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Biomedical subjects

C S Thompson

Publications and source records attributed to C S Thompson.

At least 109 records · Page 6Linked to original sources

Does furosemide alter the hemodynamic response to rapid intravascular transfusion of the anemic fetal lamb?

The purpose of this study was to define the hemodynamic response to rapid intravascular transfusion of the anemic fetal lamb and to determine whether furosemide alters that response. Sixteen experiments were performed in nine chronically instrumented gravid ewes between 0.8 and 0.9 of timed gestation. On day 1 of each experiment, each fetus was subjected to hemorrhage (40 ml/kg of estimated fetal weight) over 1 hour. On day 2, plasma was withdrawn from the stored fetal blood until the hematocrit was approximately 70%, and the packed red blood cells were returned to the fetus intravenously over 10 minutes. Each fetus received either furosemide (2 mg/kg) or control saline solution intravenously at time zero and again at 5 minutes. The order of experiments was randomly determined for each animal. Hemorrhage resulted in a similar decrease in fetal hematocrit in the two groups. The mean +/- SEM fetal hematocrit before hemorrhage was 38 +/- 3% in the furosemide group (n = 8) and 36 +/- 2% in the control group (n = 8). On day 2, the mean +/- SEM fetal hematocrit before transfusion was 28 +/- 2% in the furosemide group and 25 +/- 1% in the control group. There was no significant difference between groups in the fetal hemodynamic response to transfusion. At the end of the transfusion, the fetal central venous pressure had increased from 4.9 +/- 0.5 to 6.2 +/- 0.5 mm Hg in the furosemide group (p = 0.01) and from 3.9 +/- 0.2 to 5.8 +/- 0.3 mm Hg in the control group (p = 0.0001). Fetal mean arterial pressure increased from 42 +/- 1 to 50 +/- 1 mm Hg in the furosemide group (p = 0.0001) and from 40 +/- 1 to 46 +/- 1 mm Hg in the control group (p = 0.0007). Fetal heart rate decreased from 187 +/- 2 to 169 +/- 5 beats/min in the furosemide group (p = 0.004) and from 188 +/- 4 to 170 +/- 5 beats/min in the control group (p = 0.0008). Transfusion did not significantly change fetal pH in either group. At 120 minutes, the fetal PO2 had increased from 17 +/- 1 to 19 +/- 1 mm Hg in the furosemide group (p = 0.03) and from 19 +/- 1 to 21 +/- 2 mm Hg in the control group (p = 0.05). We conclude that rapid transfusion of the anemic fetal lamb resulted in modest increases in fetal central venous pressure and mean arterial pressure.(ABSTRACT TRUNCATED AT 400 WORDS)

Anemia, Hemolytic↗

Effect of starvation and sampling time on plasma alkaline phosphatase activity and calcium homeostasis in the rat.

The effect of starvation and sampling time on plasma alkaline phosphatase activity, total plasma calcium concentration and whole blood ionized calcium concentration was determined in the rat. Starvation caused a significant fall in total and ionized calcium concentrations as well as in alkaline phosphatase activity. These changes were accompanied by a fall in whole blood pH and an increase in the anion gap and a decrease in urinary excretion of calcium. These indices were restored to normal following refeeding. There was no change in serum 25-OH vitamin D concentrations following starvation for 3 days. Alkaline phosphatase activity showed a pattern compatible with the presence of a circadian rhythm when sampling took place between 0800 and 1800 h. Total and ionized calcium concentrations did not show such a rhythm when animals were fed the present diet.

25-Hydroxyvitamin D 2↗

Does the intravenous infusion of ritodrine or magnesium sulfate alter the hemodynamic response to hemorrhage in gravid ewes?

