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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the past decades insulin has been given in relatively high doses when treating diabetic coma. Recently low-dose insulin treatment has been proposed by several groups. In the reported investigation insulin was initially given in moderate to high doses (12-200 U/h) with a steady reduction in dose during the course of treatment. Insulin infusion was regulated either manually with an adjustable infusion pump (7 patients) or automatically with an artificial endocrine pancreas (glucose-controlled insulin infusion system; 11 patients). Thus 18 patients with decompensated diabetes mellitus (coma or precoma) were treated. In 14 patients with ketoacidotic decompensation laboratory data on hospital admission were: blood glucose 7.35 +/- 0.61 g/l, serum potassium 4.7 +/- 0.4 mmol/l, pH 7.1 +/- 0.04, base excess - 19,7 +/- 2.2 mmol/l (x +/- SEM). The other patients had hyperglycaemic or hyperosmolar non-ketotic decompensation. In all patients controlled reduction of blood glucose levels was achieved within 2.3 to 18 hours. The amounts of insulin infused during this ranged from 17 to 320 units, but in one instance was 1950 units. There were no complications.
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PMID:[Insulin treatment of decompensated diabetes mellitus with a new artificial endocrine pancreas (author's transl)]. 33 2

Utilizing a specific and sensitive radioimmunoassay, palsma and urine tyramine were measured in 14 consecutive patients with liver biopsy-proven Reye's syndrome. Plasma tyrosine was measured in 11 of these patients. The results revealed significant (P less than .003) elevation in plasma (3.4 +/- .52 ng/ml) (mean +/- SEM) and urine (1.00 +/- .26 mg/24 hr) tyramine as well as plasma tyrosine (204 +/- 52.5 mumole/liter) at the onset of the disease when compared to the levels of tyramine and tyrosine in a group of hospitalized patients without hepatic disorders. Furthermore, there was a positive correlation between plasma tyramine and days in coma (r = .86; P less than .001), and between plasma tyramine and tyrosine (r = 0.80; P less than .001). These data suggest that there is s substantial disturbance of tyrosine metabolism in Reye's syndrome and that the accumulation of this amino acid and its metabolite, tyramine, may contribute to the encephalopathy of this disease.
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PMID:Evidence for hypertyraminemia in Reye's syndrome. 45 May 66

An experimental model of clinical liver failure, using total devascularization of the liver is described in the pit. The survival time was 1495 +/- 75 (SEM) minutes. Clinically the pigs showed a uniform course. They became lethargic after eight to ten hours and following a period of increasing drowsiness they became comatose. The immediate cause of death was cardio-vasculary collaps. The ammonium ion concentration in the blood increased to 696 +/- 57 umol/l and in cerebrospinal fluid to 664 +/- 57 umol/l. Cerebrospinal fluid glucose concentration was significantly decreased.
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PMID:Total devascularization of the Liver: an experimental model of acute liver failure. 106 34

Cerebral circulation and metabolism in septic encephalopathy have not been well documented. The authors measured cerebral blood flow (CBF) and metabolic rate for oxygen (CMRO2) in six patients with septic encephalopathy associated with multiple organ failure (three to five organs). They found that CBF and CMRO2 were significantly lower than awake control values of 46 +/- 2 to 28 +/- 3 mL/100g/min (mean +/- SEM) and 3.1 +/- 0.2 to 1.2 +/- 0.2 mL/100g/min, respectively. Cerebral vascular resistance (CVR) and cerebral circulatory index (CCI:CBF/CMRO2) were significantly higher than the control values of 2.0 +/- 0.1 to 3.0 +/- 0.4 mm Hg/mL/100g/min and 15.1 +/- 0.8 to 24.2 +/- 3.3, respectively. At the time of cerebral circulatory and metabolic measurements, their consciousness varied between 4 and 10 as evaluated by the Glasgow coma scale. The electroencephalogram showed diffuse slow wave activity and the latency of the auditory brain stem evoked response was prolonged in four of six patients. Computed brain tomography showed either no abnormality or mild atrophy. It is concluded that CBF and CMRO2 are disproportionally decreased during septic encephalopathy in association with dysfunction of the CNS and decreased electrical activity.
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PMID:Cerebral circulation and metabolism in patients with septic encephalopathy. 199 41

