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Biomedical subjects

N J Gurll

Publications and source records attributed to N J Gurll.

At least 19 recordsLinked to original sources
PubMed1995

Tc-99m MIBI scintigraphic detection of metastatic insular thyroid carcinoma.

Thallium-201 and, recently, Tc-99m MIBI have been used in conjunction with I-131 scintigraphy for follow-up of patients with well-differentiated thyroid cancer. Insular carcinoma of the thyroid is a fairly aggressive thyroid neoplasm that is believed to arise from follicular cells and usually concentrates I-131. The authors report a patient with recurrent insular thyroid carcinoma in whom bilateral adrenal and lung metastatic lesions developed 3 years after ablative I-131 therapy for cervical lymph node and skeletal metastases. Tc-99m MIBI planar and SPECT images demonstrated these new lesions better than pretherapy I-131 scintigraphy and affords an imaging technique for post-I-131 therapy follow-up that does not require withholding thyroid hormone suppression.

Adenocarcinoma, Follicular↗
PubMed1991

Insular carcinoma: a distinct thyroid carcinoma with associated iodine-131 localization.

Insular carcinoma, once considered a poorly-differentiated thyroid cancer, has been reclassified as a distinct thyroid neoplasm. Since this neoplasm is composed of follicular epithelial cells, it may concentrate radioiodide (131I) making postoperative 131I imaging for detection of metastases and radiotherapy possible. A 20-yr review of 35 cases diagnosed as anaplastic or undifferentiated thyroid carcinoma at this medical center revealed five patients with insular carcinoma. Four patients showed postoperative 131I localization and received therapeutic doses of 131I. Three of the four showed extrathyroidal 131I localization in neoplastic lesions. In one patient, the resolution of metastatic lesions by magnetic resonance and 131I imaging suggests that 131I may have an important therapeutic role in this aggressive neoplasm.

Adult↗
PubMed1989

Cytogenetic abnormalities in tumors of patients with von Hippel-Lindau disease.

Von Hippel-Lindau (VHL) disease is an autosomal dominant disorder that causes the development of benign and malignant tumors in several organ systems. Tumors causing significant morbidity include retinal angioma, cerebellar hemangioblastoma (CH), renal cell carcinoma (RCC), and pheochromocytoma (Pheo). Cytogenetic studies of tumors in VHL patients are rare. Cytogenetic findings in tumors from 12 patients with VHL disease, including four RCCs, three CHs, and five Pheos are presented. Three of the four RCC cases were abnormal. Monosomy 3 or a deletion of 3p was present in all three abnormal cases. Complete or partial trisomy of chromosome 5 was present in two cases. A deletion of 14q, trisomy 7, and a missing Y were each observed in one case. These findings indicate that a deletion of 3p may be a primary cytogenetic change in RCCs associated with VHL disease in addition to playing a role in sporadic RCC. Duplications of 5q and deletions of 14q may be important secondary changes in the progression of the malignant phenotype. No visible cytogenetic abnormalities were observed in the three CHs, or in four of the Pheos. One of the five Pheos was found to exhibit mosaic trisomy 7; its significance is unclear at the present time.

Adrenal Gland Neoplasms↗
PubMed1989

The therapeutic efficacy of opiate antagonists in hemorrhagic shock.

The endogenous opioids have been implicated as contributing factors to the cardiovascular dysfunction of shock. Opiate receptor antagonists improve cardiovascular function and long-term survival in laboratory animal models of shock. In this communication, evidence of the therapeutic efficacy of opiate antagonists in canine and primate hemorrhagic shock is presented. The animals were hemorrhaged into a reservoir to lower MAP to 45 mmHg and that pressure was maintained for 1 h at which time the reservoir was clamped and treatment initiated. The "shed blood" was returned at t = 120 min and treatment continued until t = 180 min. Opiate antagonists employed included naloxone, naltrexone and the mixed agonist/antagonist agent, nalbuphine. Both naloxone and naltrexone improved cardiac function at doses of 1 and 2 mg/kg. Animal survival was significantly enhanced in the high dose format. Nalbuphine also improved cardiovascular performance at doses from 1 to 4 mg/kg but at higher doses it depressed cardiac performance. The efficacy of the antagonists is attenuated by acidosis and hypothermia. Opiate antagonists may induce cardiac arrhythmias in combination with beta-adrenergic blocking drugs and the efficacy is reduced in animals that received high dose steroid therapy. Thus the use of opiate antagonists would be contraindicated in patients that received drugs such as propranolol or methylprednisolone. There have been no controlled clinical trials of opiate antagonists in human hemorrhagic shock; these are needed for final clarification.

