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Biomedical subjects

D E Longnecker

Publications and source records attributed to D E Longnecker.

At least 55 records · Page 3Linked to original sources
PubMed1984

Methylprednisolone plus ibuprofen increases mortality in septic rats.

Steroids and cyclooxygenase inhibitors have been advocated as adjunctive treatment for sepsis. We studied the influences of these treatments on the survival of 98 male Sprague-Dawley rats in which sepsis was induced by cecal ligation and puncture. Rats received one of four treatments: sodium chloride (NaCl); methylprednisolone, 30 mg/kg (MP); ibuprofen, 12.5 mg/kg (I); methylprednisolone, 30 mg/kg, plus ibuprofen, 12.5 mg/kg (MP + I). Cumulative survival statistics were determined daily for 14 days thereafter. Survival was not altered by either MP or I when compared to animals receiving NaCl only. However, the combination of MP + I increased mortality from day 2 through day 14. The authors conclude that (1) MP administration alone does not increase mortality in septic rats; therefore, the results do not support the contention that steroid treatment in the absence of antibiotic therapy may be detrimental; (2) the cyclooxygenase inhibitor I does not improve survival in septic rats; and (3) the combined administration of MP and I increases mortality in septic rats and the possibility that this combination might be harmful in septic patients should be considered also.

Animals↗
PubMed1982

Anesthetic influence on arteriolar diameters and tissue oxygen tension in hemorrhaged rats.

Arteriolar diameters and tissue oxygen tensions were measured in the cremaster muscles of 68 hemorrhaged rats which were anesthetized with either intramuscular ketamine, 125 mg/kg, plus 30 mg/kg supplements as needed, or enflurane, 2.2% inspired. Animals breathed room air, or room air plus enflurane, throughout the experiments. Arterioles in the cremaster muscle were identified according to successive orders of branching, and the internal diameters of first-, third-, and fourth-order vessels were measured at 30-s intervals. Cremaster muscle oxygen tension was measured polarographically with platinum-iridium microelectrodes. Mean arterial pressure was controlled at 30-35 mmHg during 30 min of hemorrhage, and maximum shed blood volumes were similar (2.6 ml/100 g) in both groups. Principal responses to hemorrhage in rats receiving enflurane were 1) constriction in first-, third-, and fourth-order arterioles, and 2) tissue hypoxia. In hemorrhaged rats receiving ketamine, the constrictor response to hemorrhage either was diminished (first-, and third-order arterioles) or abolished (fourth-order arterioles), and tissue hypoxia did not occur. The authors conclude that ketamine, as compared with enflurane, diminishes or prevents arteriolar constriction and tissue hypoxia in the cremaster muscle of hemorrhaged rats.

Anesthetics↗
PubMed1981

Effects of propranolol on the cardiovascular and renin-angiotensin systems during hypotension produced by sodium nitroprusside in humans.

The authors examined the effects of controlled hypotension induced with sodium nitroprusside (SNP) with and without propranolol on the cardiovascular, pulmonary, and renin-angiotensin systems in 10 consecutive anesthetized patients with kyphoscoliosis undergoing posterior spinal fusion. SNP infusion (4.1 microgram . kg-1 . min-1) alone decreased mean systemic arterial pressure (SAP) by 25 torr +/- 3 SE (P less than 0.001), systemic vascular resistance index (SVRI) by 1113 dyne . sec. cm-5 . m2 +/- 125 SE (P less than 0.001), mean pulmonary artery pressure (PAP) by 6 torr +/- 2 SE (P less than 0.02), pulmonary capillary wedge pressure (PCWP) by 4 torr +/- 1 SE (P less than 0.01), pulmonary vascular resistance (PVR) by 50 dyne . sec . cm-5 +/- 18 (P less than 0.05), and PaO2 by 16 torr +/- 7 SE (P less than 0.05), whereas cardiac index increased by 1.08 l . min-1 . m2 +/- 0.24 SE (P less than 0.01) and heart rate increased 16 beats/min +/- 5 SE (P less than 0.02). After 40 min of hypotension, 0.03 mg/kg propranolol was injected intravenously while the SNP infusion rate was held constant. Ten min later there was a significant decrease in the heart rate (10 beats/min +/- 4 SE, P less than 0.02) and cardiac index (0.65 l . min-1 . m-2 +/- 0.21, P less than 0.02). Plasma renin activity (PRA) increased from 2.37 ng . ml-1 . h-1 +/- 0.7 SE before anesthesia to 6.50 ng . ml-1 . h-1 +/- 1.45 SE (P less than 0.05) after 40 min of nitroprusside infusion. Forty min after propranolol there was a significant reduction in PRA to 4.07 ng . ml-1 . h-1 +/- 0.73 SE (P less than 0.05). Thus propranolol, when given during SNP hypotension, exhibits an early cardiovascular response manifested as a decrease in cardiac output and heart rate and a delayed action of the kidney resulting in an inhibition of renin release.