Ninety-seven patients with insulin dependent diabetes mellitus (IDDM) were randomized to intensified conventional treatment (ICT, n = 44) or regular treatment (RT, n = 53). The mean HbA1c level (+/- SEM) was reduced from 9.5 +/- 0.2% to 7.4 +/- 0.1% in the ICT group (P less than 0.001), and from 9.4 +/- 0.2% to 9.0 +/- 0.2% (P less than 0.01) in the RT group. The difference between the groups was significant (P less than 0.001). During a period of 3 years, 57% of the ICT patients (95% confidence interval 44-73%) and 23% of the RT patients (95% CI, 11-34%) (P less than 0.001) had at least one episode of serious hypoglycaemia, with the need for third-party assistance or resulting in coma. Eighteen of the 32 ICT patients who initially had adrenergic symptoms during hypoglycaemia changed to predominantly neuroglycopenic symptoms. This was the case with only 8 of 38 RT patients (P less than 0.01). The change in symptoms was related to the increased frequency of serious hypoglycaemia, but neither symptoms nor frequency of hypoglycaemia bor any relationship to insulin dose, body mass index, duration of diabetes or autonomic nerve function. The results of several neuropsychological tests did not differ between the groups at baseline, and did not change during the study. There were no signs of deteriorating cognitive function in the patients with serious hypoglycaemic episodes.
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PMID:Hypoglycaemic episodes during intensified insulin treatment: increased frequency but no effect on cognitive function. 199 69

We studied the changes in plasma arginine vasopressin in 5 patients with diabetic ketoacidosis and one patient with non-ketotic hyperosmolar coma who had marked hyperglycemia (36.6 +/- 4.6 mmol/l, mean +/- SEM) and dehydration. Plasma osmolality (Posm) was 342.2 +/- 11.4 mOsm/kg H2O, and hematocrit, serum protein, and blood urea nitrogen were also elevated at hospitalization. Circulating blood volume was decreased by approximately 21% as compared with that on day 7. Plasma AVP level was increased to 8.5 +/- 1.6 pmol/l at hospitalization. When hyperglycemia was improved by iv infusion of a small dose of insulin plus fluid administration, plasma AVP level promptly decreased to 2.4 +/- 0.4 pmol/l within six hours. When plasma AVP level had normalized, Posm was still as high as 305 mOsm/kg H2O, but the loss of circulating blood volume was only 4.2% of the control state. Plasma AVP level was positively correlated with change in hematocrit (plasma AVP = 3.58 + 0.45.hematocrit, r = 0.468, p less than 0.01), serum protein (r = 0.487, p less than 0.01), Posm (r = 0.388, p less than 0.01), and blood glucose (r = 0.582, p less than 0.01). Plasma AVP level was negatively correlated with the change in circulating blood volume (plasma AVP = 3.6 - 0.14.change in circulating blood volume, r = -0.469, p less than 0.01). These results indicate that both non-osmotic and osmotic stimuli are involved in the mechanism for AVP release in patients with diabetic coma, and that the non-osmotic control of AVP may contribute to circulating homeostasis, protecting against severe blood volume depletion in diabetic patients suffering from hyperglycemia and dehydration.
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PMID:Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid. 211 Apr 10

To understand the effect of positioning of patients on intracranial pressure, studies were performed in 30 patients with head injuries severe enough to produce prolonged coma with Glasgow Coma Scale scores less than 8. Intracranial pressure was measured with the patient in four different positions: head at 0 degrees, head down 30 degrees, three fourths supine, and three fourths prone without turning the head. Intracranial pressure results were as follows: at 0 degrees, 20.50 +/- 1.75 (mean +/- SEM) mm Hg; head down 30 degrees, 24.15 +/- 1.75 mm Hg; three fourths supine, 28.83 +/- 2.69 mm Hg; and three fourths prone 30.85 +/- 2.90 mm Hg. Intracranial pressures were higher in the latter three positions as compared with the standard 0 degrees supine position, but some individual differences in response were noted. The data suggest that the head-down, three-fourths supine, and three-fourths prone positions have a greater chance of increasing the intracranial pressure in patients with severe head injury having prolonged comas. When patients are placed in the above three postures the duration should be as short as possible, and they should be used only when absolutely necessary.
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PMID:Intracranial pressure changes during positioning of patients with severe head injury. 274 9

