Surgical treatment of carotid body tumors

Karotidno tjelešce kemoreceptorski je organ smješten u adventiciji karotidne bifurkacije, odgovoran za održavanje homeostaze pO2, pCO2 i pH. Tumori karotidnog tjelešca pripadaju skupini rijetkih tumora i mogu se podijeliti na tri tipa; sporadični, obiteljski i hiperplastični. Najčešće se očituju kao bezbolne tvorbe na lateralnoj strani vrata, koje u uznapredovaloj fazi mogu uzrokovati neurološke simptome i simptome lokalne kompresije. Temelj dijagnostike je ultrazvuk, a CTA, MRA i DSA koriste se u prijeoperacijskoj obradi. Shamblinova klasifikacije dijeli tumore u tri skupine na temelju odnosa tumora s karotidnim arterijama. Zlatni standard liječenja je subadventicijska resekcija; radioterapija i opservacija alternativne su opcije. Kirurška resekcija danas je praćena niskim mortalitetom, ali još uvijek se veže uz značajan rizik neurovaskularne ozljede. Uspješnost operacije može se potencirati primjenom prijeoperacijske devaskularizacije putem embolizacije, ugradnje stenta ili prijeoperacijske radioterapije.The carotid body is a chemoreceptor organ found in adventitia of carotid bifurcation responsible for maintaining homeostatis of pO2, pCO2 i pH. Carotid body tumors belong to the group of rare tumors and can be divided into three types: sporadic, familial and hyperplastic. They most often present as painless mass on the lateral side of the neck and can, in advanced stages, cause neurological symptoms and symptoms of local compression. The base for diagnosis is ultrasound,while CT, MR and angiography are used in preoperative assesment. Shamblin's classification divides these tumors into three groups based on the relationship of the tumor to the carotid arteries. The gold standard of treatment is subadventricular resection; radiotherapy and observation are alternative options. Surgical resection today is accompanied with low mortality, but is still associated with a significant risk of neurovascular injury. The success of the operation can be enhanced by preoperative devascularization, stent implantation or preoperative radiotherapy

Surgical treatment of carotid body tumors

Karotidno tjelešce kemoreceptorski je organ smješten u adventiciji karotidne bifurkacije, odgovoran za održavanje homeostaze pO2, pCO2 i pH. Tumori karotidnog tjelešca pripadaju skupini rijetkih tumora i mogu se podijeliti na tri tipa; sporadični, obiteljski i hiperplastični. Najčešće se očituju kao bezbolne tvorbe na lateralnoj strani vrata, koje u uznapredovaloj fazi mogu uzrokovati neurološke simptome i simptome lokalne kompresije. Temelj dijagnostike je ultrazvuk, a CTA, MRA i DSA koriste se u prijeoperacijskoj obradi. Shamblinova klasifikacije dijeli tumore u tri skupine na temelju odnosa tumora s karotidnim arterijama. Zlatni standard liječenja je subadventicijska resekcija; radioterapija i opservacija alternativne su opcije. Kirurška resekcija danas je praćena niskim mortalitetom, ali još uvijek se veže uz značajan rizik neurovaskularne ozljede. Uspješnost operacije može se potencirati primjenom prijeoperacijske devaskularizacije putem embolizacije, ugradnje stenta ili prijeoperacijske radioterapije.The carotid body is a chemoreceptor organ found in adventitia of carotid bifurcation responsible for maintaining homeostatis of pO2, pCO2 i pH. Carotid body tumors belong to the group of rare tumors and can be divided into three types: sporadic, familial and hyperplastic. They most often present as painless mass on the lateral side of the neck and can, in advanced stages, cause neurological symptoms and symptoms of local compression. The base for diagnosis is ultrasound,while CT, MR and angiography are used in preoperative assesment. Shamblin's classification divides these tumors into three groups based on the relationship of the tumor to the carotid arteries. The gold standard of treatment is subadventricular resection; radiotherapy and observation are alternative options. Surgical resection today is accompanied with low mortality, but is still associated with a significant risk of neurovascular injury. The success of the operation can be enhanced by preoperative devascularization, stent implantation or preoperative radiotherapy

