Sensory innervation of the rat portal vein and the hepatic artery

Barja, Francisco; Mathison, Ron

doi:10.1016/0165-1838(84)90050-x

Cited by 49 publications

(43 citation statements)

References 24 publications

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“…The portohepatis of the rat is extensively innervated by sensory fibers originating from dorsal root ganglia at the T7ϪT13 level of the thoracic spine (21). The pattern of spinal afferent innervation in the rat, as indicated by calcitonin gene-related peptide (CGRP) immunohistochemistry, is very dense for the portal vein while being virtually absent from the liver parenchyma (36,37).…”

Section: Discussionmentioning

confidence: 99%

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Celiac-Superior Mesenteric Ganglionectomy, but Not Vagotomy, Suppresses the Sympathoadrenal Response to Insulin-Induced Hypoglycemia

Fujita

Donovan

2005

Diabetes

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Afferent innervation of the portal vein has been shown to be critical in hypoglycemic detection, but the neural pathway by which these afferents ascend remains unknown. To ascertain the role of vagal afferents versus spinal afferents in hypoglycemic detection, the catecholamine response to hypoglycemia was assessed in male Wistar rats undergoing hepatic vagotomy (HV), total subdiaphragmatic vagotomy (TSV), or celiac-superior mesenteric ganglionectomy (CSMG). After recovering from the surgery, the animals were exposed to a hyperinsulinemic-hypoglycemic clamp, with glucose infused peripherally via the jugular vein. In all animals, systemic hypoglycemia (2.64 ؎ 0.03 mmol/l) was induced via jugular vein insulin infusion (25 mU ⅐ kg ؊1 ⅐ min ؊1 ). No significant differences were observed among the groups with respect to arterial glucose or insulin concentration. When hypoglycemia was induced in shamoperated control animals, epinephrine was observed to rise from a basal value of 0.84 ؎ 0.10 to 25.18 ؎ 1.24 nmol/l. Neither HV nor TSV had any significant impact on the epinephrine response to hypoglycemia. In contrast, CSMG animals demonstrated a significant suppression in the epinephrine response to whole-body hypoglycemia (11.25 ؎ 1.21 vs. 22.32 ؎ 0.86 nmol/l in CSMG vs. controls; P < 0.05). The norepinephrine response for controls, 2.00 ؎ 0.22 at basal and rising to 8.95 ؎ 0.20 nmol/l in hypoglycemia, was not significantly different from that of the HV and TSV animals. As with epinephrine, the norepinephrine response to hypoglycemia was significantly suppressed in CSMG compared with control animals (4.72 ؎ 0.48 vs. 7.15 ؎ 0.76 nmol/l; P < 0.05). These findings are consistent with the idea that hypoglycemic detection at the portal vein is mediated by spinal, and not vagal, glucose-sensitive afferents. Diabetes 54:3258 -3264, 2005

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Section: Discussionmentioning

confidence: 99%

“…Visceral spinal afferents, although generally associated with nociception, are now recognized to support a variety of functions, including metabolic sensing (17). The vasculature of the gut, including the portal vein, has been shown to be richly innervated by afferents emerging from the dorsal root ganglia at T7ϪT13 (21).…”

mentioning

confidence: 99%

Celiac-Superior Mesenteric Ganglionectomy, but Not Vagotomy, Suppresses the Sympathoadrenal Response to Insulin-Induced Hypoglycemia

Fujita

Donovan

2005

Diabetes

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“…The influence of efferent output from the ventromedial hypothalamus upon glucose metabolism has been well characterized (13). Histological studies have revealed extensive innervation of the portohepatic region, with afferent fibers composing a significant portion of those neurons (14)(15)(16). Although the extent and signific a n c e (15).…”

Section: Discussionmentioning

confidence: 99%

Portal vein afferents are critical for the sympathoadrenal response to hypoglycemia.

2000

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We sought to elucidate the role of the portal vein a fferents in the sympathetic response to hypoglycemia. Laparotomy was performed on 27 male Wi s t a r rats. Portal veins were painted with either 90% phenol (denervation group [PDN]) or 0.9% saline solution (sham-operated group [SHAM]). Rats were chronically cannulated in the carotid artery (sampling), jugular vein (infusion), and portal vein (infusion). After a recovery period of 5 days, animals were exposed to a hyperinsulinemic-hypoglycemic clamp, with glucose infused either portally (POR) or peripherally (PER). In all animals, systemic hypoglycemia (2.48 ± 0 . 0 9 mmol/l) was induced via jugular vein insulin infusion (50 mU · k g -1 · min -1 ). Arterial plasma catecholamines were assessed at basal (-30 and 0 m i n ) and during sustained hypoglycemia (60, 75, 90, and 105 min). By design, portal vein glucose concentrations were significantly elevated during POR versus PER (4.4 ± 0.14 vs. 2.5 ± 0.07 mmol/l; P < 0.01, respectively) for both PDN and SHAM. There were no significant differences in arterial glucose or insulin concentration between the four experimental conditions at any point in time. When portal glycemia and systemic glycemia fell concomitantly (SHAM-PER), epinephrine increased 12-fold above basal (3.75 ± 0.34 and 44.56 ± 6.1 nmol/l; P < 0.001). However, maintenance of portal normoglycemia (SHAM-POR) caused a 50% suppression of the epinephrine response, despite cerebral hypoglycemia (22.2 ± 3.1 nmol/l, P < 0.001). Portal denervation resulted in a significant blunting of the sympathoadrenal response to whole-body hypoglycemia (PDN-PER 27.6 ± 3.8 nmol/l vs. SHAM-PER; P < 0.002). In contrast to the sham experiments, there was no further suppression in arterial epinephrine concentrations observed during PDN-POR versus PDN-PER (P = 0.8). These findings indicate that portal vein afferent innervation is critical for hypoglycemic detection and normal sympathoadrenal counterregulation. D i a b e t e s 4 9 :8-12, 2000 C atecholamines constitute the primary defense against hypoglycemia for individuals with type 1 diabetes, in which the ability to suppress insulin is absent and the capacity to secrete glucagon is diminished. The catecholamine response has been well characterized for both normal and diabetic individuals (1-4). Under normal conditions, this sympathetic response appears sufficient to compensate for the loss of other counterregulatory measures (1,2). Unfortunately, over time, the catecholamine response for individuals with type 1 diabetes diminishes relative to the fall in blood glucose (1,2). The diminished catecholamine response appears to have been further exacerbated by increasingly aggressive attempts to control blood glucose levels in type 1 diabetic patients (3,4).Although iatrogenic hypoglycemia has been invoked as a partial explanation, in general, the pathology of the diminished sympathetic response in patients with type 1 diabetes remains poorly understood. In part, this can be attributed to the lack of knowledge concerning the locus f...