Animals↗
PubMed1989

Brown tumor of bone: a potential source of false-positive thallium-201 localization.

Brown tumor of bone (osteitis fibrosa cystica) should be included in the differential diagnosis of lesions that cause false-positive thallium-201 localization in patients with primary hyperparathyroidism. We report a case of a brown tumor of the upper sternum mimicking a superior mediastinal parathyroid neoplasm in a patient with persistent hyperparathyroidism 9 years after a negative neck exploration (with subtotal thyroidectomy and thymectomy). A 201TI/99mTc pertechnetate subtraction scintigram demonstrated complete subtraction of this 201TI focus.

Bone and Bones↗
PubMed1988

Naloxone requires circulating catecholamines to attenuate the cardiovascular suppression of endotoxic shock.

The opiate antagonist naloxone (NAL) improves cardiovascular performance in canine hemorrhagic and endotoxic shock. If the release of neural and adrenal catecholamines is attenuated, NAL does not produce the expected improvement in cardiovascular function in canine hemorrhagic shock. This study tests the hypothesis that an endorphin-catecholamine interaction at the heart is responsible for a part of the cardiovascular depression of endotoxic shock. Two groups of five dogs were instrumented to measure mean arterial pressure (MAP), the first derivative of left ventricular pressure over time (LV dP/dt max), cardiac output, and heart rate (HR); they were then subjected to bilateral adrenalectomy and given chlorisondamine to produce ganglionic blockade. At t = 0 min the dogs were given Escherichia coli endotoxin at 1 mg/kg (LD80). Group I animals received NAL at 2 mg/kg + 2 mg/kg.hr iv from t = 30 to t = 60. At t = 45 these animals were treated with epinephrine (EPI) at 20 micrograms/kg.hr iv until t = 60. Group II animals got EPI from t = 30 to t = 60 and NAL from t = 45 to t = 60 at the same doses as Group I. In Group I, NAL alone had no effect on MAP, LV dP/dt max, or HR. EPI significantly increased (P less than 0.002) cardiovascular parameters with MAP increasing from 52 +/- 7 to 159 +/- 14 mm Hg. In Group II, EPI produced a significant increase in all parameters, and the addition of NAL produced a further significant increase; MAP increased from 37 +/- 3 to 126 +/- 16 mm Hg with EPI and then to 175 +/- 11 mm Hg with NAL. These data support the above hypothesis and indicate that circulating catecholamines need to be present to allow naloxone to reverse the cardiovascular depression in endotoxic shock.

Animals↗
PubMed1988

Evidence for a role of endorphins in the cardiovascular pathophysiology of primate shock.