Surgical treatment of carotid body tumors

Karotidno tjelešce kemoreceptorski je organ smješten u adventiciji karotidne bifurkacije, odgovoran za održavanje homeostaze pO2, pCO2 i pH. Tumori karotidnog tjelešca pripadaju skupini rijetkih tumora i mogu se podijeliti na tri tipa; sporadični, obiteljski i hiperplastični. Najčešće se očituju kao bezbolne tvorbe na lateralnoj strani vrata, koje u uznapredovaloj fazi mogu uzrokovati neurološke simptome i simptome lokalne kompresije. Temelj dijagnostike je ultrazvuk, a CTA, MRA i DSA koriste se u prijeoperacijskoj obradi. Shamblinova klasifikacije dijeli tumore u tri skupine na temelju odnosa tumora s karotidnim arterijama. Zlatni standard liječenja je subadventicijska resekcija; radioterapija i opservacija alternativne su opcije. Kirurška resekcija danas je praćena niskim mortalitetom, ali još uvijek se veže uz značajan rizik neurovaskularne ozljede. Uspješnost operacije može se potencirati primjenom prijeoperacijske devaskularizacije putem embolizacije, ugradnje stenta ili prijeoperacijske radioterapije.The carotid body is a chemoreceptor organ found in adventitia of carotid bifurcation responsible for maintaining homeostatis of pO2, pCO2 i pH. Carotid body tumors belong to the group of rare tumors and can be divided into three types: sporadic, familial and hyperplastic. They most often present as painless mass on the lateral side of the neck and can, in advanced stages, cause neurological symptoms and symptoms of local compression. The base for diagnosis is ultrasound,while CT, MR and angiography are used in preoperative assesment. Shamblin's classification divides these tumors into three groups based on the relationship of the tumor to the carotid arteries. The gold standard of treatment is subadventricular resection; radiotherapy and observation are alternative options. Surgical resection today is accompanied with low mortality, but is still associated with a significant risk of neurovascular injury. The success of the operation can be enhanced by preoperative devascularization, stent implantation or preoperative radiotherapy

Novel Therapeutic Effects in Rat Spinal Cord Injuries: Recovery of the Definitive and Early Spinal Cord Injury by the Administration of Pentadecapeptide BPC 157 Therapy

Recently, marked therapeutic effects pertaining to the recovery of injured rat spinal cords (1 min compression injury of the sacrocaudal spinal cord (S2-Co1) resulting in tail paralysis) appeared after a single intraperitoneal administration of the stable gastric pentadecapeptide BPC 157 at 10 min post-injury. Besides the demonstrated rapid and sustained recovery (1 year), we showed the particular points of the immediate effect of the BPC 157 therapy that began rapidly after its administration, (i) soon after injury (10 min), or (ii) later (4 days), in the rats with a definitive spinal cord injury. Specifically, in counteracting spinal cord hematoma and swelling, (i) in rats that had undergone acute spinal cord injury, followed by intraperitoneal BPC 157 application at 10 min, we focused on the first 10–30 min post-injury period (assessment of gross, microscopic, and gene expression changes). Taking day 4 post-injury as the definitive injury, (ii) we focused on the immediate effects after the BPC 157 intragastric application over 20 min of the post-therapy period. Comparable long-time recovery was noted in treated rats which had definitive tail paralysis: (iii) the therapy was continuously given per orally in drinking water, beginning at day 4 after injury and lasting one month after injury. BPC 157 rats presented only discrete edema and minimal hemorrhage and increased Nos1, Nos2, and Nos3 values (30 min post-injury, (i)) or only mild hemorrhage, and only discrete vacuolation of tissue (day 4, (ii)). In the day 4–30 post-injury study (iii), BPC 157 rats rapidly presented tail function recovery, and no demyelination process (Luxol fast blue staining)

