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Biomedical subjects

D S Prough

Publications and source records attributed to D S Prough.

At least 127 records · Page 7Linked to original sources
PubMed1988

Theophylline effect on the cerebral blood flow response to hypoxemia.

Cerebral oxygen delivery (CO2D) remains nearly constant over a wide range of cerebral perfusion pressure and arterial oxygen content. In response to a decrease in arterial oxygen content secondary to hypoxemia, cerebral blood flow (CBF) increases, a response likely mediated by the release of adenosine. We studied the effect of theophylline, a potent adenosine antagonist, on CBF and cerebral oxygen delivery (CO2D) during hypoxemia in five healthy adult male volunteers. The CBF was measured using 133Xe clearance under conditions of (1) normoxemia (O2 saturation greater than 95 percent); (2) hypoxemia (O2 saturation = 80 percent); (3) normoxemia following aminophylline (the ethylene diamine salt of theophylline) 6 mg/kg intravenously; and (4) hypoxemia following aminophylline. Aminophylline decreased CBF and CO2D during both normoxemia and hypoxemia, but did not prevent the increase in CBF accompanying hypoxemia, suggesting that the increase in CBF in response to hypoxemia may not be mediated by adenosine or that customary doses of aminophylline are insufficient to inhibit adenosine-mediated cerebral vasodilation in response to hypoxemia. The significant decrease in CBF and CO2D observed following aminophylline is potentially clinically important and should be considered in the selection of bronchodilator therapy.

Adult↗
PubMed1988

Effects of nimodipine on the production of thromboxane A2 following total global cerebral ischemia.

To clarify the contribution of vasoconstrictor prostaglandins to the hypoperfusion state typically following total global cerebral ischemia, 14 mongrel dogs were subjected to 11 minutes of global cerebral ischemia. They were then randomly assigned to receive either no treatment or an intravenous bolus of the calcium channel blocker nimodipine, 10 micrograms/kg, 15 minutes after ischemia followed by a continuous infusion of nimodipine, 1.0 micrograms/kg/min. Thromboxane (Tx) A2 production, as measured by cerebral venous levels of TxB2 (the stable metabolite of TxA2) increased similarly in the two groups. In contrast to previous studies, mean postischemic cerebral blood flow did not increase sufficiently in the nimodipine-treated group to achieve statistical significance. These data suggest that the improved neurological outcome associated with nimodipine treatment following global cerebral ischemia does not relate to reduced levels of the prostaglandin precursor arachidonate.

Animals↗
PubMed1988

Monitoring renal function.

Acute renal failure is a common cause of morbidity and mortality in critically ill patients. The prompt, effective management of acute oliguria, frequently the presenting sign of renal deterioration, remains difficult because of the lack of suitable monitors. No monitor presently in common use is sufficiently specific, sensitive, or rapidly available to satisfy clinical needs.

Acute Kidney Injury↗
PubMed1988

Monitoring hepatic function.

Hepatic function can be monitored using exogenous (e.g., sulfobromophthalein, indocyanine green, antipyrine, aminopyrine, galactose) and endogenous substances (e.g., bile acids, PT/PTT, albumin, ammonia, bilirubin). Test of hepatic necrosis include aspartate aminotransferase, and alanine aminotransferase. The hepatobiliary system can be assessed using alkaline phosphatase, 5'-nucleotidase, gamma-glutamyl transpeptidase, ultrasound, and iminodiacetic acid scans.

Humans↗
PubMed1988

Triiodothyronine (T3) antagonizes adverse effects of high circulating reverse-T3 (rT3) during hemorrhagic shock.

To examine whether triiodothyronine (T3) could counteract the lethal effect of exogenous reverse T3 (rT3) in hemorrhagic shock, 21 anesthetized, heparinized mongrel dogs were given 15 micrograms/kg of rT3 IV. Thirty minutes later, the dogs were bled rapidly into a reservoir to achieve and maintain a mean arterial pressure of 40 mm Hg. After 60 minutes at 40 mm Hg (compensated shock), the reservoir line was clamped for 30 minutes (uncompensated shock). The shed blood was then reinfused over 30 minutes, and the dogs were monitored for an additional 60 minutes. At the start of uncompensated shock, 11 dogs were given at least 15 micrograms/kg of T3 IV, and 10 animals received saline. Before T3 treatment, there were no significant intergroup differences in the measured hemodynamic and blood gas variables. In the untreated group, 8 of 10 dogs (80%) died during uncompensated shock, in comparison to 3 of 11 dogs (27%) that received T3 (P less than 0.01). Long-term survival in the T3 group was 5/11 (45%), significantly higher than that (1/10, 10%) in the untreated group (P less than 0.05). These results, interpreted in relationship to previous studies, suggest that the therapeutic efficacy of T3 in canine hemorrhagic shock may be related to antagonism of adverse effects of endogenous rT3.

Animals↗
PubMed1988

Cardiac electrophysiologic effects of fentanyl and combinations of fentanyl and neuromuscular relaxants in pentobarbital-anesthetized dogs.

