Research Article: New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study1

Date Published: March 18, 2019

Publisher: Sociedade Brasileira para o Desenvolvimento da Pesquisa em
Cirurgia

Author(s): Celaleddin Soyalp, Mehmet Nuri Kocak, Ali Ahiskalioglu, Mehmet Aksoy, Canan Atalay, Mehmet Dumlu Aydin, Murteza Cakir, Cagatay Calikoglu, Sevilay Ozmen.

http://doi.org/10.1590/s0102-865020190030000003

Abstract

To evaluate whether there is a relationship between renal artery vasospasm
related low glomerular density or degeneration and neurogenic lung edema
(NLE) following subarachnoid hemorrhage.

This study was conducted on 26 rabbits. A control group was formed of five
animals, a SHAM group of 5 to which saline and a study group (n=16) injected
with homologous blood into the sylvian cisterna. Numbers of degenerated
axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE
scores were recorded.

Important vagal degeneration, severe renal artery vasospasm, intrarenal
hemorrhage and glomerular atrophy observed in high score NLE detected
animals. The mean degenerated axon density of vagal nerves
(n/mm2), atrophic glomerulus density (n/mm3) and NLE
scores of control, SHAM and study groups were estimated as 2.40±1.82,
2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61,
34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic
glomerulus and NLE scores are higher in study group than other groups and
the differences are statistically meaningful (p<0.001). Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.

Partial Text

Neurogenic lung edema (NLE) can be originated from vagosympathetic imbalance1 following SAH. Vagal insufficiency and hypo-functioned hilar parasympathetic
ganglia may be a causative role on the pathogenesis of NLE2. Vagal ischemia and cervical spinal network degenerations trigger
respiratory disturbances because vagal ischemia also cause NLE by destroying heart
functions. Cerebral fat embolism induced by SAH3 could cause worsened prognosis of NLE because NLE has an important roles on
systemic chylomicron embolism. SAH induced vagal lesions cause acute kidney
injury4. SAH is prevalent causes of morbidity and mortality among dialysis patients.
And even, chronic kidney disease is associated with higher stroke and SAH
incidence5. Sodium retention related fulminant nephrotic edema arising from sympathetic
over activity may aggravate NLE. Vagal micro-ganglia and plexus insufficiency around
renal tissue6 or increased sympathetic outflow cause renovascular hypertension7. Because the vagal stimulation prevents renal inflammation and renovascular
pathologies. Interruption of vagal impulses inhibit hyperactive sympathetic
receptors of kidneys8 and renal sympathetic activity increase in vagotomised rats9. Although renal vasospasm is a dangerous complication of subarachnoid
hemorrhage, nobody mentioned vagal insufficiency based neurogenic lung edema (NLE).
The aim of this study was to elucidate whether there is a relationship between vagal
ischemia induced renal artery vasospasm triggered glomerular degeneration and NLE
following subarachnoid hemorrhage.

Animal husbandry and the study design followed the guidelines of the National
Institutes of Health. The study plan was approved by the Ethic Committee of Ataturk
University. All experimental protocols were conducted Pharmacology Laboratory,
Ataturk University, School of Medicine, Erzurum.

Two of 15 rabbits died within the second week, likely due to cardiorespiratory
irregularities and new animals were restudied. Four animals in the study group died.
In control group, the heart rate was 252±31 beats/min, the respiration rate was 24±4
breaths/min and the arterial oxygen saturation was 96±4%. Early phase of SAH, the
heart rate decreased to 156±12 beats/min, the breathing rate was 13±3 breaths/min,
and the oxygen saturation was 83±10%. Late phase of SAH, the pulse rate increased to
349±31 beats/min, while the respiration rate increased to 41±11 breaths/min with
severe tachypnea and apneic variabilities. ST depression, ventricular extrasystols,
bigeminal pulses, QRS separation, and fibrillations were observed in animals with
SAH. Finally, decreased respiration amplitude, shortening of inspiration with
prolonged expiration time, apnea-tachypnea attack, diaphragmatic breath and
respiratory arrest observed in dead animals. Massive neurogenic lung edema detected
in important glomerulus degeneration developed animals.

Vagal complex degeneration based glomerular atrophy have important roles on NLE
following SAH.

 

Source:

http://doi.org/10.1590/s0102-865020190030000003

 

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