Search PubMed⌕ Search

Biomedical subjects

E D Miller

Publications and source records attributed to E D Miller.

82 records · Page 5Linked to original sources
PubMed1975

Inhibition of angiotensin conversion and prevention of renal hypertension.

Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin-angiotensin system is responsible for the initiation of renovascular hypertension in the one-kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.

Angiotensin II↗
PubMed1972

Inhibition of angiotensin conversion in experimental renovascular hypertension.

Constriction of the renal artery and controlled reduction of renal perfusion pressure is followed by a prompt increase in systemic renin activity and a concomitant rise in blood pressure in trained, unanesthetized dogs. The elevated blood pressure induced by the renal artery stenosis can be prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro, which blocks conversion of angiotensin I to angiotensin II. Further, the nonapeptide can restore systemic pressure to normnal in the early phase of renovascular hypertension. These results offer strong evidence that the renin-angiotensin system is responsible for the initiation of hypertension in the unilaterally nephrectomized dog with renal artery constriction.

Angiotensin II↗
PubMedDate not supplied

Morphological differentiation of bipolar cells in the ferret retina.

Bipolar cells are not only important for visual processing but input from these cells may underlie the reorganization of ganglion cell dendrites in the inner plexiform layer (IPL) during development. Because little is known about the development of bipolar cells, here we have used immunocytochemical markers and dye labeling to identify and follow their differentiation in the neonatal ferret retina. Putative cone bipolar cells were immunoreacted for calbindin and recoverin, and rod bipolar cells were immunostained for protein kinase C (PKC). Our results show that calbindin-immunoreactive cone bipolar cells appear at postnatal day 15 (P15), at which time their axonal terminals are already localized to the inner half of the IPL. By contrast, recoverin-immunoreactive cells with terminals in the IPL are present at birth, but many of these cells may be immature photoreceptors. By the second postnatal week, recoverin-positive cells resembling cone bipolar cells were clearly present, and with increasing age, two distinct strata of immunolabeled processes occupied the IPL. PKC-containing rod bipolar cells emerged by the fourth postnatal week and at this age have stratified arbors in the inner IPL. The early bias of bipolar axonal arbors in terminating in the inner or outer half of the IPL is confirmed by dye labeling of cells with somata in the inner nuclear layer. At P10, several days before ribbon synapses have been previously observed in the ferret IPL, the axon terminals of all dye-labeled bipolar cells were clearly stratified. The results suggest that bipolar cells could provide spatially localized interactions that are suitable for guiding dendritic lamination in the inner retina.

Animals↗
PubMedDate not supplied

Saralasin dilates arterioles in SHR but not WKY rats.

Microvascular responses to topical or intravascular saralasin were determined in the cremaster muscle arterioles of adult spontaneously hypertensive rats (SHR, n = 19) and Wistar-Kyoto (WKY, n = 16) normotensive rats. Animals were anesthetized with chloralose and urethane, and they breathed room air spontaneously. Mean arterial pressure was obtained from a catheter in a carotid artery, and microvascular diameters were determined by video microscopy. Plasma renin activity was measured in animals that were treated identically except that saralasin was not administered. For all animals, mean arterial pressure averaged 126 +/- 4 mm Hg in SHR and 82 +/- 4 mm Hg (p less than 0.001) in WKY rats. Topical saralasin, 10(-6)M, was applied to the cremaster muscles of SHR (n = 9) or WKY (n = 8) rats while internal diameters of first-through fourth-order arterioles (A1, A2, A3, A4) were measured. Topical saralasin did not alter arteriolar diameters (A1 through A4) in WKY rats, but A3 and A4 vessels dilated significantly (29% +/- 5% and 38% +/- 7% respectively; p less than 0.01) in SHR. Fourth-order diameters were measured in other SHR (n = 10) and WKY (n = 8) rats while saralasin was administered intraarterially (300 micrograms bolus into the hypogastric artery) or intravenously (10 micrograms/kg/min for 30 minutes). Intraarterial or intravenous saralasin caused significant dilation (32% +/- 12% and 20% +/- 4%, respectively; p less than 0.01) of A4 arterioles in SHR, but no dilation occurred in the arterioles of WKY rats. Arteriolar responses were significantly different (p less than 0.001) in SHR vs WKY rats for both the topical and the intravascular administration of saralasin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

The effect of dichloroacetate on brain lactate levels following incomplete ischemia in the hyperglycemic rat.