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“…It is known that SP-and CGRP-immunoreactive (IR) nerve fibers have an afferent course to the spinal sensory ganglia and have sensory function in the alimentary tract and its glands [22,23]. Comparative anatomical studies concerning SP nerve fibers have been conducted in many species including human but not in porcine.…”

Section: Discussionmentioning

confidence: 99%

Alterations in porcine intrahepatic sympathetic nerves after bisphenol A administration

Thoene

Godlewski

Rytel

et al. 2018

Folia Histochem Cytobiol.

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Introduction. Bisphenol A (BPA) is used in the chemical industry for manufacturing plastics which are used as food packaging. Data indicate that BPA is released from such products and is widely present in the environment and the human body. So far, the EFSA and the US FDA have determined "safe" BPA oral exposure levels, and a large amount of data indicates that BPA is harmful even at low-doses. Our previously performed analyses concerning BPA exposure demonstrated the impact of this substance on parasympathetic and peptidergic nerve fibers present within the liver. Therefore, this study concerns BPA exposure and sympathetic intrahepatic innervation in reference to several neuropeptides which modulate neuronal responses: cocaine and amphetamine regulated transcript (CART), galanin (GAL), calcitonin gene-regulated peptide (CGRP) and substance P (SP). Materials and methods. Fifteen young swine at 8 weeks of age were used as experimental models of the juvenile human liver. The pigs were divided into 3 groups and received capsules orally with bisphenol at a dose of 0.05 mg/kg b.w./day; a dose of 0.5 mg/kg b.w./day and placebo capsules as a control. After 28 days of oral BPA intake, the animals were euthanized, perfused with 4% paraformaldehyde (PFA), and livers were collected and fixed in PFA. The cryostat sections were subjected to a routine double-labeling immunofluorescence technique. The primary antibodies were directed against dopamine beta hydroxylase (DbH), which is a marker for sympathetic nerves, and one of the investigated neuropeptides: CART, GAL, CGRP and SP, which co-localized the investigated nerves. Immunoreactive nerves were counted in the liver and the percentage presence of each neuronal combination in particular samples of each experimental group were determined and analyzed statistically. Results. The BPA oral intake at low and ten times higher dosage caused an increase of the number of sympathetic nerve fibers within the porcine liver by 48.6% and 63.7%, respectively. Moreover, BPA exposure caused an increased presence of sympathetic nerve fibers in these two experimental groups, which were co-localized with CART and GAL up to 65.9%/173.2% and 147.4%/126.3%, respectively. At the lower BPA doses of 50 μg/kg b.w./day, the percentages of SP+/DbH+ and CGRP+/DbH+ nerve fibers were similar to the control. 114Michael Thoene et al. However at a ten times higher dose, BPA caused an increased number of SP+/ DbH+ and CGRP+/ DbH+ nerve fibers in the liver, up to 46.4% and 73.5% respectively. Conclusions. BPA caused an increase in the number of sympathetic nerve fibers as well as sympathetic nerve fibers which co-localized with neuropeptides in the porcine liver. The increase in CART and GAL were exceptionally high even at low BPA doses. BPA food contamination may dysregulate liver sympathetic innervation, and thereby may change the oxygenated blood supply, alter metabolism and disrupt the activity of hepatic parenchymal cells.

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Sensory innervation of the rat portal vein and the hepatic artery

Cited by 49 publications

References 24 publications

Celiac-Superior Mesenteric Ganglionectomy, but Not Vagotomy, Suppresses the Sympathoadrenal Response to Insulin-Induced Hypoglycemia

Celiac-Superior Mesenteric Ganglionectomy, but Not Vagotomy, Suppresses the Sympathoadrenal Response to Insulin-Induced Hypoglycemia

Portal vein afferents are critical for the sympathoadrenal response to hypoglycemia.

Alterations in porcine intrahepatic sympathetic nerves after bisphenol A administration

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