Using the opiate receptor antagonist naloxone, we tested the hypothesis that endorphins act on opiate receptors to cause cardiovascular depression in primate shock. Mean arterial pressure (MAP), cardiac output, and left ventricular contractility (LV dP/dtmax) were measured in 34 anesthetized cynomolgus monkeys. Hemorrhagic shock was induced by bleeding into a heparinized reservoir to achieve (t = 0) and maintain MAP at 45 mm Hg. At t = 60 min, the reservoir was clamped and the animals were treated with 2 mg/kg plus 2 mg/kg.h naloxone (n = 5) or 0.9% NaCl as a control (n = 5). There were no significant differences in the cardiovascular responses to naloxone and saline when acid-base balance and core body temperature were not controlled. Pressor responses to naloxone, however, were present in proportion to arterial pH and body temperature. When these factors were controlled, naloxone (n = 6) significantly increased MAP and LV dP/dtmax by 48% and 83%, respectively, whereas saline (n = 6) had no significant effect. Blood was reinfused at t = 120 min, and survival rate at 72 h was significantly (p = .01) higher with naloxone (3/6) than saline controls (0/6). In the endotoxic shock model, cynomolgus monkeys were treated with 2 mg/kg plus 2 mg/kg.h naloxone (n = 6) or 0.9% NaCl (n = 6) when MAP reached 75 mm Hg or its nadir 60 to 90 min after Escherichia coli endotoxin, 5 mg/kg iv. Naloxone significantly increased MAP and LV dP/dtmax by 24% and 22%, respectively, whereas saline had no effect. Survival rate at 48 h was significantly (p = .01) higher with naloxone (6/6) than saline (1/6). Plasma beta-endorphin and beta-lipotropin concentrations rose three to five-fold in both shock models and were not affected by treatment. We conclude that endorphins are activated in primate shock and act on opiate receptors to contribute to the cardiovascular depression found with hemorrhage and endotoxemia.

Acidosis↗
PubMed1987

Naloxone pretreatment prevents the bloody diarrhea of canine endotoxic shock.

We examined the importance of timing with endorphin involvement in shock by giving the opiate receptor antagonist naloxone as a pretreatment in canine endotoxic shock. Dogs anesthetized with pentobarbital (30 mg/kg iv) were given Escherichia coli endotoxin at LD80 doses iv. Naloxone (2 mg/kg plus 2 mg/kg/hr iv, N = 10) started 15 min before endotoxin attenuated the fall in mean arterial pressure, cardiac index, and the first derivative of left ventricular pressure due to endotoxin in comparison with control animals given 0.9% NaCl (N = 10). Naloxone attenuated the endotoxin-induced decrease in superior mesenteric arterial blood flow and the increases in portal venous pressure and pulmonary arterial pressures. Moreover, naloxone pretreatment prevented the characteristic bloody diarrhea and reduced mortality. Our findings implicate endorphins acting on opiate receptors as important mediators of endotoxin-induced cardiovascular failure and bloody diarrhea in canine endotoxemia. These are early manifestations and dictate expeditious use of naloxone in endotoxic shock.

Animals↗
PubMed1987

Thyrotropin releasing hormone: effects in monkeys and dogs subjected to experimental circulatory shock.

We tested the hypothesis that thyrotropin releasing hormone (TRH) would improve cardiovascular function and survival in circulatory shock by opposing the adverse effects of endogenous opioids and other pathophysiologic mediators. Cynomolgus monkeys and mongrel dogs were anesthetized and catheterized to measure mean arterial pressure (MAP) and left ventricular contractility (LV dp/dtmax). Hemorrhagic shock was induced by bleeding into a reservoir to achieve and maintain MAP at 45 mm Hg for one hour. Endotoxic shock was produced by the iv injection of an LD80 dose of Escherichia coli lipopolysaccharide endotoxin (3 mg/kg in dogs and 5 mg/kg in monkeys). Animals were treated iv with either TRH (2 mg/kg plus 2 mg/kg X h) or equivolume saline. TRH significantly increased MAP and LV dp/dtmax in primate hemorrhagic and endotoxic shock. In primate hemorrhagic shock, TRH significantly (p = .02) improved survival (alive/total = 4/5 vs. 0/5). However, TRH had no effect on survival in endotoxemic primates. In contrast, TRH treatment in dogs produced only a transient hemodynamic response after endotoxemia and no significant hemodynamic effect after acute hemorrhage (even at twice the TRH dose). TRH did not affect survival in either dog model of circulatory shock. Based on extensive evidence with the opiate receptor antagonist naloxone in other studies, endogenous opioids play a role in the cardiovascular depression in primate and canine circulatory shock. From these studies with TRH, we conclude that TRH is relatively ineffective in canine circulatory shock, and physiologic antagonism of the adverse effects of opioids and other cardiodepressant substances by TRH administration may prove to be a useful alternative treatment of primate hemorrhagic shock.

