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Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infants of diabetic mothers are at increased risk of a number of problems at birth. Among these problems are increased risks of respiratory distress syndrome and transient tachypnea of the newborn. Because surfactant synthesis, surfactant secretion, and lung fluid resorption are all mediated in part by beta-adrenergic responses, we asked if excess insulin interferes with the beta-adrenergic response cascade in fetal lung. Lungs from fetal rabbits (26 day) were grown in explant culture in hormone-supplemented culture medium. The explants were harvested after 48 h exposure to hormones and processed for determination of beta-adrenergic receptor concentration, guanine nucleotide regulatory proteins (Gs, Gi), beta-agonist stimulated adenosine 3',5'-cyclic monophosphate (cAMP) generation, cAMP-dependent phosphodiesterase activity, and choline incorporation into phosphatidylcholine. Although insulin did not change the concentration of beta-adrenergic receptors, it decreased the ability of isoproterenol to stimulate cAMP generation. Increase in stimulation over basal was similar in explants treated with dexamethasone and dexamethasone plus insulin, but absolute levels of isoproterenol-stimulated cAMP were less in the explants treated with dexamethasone plus insulin. We speculate that insulin inhibition of cAMP generation may be important in the pathogenesis of the respiratory problems of infants of diabetic mothers.
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PMID:Insulin inhibits beta-adrenergic responses in fetal rabbit lung in explant culture. 133 1

Complications in 42 newborn infants of diabetic mothers (IDM), both insulin- and non-insulin-dependent, were studied prospectively over a period of 16 months at Harare Maternity Hospital. Hypoglycaemia, the most common complication observed, was present in 23 (55%): only seven of these were symptomatic. In 21 of these 23 cases, blood glucose was stabilized during the first 24 hours of life. Jaundice and transient tachypnoea were each seen in 12 cases (29%). There were no cases of respiratory distress syndrome. One infant had polycythaemia requiring partial exchange transfusion. No life-threatening congenital malformations were seen. All infants were given special care initially and in the majority of cases this could be discontinued after 24 hours. With simple interventions, the morbidity of IDM born was found to be comparable to levels reported from developed countries.
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PMID:Infants of diabetic mothers: a prospective study of neonatal complications in Harare, Zimbabwe. 248 98

In a prospective study of 50 infants of diabetic mothers, 40% were large, 44% appropriate and 16% small for gestational age, 36% were preterm, 24% of the mothers were managed by dietary modification, 62% received insulin, 10% were treated with oral hypoglycemic agents while 4% did not receive any treatment as they were diagnosed postpartum, 58% mothers, underwent cesarean section (38% elective and 20% emergency procedures), 34% had normal vaginal deliveries, 6% were delivered by forceps and 2% by vacuum. Sixty-four per cent were infants of gestational diabetic (IGDM) and 36% of preconceptional diabetic mothers (IPDM). The morbidity and mortality was lesser in IGDM compared to IPDM. Hypoglycemia was documented in 50%, polycythemia in 20%, birth asphyxia in 18%, respiratory distress syndrome and hypocalcemia in 14% each, transient tachypnea of the newborn in 12%, hyperbilirubinemia in 8%, congenital anomalies in 4% and cardiomyopathy, birth trauma and meconium aspiration in 2% each. Pretherapy serum insulin levels were estimated in 10 babies, and 6 babies were subjected to 2D-echocardiography. The overall mortality was 20%. Infants born to mothers on oral hypoglycemic agents had a poor outcome.
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PMID:Infants of diabetic mothers--an analysis of 50 cases. 259 99