Adolescent↗
PubMed1980

Microcirculatory actions of general anesthetics.

General anesthesia, either with the inhalation or the nonvolatile anesthetics, results in significant changes in the microvasculature. The anesthetics alter microvascular diameters in the resting animal and they change the responses to stress (i.e., catecholamine stimulation or hemorrhage) also. Alterations in the microvasculature involve primarily changes in the diameters of arterioles and venules and these, combined with the associated changes in arterial pressure and cardiac output, are responsible for the changes in organ blood flow that occur during general anesthesia. General anesthetics alter the in vivo vascular smooth muscle responses to topically applied vasoactive substances such as epinephrine or norepinephrine. The microvascular responses to hemorrhage are altered by the anesthetics and the changes are most pronounced in the smaller (approximately 20 micrometers) arterioles. Anesthetic influences on the microcirculation are unique for each agent and are not the result of the general state of narcosis. Anesthetic influences on the microvasculature are both dose-dependent and tissue-specitic. The peripheral vascular effects of the anesthetics may influence the choice of anesthesia and may alter the results of experimental investigations performed in anesthetized animals.

Anesthetics↗
PubMed1979

Influence of anaesthetic agents on the survival of rats following acute ischaemia of the bowel.

We compared the effects of ketamine and halothane anaesthesia on the survival of rats subjected to superior mesenteric artery occlusion. Survival was significantly greater with halothane. Animals anaesthetized with ketamine developed arterial hypocarbia during bowel ischaemic shock, while those receiving halothane did not. Arterial hypoxaemia was not present in either group. Haematocrits increased in both groups following bowel ischaemia. Excess lactate was increased significantly in non-survivors compared with survivors. The survival data contrast with previous results obtained after haemorrhagic hypotension and emphasize the need to consider differing therapeutic approaches in the various shock states.

Anesthesia, Inhalation↗
PubMed1979

Halothane mimics oxygen in oxygen microelectrodes.

The effects of halothane and enflurane on the polarographic measurement of oxygen with five platinum and three gold microelectrodes were examined. Oxygen microelectrodes were calibrated in saline solution equilibrated with either nitrogen (N2) or air, then either halothane, 1.0 per cent, or enflurane, 2.0 per cent, was added to the gas mixture. For each electrode, polarographic curves were determined during exposure to five equilibrating gas mixtures: N2, air, N2 plus halothane, air plus halothane, and N2 plus enflurane. Halothane variably increased the current produced (and therefore the estimated oxygen tension) at all polarizing voltages in saline solution equilibrated with either N2 or air. The effect was present in both conical platinum electrodes and recessed-tip gold electrodes and was not prevented by membrane coatings of polystyrol, Rhoplex or collodion. Enflurane did not alter the polarographic measurement of oxygen. It is concluded that tissue oxygen tension measurements, made with these microelectrodes and membranes, may be unreliable in the presence of halothane.

Calibration↗
PubMed1979

Renin response to hemorrhage in awake and anesthetized rats.

Anesthetic agents have been shown to alter survival in animals subjected to hemorrhage. Since survival after hemorrhage is increased by inhibitors of the renin-angiotensin system, we asked whether anesthetic agents altered renin release during hemorrhage. We studied 33 rats which were subjected to one hour of hemorrhagic hypotension at a mean arterial pressure of 40 mm Hg. Animals were either awake or anesthetized with halothane or ketamine. Anesthesia alone did not alter plasma renin activity (PRA), whereas hemorrhage resulted in approximately a ten-fold increase in PRA in both awake and anesthetized animals. After the shed blood was returned to the animal, intravenous saralasin, an angiotensin II competitive inhibitor, produced a 21-24 mm Hg decrease in blood pressure in all animals, regardless of the severe hemorrhage is unaltered by halothane or ketamine anesthesia, that the renin-angiotensin system provides a similar amount of blood pressure support in both awake and anesthetized animals, and that the anesthetic influence on survival following severe hemorrhage does not result from anesthetic-induced alterations of the renin-angiotensin system.