Dichloroacetate (DCA) is known to prevent the phosphorylation of the pyruvate dehydrogenase complex (PDHC) by blocking the action of PDH kinase. This action allows the active PDHC to exert its effect on the metabolism of glucose, lactate and alanine to acetyl CoA. DCA has been shown to reduce serum lactate levels in humans and animals in such conditions as diabetes, phenformin-induced hepatic failure, exercise, and endotoxin-induced shock. Lactic acidosis in the brain has often been postulated as a cause of neuronal damage following ischemia and hypoxia. Therefore, we examined the effect of intravenously administered DCA (100 mg/kg) in rats that were rendered hyperglycemic by intravenous glucose (2 g/kg), and then made to undergo 15 minutes of incomplete cerebral ischemia by bilateral carotid ligation and systemic hypotension (mean arterial pressure of 50 mm Hg). DCA significantly reduced serum lactate levels pre-ischemia, but had no effect on serum lactate levels after ischemia induction. Brain levels of lactate, ATP and PCr after 15 minutes of incomplete ischemia were unaffected by DCA. We conclude that in this in-vivo model the control of PDHC activity in the brain may be different than that in the periphery, and that DCA was not effective in reducing brain tissue lactate levels.

Acetates↗
PubMedDate not supplied

Postoperative analgesia for thoracotomy patients.

Severe postoperative pain, which may persist for up to 3 days and may lead to postoperative complications, due to the patient's inability to breathe deeply and cough, is frequently experienced in the area of the incision and chest tubes by thoracotomy patients. Eighteen patients undergoing routine thoracotomies were tested preoperatively for arterial blood gases and pulmonary function and given chest x-rays. Anesthesia consisted of thiopental, succinylcholine, N2O, enflurane, and pancuronium. Before incision closure, 6 intercostal spaces were injected by the surgeon with 3 ml of a randomly determined drug mixture. Patients received either bupivacaine and saline solution, bupivacaine and LMW dextran 40, or saline and LMW dextran 40. Arterial blood gases, pulmonary function, chest x-rays, narcotic dosage, sensory level, and subjective responses were evaluated for 3 days postoperatively. Results demonstrate that intercostal nerve blocks can markedly reduce postoperative pain and improve pulmonary function in such patients. Significant differences from controls were seen in Pao2, Paco2, vital capacity, forced expiratory flow rates, analgesic requirements, and patient comfort. The duration of the block with bupivacaine and saline was less than 12 hours, while the mean duration of the block with bupivacaine and dextran 40 was 36 hours.

Aged↗
PubMedDate not supplied

Cardiovascular effects of enflurane and halothane on the rhesus monkey.

Ten rhesus monkeys were chronically instrumented to compare the cardiovascular effects of enflurane and halothane. In 17 experiments, each monkey was evaluated in the awake state and after equilibration at each of many anesthetic levels. End-expired gas concentrations were expressed in multiples of human minimum alveolar concentrations (MAC) for comparison. There was a predictable dose-related decrease in heart rate, mean arterial pressure, peak left ventricular dp/dt, and the latter divided by left ventricular developed pressure (see article) with both agents. Central venous pressure was increased by both. At equal MAC levels, no significant differences were detected between halothane and enflurane. Cardiac output and aortic flow acceleration were obtained on one of the animals for both agents. Results were consistent with those for the other measured parameters.

Animals↗
PubMedDate not supplied

A comparative study of enflurane and halothane using systolic time intervals.

The effects of enflurane and halothane anesthesia on systolic time intervals were studied in 12 healthy patients. Cardiovascular measurements were made at equipotent levels of anesthesia: enflurane 1.23% end-tidal and halothane 0.65% end-tidal. These agents were studied first with 50% N2O and then without N2O. Systolic, diastolic, and mean arterial blood pressure were decreased more by enflurane than by halothane (p less than 0.05). However, halothane caused significantly more myocardial depression than enflurane, as indicated by a larger preejection period (PEP) and preejection period/left ventricular ejection time (PEP/LVET) and a smaller 1/PEP2 and ejection fraction. When N2O was discontinued, both agents increased PEP and PEP/LVET and decreased 1/PEP2 and the ejection fraction.

Adult↗
PubMedDate not supplied

Limitations of the cyanide electrode for use in plasma and whole blood.

Although the cyanide ion-specific electrode has been used for the measurement of cyanide in biologic fluids, its validity has not been documented under these conditions. Therefore, we analyzed 60 paired samples of blood and plasma in a blinded fashion and compared the cyanide ion concentrations obtained from the ion-specific electrode with those obtained from a standard chemical assay. There was poor correlation between results in plasma samples (r = .52, n = 26) and no correlation in whole blood (r = .02, n = 34). Until refinements of the electrode technique are made, this method cannot be recommended for the measurement of cyanide in biologic fluids.

Animals↗