Catecholamine release during and after cross clamping of descending thoracic aorta

Normann, Nils A.; Taylor, Addison A.; Crawford, E. Stanley; DeBakey, Michael E.; Saleh, S A

doi:10.1016/0022-4804(83)90047-1

Cited by 35 publications

(23 citation statements)

References 14 publications

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“…On the other hand, it is known that clamping of the thoracic aorta and the subsequent distal ischaemia results in sympathoadrenal activation and an increase in catecholamine levels (Normann et al 1983). Spinal cord impact injury leads to arterial hypertension (Griffiths et al 1978).…”

Section: Discussionmentioning

confidence: 99%

Post anaesthetic myelopathy in the horse: a case report

Patschova¹,

Kabeš²,

Ludvíková³

2014

Vet. Med. - Czech

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ABSTRACT:The first case of post anaesthetic myelopathy in a horse is described. A two year old 530 kg Shire stallion underwent surgical removal of a granuloma in the ventral sternal region under general inhalation anaesthesia in dorsal recumbency. Total duration of the operation was 85 min. The anaesthesia was uneventful except for profuse sweating and arterial hypertension observed during the whole period. During recovery the horse was not able to stand, and flaccid paralysis of hind limbs, absence of reaction to an induced pain stimulus on the hind limbs and no patellar or anal reflex was recorded; in addition, tail tonus was weak. Panniculus reflex was absent distally from the 17 th intercostal space. Head, neck and front limb movement was not affected. The horse did not respond to treatment by intravenous administration of dexamethasone, hypertonic or isotonic saline. The status deteriorated and the horse was euthanised 4 h after the end of anaesthesia. The main pathological findings were haemorrhage, oedema and malacia of L5-L6 spinal cord segments and cauda equina. Histological examination of the spinal cord revealed haemorrhage and areas of necrosis predominantly in the grey matter of L5 and L6 segments. Impairment of spinal cord perfusion due to haemodynamic changes associated with dorsal recumbency and general anaesthesia is presumed. Predisposition factors could include young age, dorsal recumbency and high weight.

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Section: Discussionmentioning

confidence: 99%

Post anaesthetic myelopathy in the horse: a case report

Patschova¹,

Kabeš²,

Ludvíková³

2014

Vet. Med. - Czech

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“…5 However, both neurogenic spinal cord excitation and a direct effect of underperfusion on the adrenal gland may be involved. 7 In conclusion, in the present study, hormone assays (AVP, PRA, epinephrine, and norepinephrine) carried out on blood collected from conscious rats at 15 and 45 minutes of AoC provided results that support a role for PRA in the early stage and a combined role for both PRA and AVP in the maintenance (45 minutes) of proximal hypertension. In addition, the results rule out a significant role for catecholamines in the onset (up to 45 minutes) of hypertension.…”

Section: Catecholamine Responsesmentioning

confidence: 72%

“…One can hypothesize from these data that lengthening of the duration of the experimental proto-col over 45 minutes may substantially enhance plasma epinephrine levels. In fact, anesthetized dogs 6 and patients 7 exhibited a marked increase in epinephrine secretion rate when submitted to cross-clamping of the aorta. The mechanisms by which the lower pressure distal to the coarctation affects adrenal medullary function remain unclear.…”

Section: Catecholamine Responsesmentioning

confidence: 99%

“…Because norepinephrine is not released from the adrenal medulla in appreciable amounts, plasma norepinephrine concentration mostly reflects release from peripheral nerve endings. 7 In fact, rodents have approximately 10% of norepinephrine released from the adrenal medulla at rest versus 90% of epinephrine, whereas this ratio in humans and dogs is 20% of norepinephrine versus 80% of epinephrine. 22 It is well known that a number of factors determine the concentration of plasma norepinephrine.…”

Section: Catecholamine Responsesmentioning

confidence: 99%

“…5 - 7 We have recently evaluated the role of arginine vasopressin (AVP) in the acute hypertensive response to aortic constriction. 4 In conscious rats the expected prompt rise in aortic proximal pressure was observed even in the presence of an AVP V, vascular receptor antagonist; however, the initial increase in proximal pressure progressively declined.…”

Section: Introductionmentioning

confidence: 99%

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Physiopathogenesis of acute aortic coarctation hypertension in conscious rats.