Injections of 10 micrograms/kg thyrotropin-releasing hormone (TRH) 150 microliter intracisternally (i.c.) in conscious rabbits evoked behavioral excitation and compulsive scratching, tachypnoea, an increase of heart rate and blood pressure, oxygen consumption and hyperthermia. TRH i.c. significantly increased free thyroid hormone and calcitonin secretion during depressed thyrotropin (TSH) secretion. The rise of calcitonin correlated with a fall of serum calcium. The ergotropic function of TRH i.c. was further demonstrated by rapid increases of glucagon, serum glucose, free fatty acid and free glycerol, with a delayed rise of insulin depending on glucose levels. The increases of free thyroid hormones, calcitonin, cortisol and lipolysis following TRH i.c. were augmented after spinal transection, while glucagon secretion increased at a slower rate, however, not accompanied by rises of glucose and insulin. Behavioral excitation and lipolysis were augmented by TRH i.c. after total thyroidal denervation, which completely prevented the rise in thyroid hormone and calcitonin secretion, although the thyroid follicles and C cells responded properly to TSH. Section of all thyroidal nerves except the recurrent laryngeal nerve reduced mainly calcitonin secretion following TRH i.c., while the behavioral, autonomic and other endocrine responses were augmented. Additional abdominal vagotomy in these rabbits diminished glucagon secretion by about 50% without significantly changing the other effector responses. Taking 125I-labelled TRH concentration in the cerebrospinal fluid at the site of i.c. injection as 100%, then 58% of TRH penetrated into outer parts of the dorsal and ventral medulla oblongata and pons, and 8% into the neuropil of the aqueductal region. Radioactivity in other brain areas including the hypothalamus was below 1%, while the hypophysis was practically devoid of radiolabelled TRH. It is suggested that the observed behavioral, autonomic and endocrine activity pattern elicited by injection of TRH into the cisterna magna was caused by excitation of neurons confined to that compartment and was mediated by pathways of the reticular formation of the lower brainstem, with the concept that TRH-containing neurons are intrinsic excitatory constituents of the 'activating reticular system'.
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PMID:Selective autonomic nervous control of thyroid hormone and calcitonin secretion during metabolic and cardiorespiratory activation by intracisternal thyrotropin-releasing hormone (TRH). 314 96

At present, the role of Doppler velocimetry in monitoring fetal well-being in diabetic pregnancies is controversial. The present study was conducted to determine if fetal aortic velocity waveforms were correlated with fetal outcome in pregnancies complicated by diabetes mellitus. Fetal aortic blood flow was prospectively assessed in 30 pregnant women with insulin-dependent diabetes mellitus. Systolic-diastolic ratios were obtained at 2 week intervals between 18 and 38 weeks of gestation. They were analyzed according to several fetal outcome variables. Infants with presumed fetal distress during labor and neonates with respiratory abnormalities (respiratory distress syndrome, persistent fetal circulation, or transient tachypnea of the newborn) showed statistically significant elevations of aortic Doppler indices (P < 0.031 and < 0.011, respectively). However, these correlations lacked clinical relevance. The infants demonstrated no evidence of fetal distress at birth since Apgar scores were > 7 at 5 min in all but one neonate. No relationship was found between the mean third trimester fetal aortic systolic-diastolic ratios and perinatal death, preterm deliveries, birth weight, Apgar scores at 1 and 5 min, and neonatal metabolic abnormalities. These data demonstrate a poor correlation between fetal aortic Doppler waveform analysis and fetal outcome. Therefore, fetal aortic Doppler velocimetry cannot be used as a means of assessing impending fetal compromise in offspring of diabetic mothers.
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PMID:Is there a correlation between aortic Doppler velocimetric findings in diabetic pregnant women and fetal outcome? 873 87