While in animal experiments neurogenically initiated pulmonary edema is a well known event and is supposed to be due to centrally initiated hemodynamic disturbances ("neurohemodynamics") in patients with severe cerebral lesions fulminant alveolar edema is reported to occur very rarely. The questions addressed by this study are: 1. whether and to what extent changes in extravascular lung water (EVTVL) can be demonstrated in patients with a severe isolated cerebral lesion; 2. whether a relationship between the severity of the cerebral lesion and accompanying EVTVL changes can be proven; and 3. whether or not EVTVL changes are associated with corresponding changes in intravascular hydrostatic and oncotic Starling parameters; i.e. cardiogenic or noncardiogenic pulmonary edema accompanying the cerebral lesion. This study included 44 patients presenting with a severe isolated cerebral lesion and decerebrate posturing on admission. EVTVL (by thermo-dye double-indicator technique), pulmonary gas exchange (AaDO2/pAO2), colloid oncotic pressure (COP) and mean systemic arterial (SAP), mean pulmonary arterial (PAP), and pulmonary capillary wedge pressures (PCWP) were measured from the day of admission to the 6th day after the acute cerebral lesion maximally; in addition the microvascular pressure in the pulmonary bed and intravascular filtration pressure were calculated from the above mentioned parameters. The neurological status on admission and throughout the observation period was scored using the Innsbruck Coma Scale (ICS) and the neurological outcome by the Glasgow Outcome Scale (GOS). Statistical analysis was performed using the distribution independent Kruskal Wallis test, the correlation coefficient r (Pearsan and Bravais), and the Spearman rank correlation (RSp); values are given as means +/- SEM; the significance has been set at P less than 0.05. Our results reveal an overall increase in EVTVL from 8.8 +/- 0.8 ml/kg on the day of admission up to 11.3 +/- 1.6 ml/kg on the 4th day. While survivors (n = 13) remained within the normal range of EVTVL (less than 9 ml/kg), non-survivors (n = 31) started at an already elevated level (10.05 +/- 1.04 ml/kg) and reached their maximum values (15.4 +/- 2.3 ml/kg) on day 3 to 4. In 3 non-survivors these increased initial EVTVL values were accompanied by pathologically increased intravascular pressures, indicating that hydrostatic mechanisms were involved in the EVTVL rises. While the hydrostatic pressures normalized spontaneously, EVTVL values stayed within the pathological range throughout the remaining observation period.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Cardiovascular and pulmonary changes in patients with an isolated cerebral lesion. II. Extravascular lung water and pulmonary gas exchange ("neurogenic lung edema")]. 277 40

Plasma epinephrine, norepinephrine, and dopamine responses were studied in insulin-dependent diabetic patients at rest, on standing and during insulin-induced hypoglycemia. beta-Adrenergic sensitivity was evaluated by the isoproterenol sensitivity test. Five men who had adrenergic symptoms during hypoglycemia and no severe hypoglycemic accidents (coma, seizures) (group A) and five men who had repeated severe hypoglycemic accidents but lack of adrenergic symptoms of hypoglycemia (group B) were studied. The mean resting plasma epinephrine was lower in group B (147 +/- 22 pmol/L, SEM) than in group A (398 +/- 98 pmol/L, P less than 0.02). On standing plasma epinephrine increased significantly in both groups. During hypoglycemia blood glucose decreased identically in the two groups; plasma epinephrine and norepinephrine increased significantly and to the same extent in both groups; the mean maximal heart rate was significantly greater in group A than in group B. Isoproterenol sensitivity (defined as the dose of isoproterenol required to increase heart rate by 25 beats/min) was lower in group B (5.87 +/- 1.12 micrograms) than in group A (2.37 +/- 0.22 micrograms, P less than 0.01). The group B patients had significantly fewer hypoglycemic symptoms during insulin-induced hypoglycemia than did group A patients. We conclude that decreased beta-adrenergic sensitivity contributes to the lack of adrenergic symptoms of hypoglycemia in insulin-dependent diabetic patients.
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PMID:Lack of hypoglycemic symptoms and decreased beta-adrenergic sensitivity in insulin-dependent diabetic patients. 282 5

Metabolic effects of 3 different sites of transplantation of cultured tumour cells from a radiation induced insulinoma (28 X 10(6) viable cells per rat) were examined in 15-18 weeks old male NEDH rats. Subscapular implantation consistently produced a highly vascularised encapsulated tumour associated with hyperinsulinaemia, hyperphagia and hypoglycaemia by 21 days, which progressed to fatal neuroglycopaenic coma at 37 +/- 3 days (mean +/- SEM). Implantation of tumour cells into the hepatic portal vein resulted in a multilobular hepatic tumour in two out of nine rats, with hyperinsulinaemia and fatal hypoglycaemia by 49-54 days. Irregularities of glucose homeostasis were observed in a further three rats by 62 days. Intrapancreatic implantation consistently produced a similar tumour to that observed at the subscapular site. Implantation into the pancreas produced the most rapid onset of hyperinsulinaemia, hyperphagia and hypoglycaemia, with survival for only 28 +/- 3 days. The results demonstrate an important effect of transplantation site on the function and metabolic consequences of the NEDH rat insulinoma.
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PMID:Metabolic effects of radiation induced rat insulinoma at pancreatic, hepatic and subscapular transplantation sites. 287 15


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