et al. 1994

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We investigated the role of vasopressin, angiotensin II, and catecholamines in the onset of acute (45-minute) aortic coarctation hypertension in conscious rats. Partial aortic constriction was performed by means of a pneumatic cuff placed around the abdominal aorta above the renal arteries for 15 or 45 minutes. A sham-operated group was used as control. Mean carotid pressure before aortic constriction did not differ between rat groups. Aortic constriction produced a similar increase of mean carotid pressure during 15 minutes (36±3 to 37 ±3 mm Hg above basal levels) and 45 minutes (37 ±2 to 39±3 mm Hg). Plasma vasopressin concentration after 15 minutes of coarctation (4.4 ±0.5 pg/mL) did not differ from that observed in control rats (3.0±0.8 pg/mL), whereas after 45 minutes, it was significantly higher (14.3±3.3 pg/mL). Plasma renin activity increased significantly after coarctation (21.7±4.1 and 29.9±2.9 ng angiotensin I/mL per hour, at 15 and 45 minutes, respectively) when compared with control rats (3.9±0.5 ng angiotensin I/mL per hour). After coarctation, plasma norepinephrine concentration was consistently reduced, whereas plasma epinephrine concentration did not differ from control rats. In conclusion, these data provide evidence for an effective vasopressor role for vasopressin in the genesis of acute (45-minute) aortic coarctation hypertension in conscious rats. In addition, although the results confirm that the renin-angiotensin system participates earlier in the onset of coarctation hypertension, they rule out a significant vasopressor role for catecholamines in the early development of hypertension. 15 It is well documented that clamping of the aorta above the renal arteries elicits a prompt overactivity of the reninangiotensin system, with angiotensin II (Ang II) playing a significant role as a pressor agent. 13 -46 Moreover, clamping of the aorta has also been associated with an increase of catecholamine concentration in the systemic circulation.5 - 7 We have recently evaluated the role of arginine vasopressin (AVP) in the acute hypertensive response to aortic constriction. 4 In conscious rats the expected prompt rise in aortic proximal pressure was observed even in the presence of an AVP V, vascular receptor antagonist; however, the initial increase in proximal pressure progressively declined. This pharmacologic evidence based on the use of the V! antagonist suggests a role for AVP in the sustained rise of pressure with AoC hypertension.It was clear from these studies that the rise of arterial pressure after AoC was related to a complex interplay of neural and hormonal events. The present study was designed to more directly evaluate the contributions of these various neurohumoral mechanisms in the hypertension observed with acute (45-minute) AoC hypertension in conscious rats by determining corresponding changes of plasma renin activity (PRA), epinephrine, norepinephrine, and AVP. MethodsExperiments were performed on male Wistar rats (260 to 320 g). On the day before the experiment, the ra...

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Angiotensin and Adrenoceptors in the Hemodynamic Response to Aortic Cross-clamping

Hong

Gelman²,

Henderson³

1992

Arch Surg

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This study was designed to test the hypothesis that activation of adrenoceptors and/or the renin-angiotensin system plays an important role in the overall hemodynamic response to aortic cross-clamping. The experiments were performed on anesthetized rats pretreated with either saline (control group), an angiotensin-converting enzyme inhibitor (enalapril maleate, 2 mg/kg), an alpha 1-adrenergic antagonist (prazosin hydrochloride, 0.5 mg/kg), a beta-adrenergic antagonist (propranolol hydrochloride, 5 mg/kg), or an alpha 2-adrenergic antagonist (atipamezole, 5 mg/kg). Cross-clamping of the thoracic aorta was associated with an expected increase in mean arterial pressure and systemic vascular resistance in all animals. During the period of cross-clamping, cardiac output gradually decreased in all groups. Animals pretreated with the alpha 1-adrenergic antagonist or the angiotensin-converting enzyme inhibitor developed hypertension of a lesser degree than the control animals, while rats pretreated with the beta-adrenergic or alpha 2-adrenergic antagonist demonstrated a greater arterial hypertension than the control animals. The possible mechanisms underlying the observed differences are discussed. In conclusion, the present study confirms the posed hypothesis that the reninangiotensin and sympathetic nervous systems play an important role in hemodynamic response to cross-clamping of the thoracic aorta.

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Catecholamine release during and after cross clamping of descending thoracic aorta

Cited by 35 publications

References 14 publications

Post anaesthetic myelopathy in the horse: a case report

Post anaesthetic myelopathy in the horse: a case report

Physiopathogenesis of acute aortic coarctation hypertension in conscious rats.

Angiotensin and Adrenoceptors in the Hemodynamic Response to Aortic Cross-clamping

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