Permanent neonatal diabetes mellitus (PNIDDM) is a rare form of IDDM with unclear etiology and pathogenesis. We determined the incidence and prevalence rates and studied the clinical and biochemical features of PNIDDM in the Sultanate of Oman. The mean incidence rate during the study period from January 1989 to December 1994 was 1.788 +/- 0.82 per 100,000 live births per year. At the end of December 1994 the prevalence rate was 2.4 per 100,000 children below the age of 5 years. They constituted 41.6% of all cases of IDDM in this age group. Diarrhoea, fever, lethargy, poor feeding and failure to thrive were the most common presenting symptoms. Dehydration and tachypnoea were the most common signs. All patients who developed IDDM during the neonatal period had intrauterine growth retardation and 4.5 presented with diabetic ketoacidosis (plasma glucose 37 +/- 9 mmol/L, pH 7.12 +/- 0.1). Hypertriglyceridemia was a constant feature (19.4 +/- 4.8 mmol/L). They were products of consanguineous marriage with significantly high prevalence of IDDM and NIDDM in their family members. None of the infants had clinical or immunological evidence of congenital viral infection. Three of the five children had HLA-DR2, the diabetes resistance alleles. C-peptide secretion was absent during and after metabolic control of hyperglycemia in all the studied infants and none had circulating islet cell antibody at presentation or during the first year after diagnosis. Despite marked growth retardation at birth, there was a significant improvement of growth after initiating insulin therapy. Four of the 5 patients had normal developmental milestones, one had mild developmental delay following a severe and prolonged attack of hypoglycemia. None of the patients had exocrine pancreatic deficiency. In summary, the very high rate of parental consanguinity, occurrence in both sexes and in two siblings in the same family, absence of islet cell antibodies and the presence of HLA-DR2 loci in 3/5 of patients suggest that PNIDDM is a different disease process to standard IDDM in childhood and an autosomal recessive mode of transmission.
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PMID:Permanent neonatal diabetes mellitus: epidemiology, mode of presentation, pathogenesis and growth. 1079 84

Claude Bernard in the late 19th century, was one of the first who recognized that acute injury was associated with the development of hyperglycemia. In 1942 David Cutherbertson introduced the terms ebb and flow to describe the phases of hypo- and hypermetabolism, which follow traumatic injury. Hyperglycemia during the ebb phase is promoted by hepatic glycogenolysis secondary to catecholamine release, as well as by direct sympathetic stimulation of glycogen breakdown. Hyperglycemia is a prominent feature of the flow phase in patients who sustain more severely injured or in whom septic complications develop. It results from augmented glucose production in the presence of insulin resistance in peripheral tissues. The flow phase is clinically expressed as a syndrome consisting of: hypermetabolism (manifested by hyperglycemia, hyperlactatemia and protein catabolism), hyperdynamic cardiovascular state and clinical manifestations of fever or hypothermia, tachycardia, tachypnoea and leucocytosis. The hypermetabolic response to stress may be prolonged when there is stimulus for continuous formation of mediators--a persistent focus of injury or infection. Three systems are responsible for translating the initial insult into the stress response: nervous, endocrine and humoral (cytokine). These systems are interrelated. Maximal metabolic response to stress requires the participation of all three systems. Although glycogenolysis increases hepatic glucose output during the ebb phase, this effect is transient because glycogen stores are rapidly depleted. In contrast, the flow phase is characterized by a sustained increase in gluconeogenesis, which in turn promotes hyperglycemia. Hyperglycemia is common following stress, despite the fact that many tissues exhibit increased cellular uptake and utilization of glucose. Peripheral insulin resistance is central to this process by limiting insulin-mediated glucose uptake in skeletal muscles. In addition, hepatic insulin resistance also plays a role in the genesis of hyperglycemia during stress. In general, the degree of hyperglycemia and insulin resistance are directly proportional to the severity of the stress response. Hyperlactatemia and oxygen consumption also increase concurrently with the severity of stress. Modest hyperglycemia during stress may be of potential benefit by promoting cellular glucose uptake, however, severe hyperglycemia may be associated with complications, this in turn could result in organs dysfunction.
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PMID:[Alterations of blood glucose homeostasis during septic or injury stress--hyperglycemia]. 1271 56