The purpose of this study was to determine whether the intravenous infusion of ritodrine or magnesium sulfate alters the hemodynamic response to maternal hemorrhage in gravid ewes. Twenty-seven experiments were performed in 12 chronically instrumented animals at 0.8 of timed gestation. Each animal was subjected to hemorrhage (20 ml/kg over 60 minutes) during infusion of ritodrine (0.004 mg/kg/min), magnesium sulfate (4 gm/hour), or saline solution control. Infusion of magnesium sulfate increased the mean (+/- SEM) maternal serum magnesium concentration to 4.8 +/- 0.2 mg/dl before hemorrhage and 5.3 +/- 0.3 mg/dl after hemorrhage. At the end of hemorrhage maternal mean arterial pressures were 63% +/- 4%, 82% +/- 2%, and 79% +/- 6% of baseline in the magnesium sulfate, ritodrine, and control groups, respectively. The maternal mean arterial pressure response in the magnesium sulfate group differed significantly from the maternal mean arterial pressure responses in the ritodrine and control groups (p less than 0.01). Fetal pH was decreased significantly only in the magnesium sulfate group (p = 0.0001). Fetal PO2 was decreased significantly in the magnesium sulfate and ritodrine groups (p less than 0.001) but not in the control group. We conclude that magnesium sulfate but not ritodrine, worsened the maternal hypotensive response to hemorrhage in gravid ewes.

Animals↗

Nutrient uptake by rat enterocytes during diabetes mellitus; evidence for an increased sodium electrochemical gradient.

1. The effect of streptozotocin-induced diabetes (7 day duration) in rats on D-glucose uptake in vivo, the unidirectional uptake of D-glucose and L-proline in vitro, the passive uptake of L-glucose in vitro and the potential difference across the brush-border membrane has been studied. 2. Diabetes resulted in an increased carrier-mediated glucose uptake both in vivo and in vitro and a stimulation of L-proline uptake at a concentration of the amino acid (0.025 mM) at which uptake was largely Na+ dependent. Diabetes was without effect on uptake using a proline concentration of 50 mM at which transport was predominantly Na+ independent. 3. A marked hyperpolarization of the brush-border membrane and an enhanced passive glucose uptake were also evident during diabetes. 4. We conclude that the stimulation of glucose uptake in vivo in diabetic intestine involves events at the brush-border membrane. The mechanisms include an increased surface area for uptake and an enhanced transmembrane electrical gradient. The latter will have a major effect on the transport of other substrates when the uptake pathway is primarily Na+ dependent.

Animals↗

Platelet thromboxane A2 synthesizing capacity is enhanced by fasting but diminished by diabetes mellitus in the rat.

In order to investigate whether the hyperaggregability of platelets in diabetic and starved rats was due to an increase in the inherent capability of these platelets to synthesize thromboxane A2, we assessed the total thromboxane A2 synthesizing capacity of platelets in rats with streptozotocin-induced diabetes and rats which have been semistarved (nine days) or fasted for various periods (24-72 h). Fasting for 48 h or more and semistarvation resulted in highly significant increases in thromboxane A2 synthesizing capacity. Experimental diabetes, however, resulted in a marked diminution in thromboxane A2 synthesizing capacity. This decrease in thromboxane A2 synthesizing capacity was prevented in diabetic rats treated with insulin. We conclude that while the hyperaggregability of starvation is associated with an increase in thromboxane A2 synthesizing capacity, that of diabetes is associated with a fall in this capacity. The decrease of this capacity in diabetic animals can be prevented by insulin treatment. Total thromboxane A2 synthesizing capacity is therefore not a major determinant of either platelet hyperaggregability or of agonist induced platelet thromboxane A2 release.

Animals↗

Increased histamine in plasma and tissues in diabetic rats.

In view of the previous observation that the histamine content of the aorta in rats with streptozotocin-induced diabetes mellitus is increased significantly over that in controls, we have investigated the effect of experimental diabetes on the histamine content of the plasma, the aorta, the kidney, the heart, the lung and the brain. Our data show that the histamine content of the plasma, the aorta, the heart, the kidney, the lung and the brain is significantly greater in diabetic rats than that found in controls. This increase in plasma and tissue histamine content may contribute to the increase in capillary and endothelial permeability known to occur in diabetes, and may have a role to play in the pathogenesis of diabetic micro- and macroangiopathy.

