽  
Olena M. Semenykhina ◽  
Vadim F. Sagach
Keyword(s):  
Hydrogen Sulfide ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Volume Load ◽  
Isolated Rat
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