Animals↗
PubMed1987

Central nervous system is involved in the cardiovascular responses to naloxone in canine endotoxic but not hemorrhagic shock.

We used naloxone to investigate the role of central nervous system opiate receptors in the cardiovascular depression of canine hemorrhagic and endotoxic shock. Shock was induced by bleeding dogs into a reservoir to achieve and maintain a mean arterial pressure (MAP) of 45 mmHg for 30 min; at 30 min the reservoir was clamped and the animals were treated with intracerebroventricular (ICV) perfusion of naloxone 0.1 mg/kg (n = 5) or artificial CSF (n = 5) for 30 min. Endotoxemic shock was induced by the iv injection of E. coli endotoxin 1 mg/kg; 15 min later the animals were given naloxone 0.1 mg/kg (n = 5) or artificial CSF (n = 5) ICV for 30 min. ICV naloxone significantly increased MAP, cardiac output (CO), and left ventricular performance (LV dP/dt max) compared to artificial CSF in canine endotoxic shock but not hemorrhagic shock. Naloxone 0.1 mg/kg (n = 5) given into the cisterna magna failed to significantly improve MAP, CO, or LV dP/dt max in dogs subjected to reservoir hemorrhagic shock for 60 min compared to artificial CSF (n = 5). These results are compatible with opiate-receptor-mediated central cardiovascular depression in endotoxic shock and peripheral cardiovascular depression in hemorrhagic shock. Accordingly, the sites of action of naloxone are mainly central in endotoxic shock and peripheral in hemorrhagic shock.

Animals↗
PubMed1985

Intracoronary naloxone in hemorrhagic shock: dose-dependent stereospecific effects.

Treatment with naloxone improves cardiovascular function and survival in a variety of shock models, and numerous sites and mechanisms for its action have been proposed. Data presented in this article support the hypothesis that in hemorrhagic shock naloxone exerts its beneficial hemodynamic effects by acting primarily at cardiac opiate receptors. Naloxone or its stereoisomer (d-naloxone) were administered intravenously (iv) and directly into the coronary circulation (ic) in dogs anesthetized with pentobarbital sodium and subjected to hemorrhagic shock. Treatment with naloxone (2.0 mg/kg iv or 0.2 mg/kg ic) resulted in significant improvements in arterial pressure, myocardial contractility, and cardiac output. Treatment with saline or naloxone (0.2 mg/kg iv) were without beneficial effect. The hemodynamic responses to naloxone administered into the coronary circulation were dose dependent and stereospecific. These data support the hypothesis that naloxone exerts its salubrious effects in canine hemorrhagic shock by acting at cardiac opiate receptors.

Animals↗
PubMed1985

Effects of naloxone on regional blood flow distribution in canine hemorrhagic shock.

The opiate antagonist naloxone increases arterial pressure, maximal left ventricular dp/dt and cardiac output when administered to dogs subjected to hemorrhagic shock. The purpose of this study was to investigate regional blood flow changes associated with naloxone treatment in anesthetized hypovolemic and normovolemic dogs. Hypovolemic dogs (n = 10) were bled over 30 min (t = -30 to t = 0) to a pressure of 45 mm Hg which was maintained for 1 hr. At t = 60, five dogs received naloxone (2 mg/kg + 2 mg/kg X hr), and five received an equal volume of saline. Regional blood flows were determined at t = -30, 45, and 90 min using 15-micron microspheres. Normovolemic dogs (n = 10) were subjected to the same protocol except they were not bled. During hypovolemia, naloxone produced significant increases in myocardial, intestinal, hepatic, and adrenal blood flows whereas saline treatment did not. No significant changes in skin, muscle, fat, pancreatic, renal, or brain flows were detected. The increases in blood flow were not associated with significant changes in vascular resistance. Naloxone had no significant effects on any hemodynamic parameter during normovolemia. The beneficial effects of naloxone in hemorrhagic shock include increased blood flow to vital organs due to increased perfusion pressure which is secondary to improved cardiac performance.