Animals↗

Anatomy and electrophysiology of neurons terminating in the corpora allata of the cockroach Diploptera punctata.

Intracellular recording and dye injection were used to study the structure and electrophysiological properties of individual neurons that project to the corpora allata of the cockroach, Diploptera punctata. Neurons in the pars intercerebralis generate long-duration, tetrodotoxin-sensitive action potentials. Dye injection revealed two cell types. One type extends axons to the contralateral nervi corporis cardiaci I, some of which innervate the corpora allata, and another type extends a major axon down each of the circumoesophageal connectives. Neurons in the pars lateralis also generate long-duration action potentials. These neurons extend axons to the ipsilateral nervi corporis cardiaci II, which continue on to terminate in the corpora cardiaca and the corpora allata. Small groups of all the above neuronal types are dye and electrically coupled. Penetration and dye injection into nerve terminals in the corpora allata and corpora cardiaca confirmed the innervation of the corpora allata by neurons located in the pars intercerebralis and pars lateralis and revealed a third class of neurons that have terminals in the corpora allata: intrinsic neurons of the corpora cardiaca.

Action Potentials↗

Differential regional changes of prostacyclin and thromboxane A2 synthesis in the intestinal tract of the fasted and semistarved rat.

The synthesis of prostacyclin (PGI2) and thromboxane A2 (TXA2) by the mucosal and muscular portions of the duodenum, jejunum, ileum and ascending colon, as well as that by mesenteric vessels, was investigated in starved and semistarved rats. The jejunal mucosa and muscularis showed a marked increase in PGI2 synthesis after fasting for 48 h and 72 h or semistarvation for 9 days when compared with controls. Jejunal TXA2 synthesis did not alter. In contrast, PGI2 and TXA2 synthesis in ileal mucosa and muscularis was significantly reduced after fasting for 48 h, 72 h and semistarvation for 9 days. PGI2 and TXA2 synthesis by duodenal and colonic muscularis was unaffected by fasting or semistarvation. PGI2 synthesis in mesenteric vessels was significantly increased by fasting and semistarvation. No changes in PGI2 or TXA2 were detected at 24 h in fasted rats in any of the tissues studied when compared with controls. These selective changes in PGI2/TXA2 secretion may be important mediators of adaptive changes in the small intestine in response to starvation.

Animals↗

Spectrum of gas within the kidney. Emphysematous pyelonephritis and emphysematous pyelitis.

Renal emphysema is an important clinical entity that is not addressed frequently in the medical literature. The affected patients may have gas within the renal parenchyma, emphysematous pyelonephritis, or confined to the collecting system, emphysematous pyelitis. Two patients that illustrate the spectrum of this entity are described. The literature has been reviewed to determine the clinical features of each disorder and to provide a schema for diagnosis and management. Emphysematous pyelonephritis is seen primarily in diabetic patients, whereas emphysematous pyelitis is recognized most often in association with urinary tract obstruction. The diagnosis is made radiographically by demonstrating renal gas on plain abdominal roentgenography or intravenous pyelography. Location and extent of renal gas are best evaluated by computed tomographic scanning. Intraparenchymal gas usually requires nephrectomy, whereas successful therapy of gas limited to the collecting system involves medical management, with a drainage procedure when obstruction coexists.

Adult↗

Fasting and diabetes mellitus elicit opposite effects on agonist-stimulated prostacyclin synthesis by the rat aorta.