Central neural damage caused by L-cysteine (L-Cys) was first reported more than 30 years ago. Nevertheless, the exact mechanisms of L-Cys-mediated neurotoxicity are still unclear. Preliminary study in mice demonstrated that, following L-Cys injection, animals developed tachypnea, tremor, convulsions, and death in conjunction with documented hypoglycemia. The aim of the present study was to further investigate the mechanism of L-Cys-mediated hypoglycemic effect and neural damage. Neonatal ICR mice (n=6) were injected with L-Cys (0.5-1.5 mg/g body weight [BW]), and their blood glucose and insulin levels were determined up to 90 min following the injection. Experiments were repeated in chemically (streptozotocin [STZ]) pancreatectomized animals. Brain histology was assessed. Mice injected with L-Cys exhibited dose-dependent neurotoxicity and higher mortality as compared with controls. L-Cys (1.2-1.5 mg/g BW) caused severe hypoglycemia (glucose<42 mg/dl) ( P<0.001). In STZ-treated (diabetic) animals, L-Cys (1.5 mg/g BW) increased plasma insulin levels 2.3-fold and decreased serum glucose levels by 50% ( P<0.01). Brain histology revealed destruction of as much as 51% of hippocampal neurons in the L-Cys-treated mice but not in the glucose-resuscitated animals. These findings suggest that L-Cys injection can cause pronounced hypoglycemia and central neural damage which is glucose reversible. Since L-Cys is chemically different from the other excitatory amino acids (glutamate and aspartate), L-Cys-mediated neurotoxicity may be connected to its hypoglycemic effect.
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PMID:Cysteine-induced hypoglycemic brain damage: an alternative mechanism to excitotoxicity. 1504 46

A 20-year old student had suffered since 3 years from diabetes mellitus type I, which was well-controlled by insulin-pump therapy. During a flight from Moscow to Los Angeles, the student all of a sudden had chest pain, dyspnea, and he vomitted repetitively--emergency landing at Zurich airport was necessary. The student presented at the emergency unit in a poor general condition with tachypnea (32/min) and tachycardia (136/min). Arterial blood gas analysis showed severe metabolic acidosis (pH 7.04), while pulmonary or cardiac disease could be ruled out. Diabetic ketoacidosis was caused by the pump running short of insulin. Treatment included rehydration and administration of insulin. Administration of insulin by an insulin-pump allows to continuously and flexibly adjust the dosage according to the requirement of the body. Interruption of insulin administration can cause, however, relatively fast ketoacidosis because exclusively short-acting insulin is used.
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PMID:[Emergency landing due to a passanger with chest pain, dyspnea, and vomiting]. 1533 25

Heart disease is among the leading causes of death in all populations. Cardiac dysfunctions are major complications in patients with advanced viral or bacterial infection, severe trauma and burns accompanied with multiple organ failure - collectively known as systemic inflammatory response syndrome (SIRS). SIRS, which is often subsequent to sepsis, is clinically featured by hypotension, tachypnea, hypo- or hyperthermia, leukocytosis and myocardial dysfunction. The striking association between inflammation and cardiac dysfunction not only prognoses likelihood of survival in patients with SIRS but also prompts the necessity of understanding the pathophysiology of cardiac dysfunction in SIRS, so that effective therapeutic regimen may be identified. Compelling evidence has shown significant and independent link among inflammation, sepsis, insulin resistance and cardiac dysfunction. Several cytokine signaling molecules have been speculated to play important roles in the onset of cardiac dysfunction under SIRS including endothelin-1 and toll-like receptor. Involvement of these pathways in cardiac dysfunction has been convincingly validated with transgenic studies. Nevertheless, the precise mechanism of action underscoring inflammation-induced cardiac contractile dysfunction is far from being clear. Given the substantial impact of inflammation and SIRS on health care, ecosystems and national economy, it is imperative to understand the cellular mechanisms responsible for cardiac contractile dysfunction under inflammation and sepsis so that new and effective therapeutic strategy against such devastating heart problems may be developed.
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PMID:A burning issue: do sepsis and systemic inflammatory response syndrome (SIRS) directly contribute to cardiac dysfunction? 1614 10


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