Therapy Effect of the Stable Gastric Pentadecapeptide BPC 157 on Acute Pancreatitis as Vascular Failure-Induced Severe Peripheral and Central Syndrome in Rats

We revealed the therapy effect of the stable gastric pentadecapeptide BPC 157 (10 μg/kg, 10 ng/kg ig or po) with specific activation of the collateral rescuing pathways, the azygos vein, on bile duct ligation in particular, and acute pancreatitis as local disturbances (i.e., improved gross and microscopy presentation, decreased amylase level). Additionally, we revealed the therapy’s effect on the acute pancreatitis as vascular failure and multiorgan failure, both peripherally and centrally following “occlusion-like” syndrome, major intoxication (alcohol, lithium), maintained severe intra-abdominal hypertension, and myocardial infarction, or occlusion syndrome, and major vessel occlusion. The application-sacrifice periods were ligation times of 0–30 min, 0–5 h, 0–24 h (cured periods, early regimen) and 4.30 h–5 h, 5 h–24 h (cured periods, delayed regimen). Otherwise, bile duct-ligated rats commonly presented intracranial (superior sagittal sinus), portal and caval hypertension and aortal hypotension, gross brain swelling, hemorrhage and lesions, heart dysfunction, lung lesions, liver and kidney failure, gastrointestinal lesions, and severe arterial and venous thrombosis, peripherally and centrally. Unless antagonized with the key effect of BPC 157 regimens, reversal of the inferior caval and superior mesenteric vein congestion and reversal of the failed azygos vein activated azygos vein-recruited direct delivery to rescue the inferior-superior caval vein pathway; these were all antecedent to acute pancreatitis major lesions (i.e., acinar, fat necrosis, hemorrhage). These lesions appeared in the later period, but were markedly attenuated/eliminated (i.e., hemorrhage) in BPC 157-treated rats. To summarize, while the innate vicious cycle may be peripheral (bile duct ligation), or central (rapidly developed brain disturbances), or peripheral and central, BPC 157 resolved acute pancreatitis and its adjacent syndrome

Antiarrhythmic Sotalol, Occlusion/Occlusion-like Syndrome in Rats, and Stable Gastric Pentadecapeptide BPC 157 Therapy

We focused on the first demonstration that antiarrhythmics, particularly class II and class III antiarrhythmic and beta-blocker sotalol can induce severe occlusion/occlusion-like syndrome in rats. In this syndrome, as in similar syndromes with permanent occlusion of major vessels, peripheral and central, and other similar noxious procedures that severely disable endothelium function, the stable gastric pentadecapeptide BPC 157-collateral pathways activation, was a resolving therapy. After a high dose of sotalol (80 mg/kg intragastrically) in 180 min study, there were cause-consequence lesions in the brain (swelling, intracerebral hemorrhage), congestion in the heart, lung, liver, kidney, and gastrointestinal tract, severe bradycardia, and intracranial (superior sagittal sinus), portal and caval hypertension, and aortal hypotension, and widespread thrombosis, peripherally and centrally. Major vessels failed (congested inferior caval and superior mesenteric vein, collapsed azygos vein). BPC 157 therapy (10 µg, 10 ng/kg given intragastrically at 5 min or 90 min sotalol-time) effectively counteracted sotalol-occlusion/occlusion-like syndrome. In particular, eliminated were heart dilatation, and myocardial congestion affecting coronary veins and arteries, as well as myocardial vessels; eliminated were portal and caval hypertension, lung parenchyma congestion, venous and arterial thrombosis, attenuated aortal hypotension, and centrally, attenuated intracranial (superior sagittal sinus) hypertension, brain lesions and pronounced intracerebral hemorrhage. Further, BPC 157 eliminated and/or markedly attenuated liver, kidney, and gastrointestinal tract congestion and major veins congestion. Therefore, azygos vein activation and direct blood delivery were essential for particular BPC 157 effects. Thus, preventing such and similar events, and responding adequately when that event is at risk, strongly advocates for further BPC 157 therapy