The effects of prolonged fasting and experimental nonketonuric diabetes on rat aortic prostacyclin (PGl2) synthesis were compared. Whereas fasting (for 48 hours or longer) resulted in a marked increase in trauma-, adrenaline-, and U46619-stimulated aortic PGI2 synthesis, prolonged experimental (streptozotocin-induced) nonketonuric diabetes caused a marked decrease in aortic PGI2 synthesis stimulated by the above agonists. Arachidonic acid (AA)-stimulated aortic PGI2 synthesis in fasted and diabetic rats, however, was not different from that in controls. The reduction in adrenaline- and U46619-stimulated, but not AA-induced, PGI2 synthesis in the diabetic rat suggests that the diminished production of PGI2 in diabetes may be due to diminished phospholipase A2 (or of the phospholipase C-diglyceride lipase system) activity, diminished AA stores, or both. The opposite effects of prolonged fasting and diabetes on aortic PGI2 synthesis suggest that caution should be exercised when comparing the metabolic consequences of starvation with those of diabetes.

Animals↗

Changes in eicosanoid synthesis in the cerebrum, cerebellum and brain stem of the diabetic rat.

The effect of streptozotocin-induced diabetes mellitus (DM) on rat brain prostanoid synthesis was assessed. Prostacyclin (PGI2) synthesis was significantly reduced in the DM animals in all 3 brain regions studied (cerebrum; cerebellum; brain stem). In contrast, the synthesis of the other 3 prostanoids assessed (PGF2 alpha; PGE2; TXA2) was not significantly altered in the DM animals. Insulin treatment reverted PGI2 synthesis towards the normal pattern. Since PGI2 is a vasodilator and the other 3 prostanoids (PGF2 alpha; PGE2; TXA2) are cerebral vasoconstrictors, these changes may be relevant to the pathogenesis of the previously reported abnormalities of cerebral blood flow and the increased incidence of cerebrovascular disease in DM.

Animals↗

Effect of starvation on biochemical indices of renal function in the rat.

The effect of starvation on urinary output and biochemical indices of renal function was investigated in rats. Starvation resulted in a marked fall in water intake. Urinary output paradoxically increased during the first day following starvation, but fell dramatically thereafter. Urinary creatinine excretion and creatinine clearance fell markedly, but plasma creatinine concentration did not alter. Plasma urea concentration and urinary urea excretion fell. Plasma sodium concentration increased, whilst plasma potassium concentration did not alter; urinary sodium and potassium excretion fell. Plasma bicarbonate concentration fell marginally, but the anion gap increased to a greater extent. Following re-feeding, water intake and urine output increased, as did urinary creatinine excretion and creatinine clearance. Plasma urea and urinary urea concentrations, as well as sodium and potassium excretion, increased. Plasma bicarbonate increased and the anion gap decreased. These indices improved within 2 days of re-feeding and were restored to normal in 5 days.

Animals↗

The effect of dietary protein restriction on the progression of diabetic nephropathy. A 12-month follow-up.

Eight patients with insulin-dependent diabetes mellitus and progressive renal dysfunction as determined by serial serum creatinine values were placed on a diet containing 40 g of high-biologic-value protein. Selected factors of renal function were determined over a 12-month interval. After the first 12 months of the protein-limited diet, creatinine clearance was not significantly changed. The rate of decline in renal function during the dietary protein restriction slowed from the rate over the prior 12 months in seven patients. Five of these seven demonstrated improvement in renal function. Daily urinary protein excretion decreased significantly, from 2105 +/- 1355 to 142 +/- 164 mg/d (2.11 +/- 1.36 to 0.14 +/- 0.16 g/d). Body weight did not change significantly, whereas serum albumin level increased significantly from a mean of 3.5 +/- 0.6 to 4.3 +/- 0.3 g/dL (35 +/- 6 to 43 +/- 3 g/L). These findings suggest that dietary protein restriction has a beneficial role in treating patients with diabetic nephropathy.

Adult↗

The effect of streptozotocin-induced diabetes on PGI2 synthesis by the rat bladder.