Adrenocorticotropic Hormone↗
PubMed1985

Role of the autonomic nervous system in mediating the response to naloxone in canine hemorrhagic shock.

When the opiate antagonist naloxone is administered to anesthetized dogs subjected to hemorrhagic shock, there is a transient decrease in heart rate and sustained increases in mean arterial pressure, maximum left ventricular dp/dt, and cardiac output. Surgical cardiac denervation and pharmacologic blockade of autonomic receptors were employed to investigate the mechanisms of these two responses. The transient bradycardia was prevented by beta-adrenergic receptor blockade or cardiac denervation. The sustained response was unaffected by cardiac denervation, attenuated by either alpha- or beta-adrenergic receptor blockade, and potentiated by cholinergic receptor blockade. Naloxone had no significant effect on plasma catecholamines. The sustained hemodynamic response to naloxone appears to have two components: there is an increase in parasympathetic stimulation which modestly attenuates the adrenergic component of the response. The adrenergic stimulation of the heart after naloxone administration appears to result from potentiation of existing adrenergic stimulation and not from increased sympathoadrenal discharge. These sustained sympathetic and parasympathetic responses appear to result from the action of naloxone at a myocardial site.

Adrenergic alpha-Antagonists↗
PubMed1985

Naloxone potentiates the cardiovascular effects of catecholamines in canine hemorrhagic shock.

Endogenous opioids are released during stress and appear to contribute to the cardiovascular suppression seen in shock. When the opiate receptor antagonist naloxone is administered intravenously to anesthetized dogs subjected to hemorrhage, mean arterial pressure, maximal left ventricular dp/dt, and cardiac output increase. This study tests the hypothesis that naloxone acts by potentiating the effects of neurally and adrenally released catecholamines. If this hypothesis is correct, then blockade of endogenous catecholamine release should attenuate the response to naloxone, and administration of exogenous adrenergic agonists prior to naloxone treatment should restore the response. Catecholamine release was attenuated by a combination of surgical adrenal denervation and pharmacological ganglionic blockade. Adrenal denervation or chlorisondamine alone attenuated and, in combination, blocked the response to naloxone in hemorrhaged dogs. Infusion of alpha- and beta-adrenergic agonists at a constant rate prior to treatment restored the response to naloxone. Naloxone appears to improve cardiovascular function in hemorrhagic shock by potentiating the effect of released catecholamines and not by increasing sympathoadrenal discharge.

Adrenal Glands↗
PubMed1984

Dose-dependent effects of nalbuphine in canine hemorrhagic shock.

We noted the effects of the mixed opiate agonist/antagonist nalbuphine on cardiovascular function and survival in canine hemorrhagic shock. Anesthetized adult mongrel dogs were bled to a mean arterial pressure (MAP) of 45 mmHg, which was maintained with a reservoir for 1 hr before the reservoir was clamped and the animals treated with 0.9% NaCl as a control or nalbuphine at various doses. Shed blood was reinfused 1 hr after the reservoir was clamped, and survival was followed for three days. Nalbuphine at 1-4 mg/kg bolus plus 1-4 mg/kg hr infusion intravenously for 3.5 hr increased MAP, cardiac output, left ventricular contractility, heart rate, and survival. At doses above 8 mg/kg plus 8 mg/kg hr nalbuphine had deleterious effects on these parameters and survival. These effects were dose-dependent and support the hypothesis that endorphins acting on opiate receptors contribute to the cardiovascular pathophysiology of canine hemorrhagic shock. Nalbuphine, furthermore, may be a logical alternative to naloxone, since its analgesic properties obviate the theoretical objection of enhanced pain perception with the use of naloxone in shock.

Animals↗