Animals↗
PubMed1978

Alterations in venous compliance in hemorrhagic shock.

Nine dogs and one primate were placed on total cardiopulmonary bypass and subjected to a simulated hemorrhagic shock procedure. Venous compliance was determined by occluding the venous outflow catheters; venous flow and pressure drop were used to calculate resistance. Individual measurements were made for the superior (SVC) and inferior vena caval (IVC) beds. During hypotension, compliance increased equally in the SVC and IVC; following reinfusion, IVC compliance was consistently lower than SVC compliance. Resistance of the sVC system increased slightly more rapidly during early hypotension than did that of the IVC, but SVC resistance then decreased and remained significantly below that of the IVC system throughout the posthypotension period. These results are interpreted as indicating a different response of the two vascular beds, particularly an increase in IVC arteriolar resistance with a decrease in venous tone. To the extent that the splanchnic bed contributes to the IVC system changes, they are contrary to the concept of a maintained venous tone and decreased arteriolar tone after hemorrhagic shock.

Animals↗
PubMed1976

Sensitivity of small subcutaneous vessels to altered respiratory gases and local pH.

Television microscopy was used to quantitate the responses of small arteries and veins, in the wings of unanesthetized bats, to alterations in the inspired concentrations of O2 and CO2. Mean arterial pressure, heart rate, and the diameters of small arteries (28-54 mum) and veins (50-128 mum) were measured during a 90-min protocol--30 min with an inspiratory gas mixture of 20% O2 and 80% N2 (control period); 30 min with a gas mixture containing 5% O2 (hypoxic period) or 12, 20, or 28% CO2 (hypercapnic period); and 30 min with the original control gas. The hypoxic responses were dilatation of arteries and no change in the veins in both innervated and surgically denervated wings. Hypercapnia resulted in artery dilatation in innervated wings. Hypercapnia resulted in artery dilatation in innervated wings and constriction in denervated wings. The veins constricted in both innervated and denervated wings during the hypercapnia period. In another series, topical application of Krebs solutions (pH ranging from 7.7 to 6.7) to exposed segments of small arteries and veins produced dilatation of both vessels with decreasing pH. Artery dilatation during hypoxia and vein constriction during hypercapnia involve non-neural mechanisms, while both a neural stimulus for dilatation and a non-neural stimulus for constriction are components in the response of innervated arteries to hypercapnia. The non-neural stimulus for artery and vein constriction during hypercapnia is not a local decrease in pH.

Animals↗
PubMed1976

Influence of anesthetic agent on survival following hemorrhage.

One hundred and twenty-eight Sprague-Dawley rats were each anesthetized with one of four anaesthetics and subjected to a standard hemorrhage protocol to determine the effects of anesthetics on survival following hemorrhage. The anesthetics studied were: halothane, 1.26 vol per cent; fluroxene, 4.5 vol per cent; pentobarbital, 50 mg/kg ip; ketamine, 125 mg/kg, im. Mean arterial pressure was conrolled at 40 torr during 60 minutes of hemorrhage. Cumulative survival rates were determined at the end of hemorrhage and 24 hr, 48 hr, 72 hr, and 7 days after hemorrhage. Twenty-four-hour survival rates were: halothane, 50.0 per cent; fluroxene, 56.3 per cent; pentobarbital, 59.4 per cent; ketamine, 84.4 per cent. Seven-day survival rates were: halothane, 46.9 per cent; fluroxene, 18.7 per cent; pentobarbital, 53.1 per cent; ketamine; 81.3 per cent. Survival rates were significantly higher (P less than 0.05) in animals anesthetized with ketamine compared with survival rates associated with the other anesthetics. Long-term (72-hr and seven-day) survival rates were significantly (P less than 0.05) lower in animals anesthetized with fluroxene. Microscopic examination of livers and small intestines revealed significantly fewer (P less than 0.05) athologic changes in the splanchnic organs of hemorrhaged rats anesthetized with ketamine compared with animals anesthetized with the other drugs.

Anesthetics↗