The effect of streptozotocin-induced diabetes mellitus on prostacyclin (PGI2) production by the urinary bladder in rats was investigated. Acute ketotic (two days duration) and non-ketonuric (seven days duration) diabetes had no effect on PGI2 production by the aorta or the bladder. "Chronic" untreated non-ketonuric (62 days duration) diabetes had a marked inhibitory effect on aortic PGI2 secretion which was not observed when rats were treated with insulin. Urinary bladders from animals with "chronic" untreated non-ketonuric diabetes were larger and heavier, and their walls were hypertrophic. The bladders from these latter animals produced more total PGI2, as well as more PGI2 per unit weight. Enhanced PGI2 production by bladders from animals with untreated non-ketonuric diabetes indicates that: 1) severity of the metabolic disturbance due to diabetes mellitus (ketosis) is not as important as the duration of diabetes as far as the induction of changes in PGI2 production is concerned; 2) distension and hypertrophy of the bladder and hyperosmolar urine are probably more potent stimulators of PGI2 production than diabetes is an inhibitor; 3) diabetes mellitus may have a variable effect on PGI2 secretion patterns in different tissues; 4) urinary excretion of PGI2 or its stable metabolite, 6-oxo-PGF1 alpha may not exclusively reflect PGI2 production by systemic vasculature and/or the kidneys; and 5) good control of diabetes prevents the bladder wall and PGI2 synthesis changes.

6-Ketoprostaglandin F1 alpha↗

Hyperglucagonaemia: effects on active nutrient uptake by the rat jejunum.

The effects of chronic (72 h) glucagon treatment on active nutrient uptake by the rat jejunum have been determined using in-vitro electrophysiological and autoradiographic methods together with an in-vivo technique which measures absorption across a cannulated segment of upper jejunum. Glucagon caused a marked increase in the potential difference across the brush border membrane from a mean value of -47.6 mV under control conditions to -54.2 mV following treatment with the hormone (P less than 0.025). A similar hyperpolarization was also noted after 24 h glucagon administration. The magnitude of the depolarization induced by the addition of D-galactose (4 mmol/l) to the mucosal fluid was increased from 6.0 to 14.3 mV following 72 h glucagon treatment (P less than 0.05). Phloridzin (0.1 mmol/l) abolished the galactose-induced depolarization in both control and treated animals. Glucagon induced significant increases of 49.9 and 61.0% respectively for glucose and galactose absorption measured under in-vivo conditions. Autoradiographic studies revealed that following glucagon treatment, L-valine uptake occurred earlier during enterocyte migration along the villus. This resulted in an enhanced accumulation of the amino acid at the villus tip. We conclude that glucagon increases nutrient transport across the small intestine. The raised electrical gradient for Na+- coupled nutrient entry into the enterocyte is likely to be a major factor in the transport response.

Animals↗

Autoradiographic localization of opioid receptor types in the rat small intestine.

The selective mu and delta ligands [3H]DAGO and [3H]DPDPE have been used to investigate the distribution of specific opioid subtypes in the rat small intestine by in vitro autoradiography. There was a greater density of [3H]DPDPE binding at regions of the villi and crypts than [3H]DAGO binding. These results suggest that the opioid receptors located in these regions are predominantly of the delta subtype.

Animals↗

The effect of cigarette smoke and diabetes mellitus on muscarinic stimulation of prostacyclin synthesis by the rat penis.

The effect of cigarette smoke extracts and experimental diabetes on rat penile prostacyclin (PGI2) synthesis was investigated. Cigarette smoke extracts induced a dose-related inhibition of methacholine-stimulated PGI2 secretion. Induction of diabetes by streptozotocin resulted in diminished PGI2 secretion, which was further inhibited by cigarette smoke extracts in an additive fashion. Treatment with insulin prevented the inhibition of PGI2 in diabetic animals. Since PGI2 is a potent vasodilator, it may mediate the increased blood flow to the penis responsible for erection following parasympathetic stimulation. The inhibition of PGI2 secretion by cigarette smoke extracts or diabetes, or both, may therefore provide a mechanism to account for the epidemiological observation that smoking and diabetes are major risk factors for male impotence.

Animals↗