The effects of fentanyl, both alone and in combination with pancuronium bromide or succinylcholine, on atrioventricular (AV) node and ventricular conduction times and refractory periods were studied. Twenty-four pentobarbital-anesthetized dogs were instrumented both with an intraaortic catheter to measure cardiac conduction times and, through a thoracotomy, with atrial and ventricular epicardial pacing electrodes to provide premature stimulation that would allow measurement of atrial and ventricular refractoriness. Fentanyl prolonged the RR interval in both low- (100 micrograms/kg) and high-dose (400 micrograms/kg) groups by 26 and 45%, respectively, and prolonged AV node conduction time by 28 and 25%, respectively. During atrial pacing at a rate sufficient to capture the atria, AV node conduction time lengthened in the low- and high-dose groups by 27 and 25%, respectively. Fentanyl also significantly lengthened AV node effective and functional refractory periods and ventricular effective refractory periods in both groups. Pancuronium (0.1 mg/kg) administered after fentanyl shortened RR intervals in the low- and high-dose groups by 14 and 22%, respectively, and shortened AV conduction times by 18 and 20%, respectively, but did not restore all values to baseline. Pancuronium significantly shortened AV node refractory periods in the low-dose but not the high-dose group. When administered after fentanyl, succinylcholine (2 mg/kg) significantly shortened the RR interval in the low- and high-dose groups by 14 and 12%, respectively. Succinylcholine shortened AV node conduction slightly but without significance and had no effect on cardiac refractoriness. His-Purkinje conduction remained unaffected by any drug intervention. These data demonstrate that fentanyl depresses cardiac conduction; subsequent administration of pancuronium and succinylcholine partially reverses this effect.

Animals↗
PubMed1987

Effects of resuscitation from hemorrhagic shock on cerebral hemodynamics in the presence of an intracranial mass.

This study compares intracranial pressure, cerebral blood flow, and cerebral oxygen transport during hemorrhagic shock and following fluid resuscitation with crystalloid or colloid solution in a canine model with an epidural mass lesion. After placement of an epidural balloon, intracranial pressure was increased to 30 mm Hg for 5 minutes and then permitted to vary without further manipulation. Hemorrhagic shock was produced by the rapid removal of blood to achieve a mean arterial pressure of 55 mm Hg for 30 minutes. Resuscitation then was performed with intravenous lactated Ringer's solution, 60 ml/kg, or with 6.0% hetastarch, 20 ml/kg. Following both solutions mean arterial pressure and cardiac output were increased and hemoglobin concentration was reduced. Intracranial pressure was significantly lower immediately after resuscitation in the hetastarch group; it then gradually increased so that the difference was much less 1 hour later. Cerebral blood flow decreased during shock and was not restored by either fluid; cerebral oxygen transport fell further with resuscitation in both groups due to hemodilutional reductions in hemoglobin. Although colloid resuscitation improved systemic hemodynamics and maintained lower intracranial pressure, it failed, as did crystalloid resuscitation, to restore cerebral oxygen transport to prehemorrhagic shock levels.

Animals↗
PubMed1987

The effect of aminophylline on cerebral blood flow in patients with chronic obstructive pulmonary disease.

Aminophylline has been shown to produce a reduction in cerebral blood flow (CBF) in animal models and patients with neurologic symptoms or signs. The effect of aminophylline on regional CBF (rCBF) in patients with chronic obstructive pulmonary disease (COPD) has not previously been reported to our knowledge. We studied the effect of loading and maintenance infusions of aminophylline on CBF in five subjects with moderate to severe COPD. rCBF was determined in eight homologous regions of each cerebral hemisphere at three intervals: (1) baseline; (2) following the IV loading dose of aminophylline (6.0 mg/kg body weight); and (3) early and late in the maintenance infusion (0.5 mg/kg/hr) period. Aminophylline loading caused a 26 percent reduction (p = 0.005) in mean rCBF from 40.6 +/- 5.2 (SD) ml/100 g/min to 30.1 +/- 6.0 ml/100 g/min. A 23 percent reduction (31.5 +/- 6.9 ml/100 g/min) persisted throughout the maintenance phase. Thus, aminophylline, as customarily used in subjects with COPD, is associated with a significant reduction in rCBF.

Adult↗
PubMed1986

Response of cerebral blood flow to changes in carbon dioxide tension during hypothermic cardiopulmonary bypass.

Changes in cerebral blood flow (CBF) in response to changes in PaCO2 were measured by intraaortic injection of 133Xe in 12 patients during hypothermic (23-30 degrees C) cardiopulmonary bypass. In each patient, CBF was determined at two randomly ordered levels of PaCO2 obtained by varying the rate of gas inflow into the pump oxygenator (Group I, n = 6) or by varying the percentage of CO2 added to the gas inflow (Group II, n = 6). Nasopharyngeal temperature, mean arterial pressure, pump-oxygenator flow, and hematocrit were maintained within a narrow range. In group I, a PaCO2 (uncorrected for body temperature) of 36 +/- 4 mmHg (mean +/- SD) was associated with a CBF of 13 +/- 5 ml X 100 g-1 X min-1, while a PaCO2 of 42 +/- 4 mmHg was associated with a CBF of 19 +/- 10 ml X 100 g-1 X min-1. In group II, a PaCO2 of 47 +/- 3 mmHg was associated with a CBF of 20 +/- 8 ml X 100 g-1 X min-1, and a PaCO2 of 53 +/- 3 mmHg was associated with a CBF of 26 +/- 9 ml X 100 g-1 X min-1. Within group I, the difference in CBF was significant (P less than 0.05); within group II, the difference in CBF was significant at the P less than 0.002 level. All CBF measurements were lower than those reported for normothermic, unanesthetized subjects of similar age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Cerebral hemodynamics after hemorrhagic shock: effects of the type of resuscitation fluid.

Cerebral blood flow (CBF), cerebral oxygen delivery, and intracranial pressure were measured in 12 dogs subjected to hemorrhagic shock and then resuscitated with lactated Ringer's solution or 6% hetastarch. Hemorrhagic shock was produced by the rapid removal of blood to achieve a mean arterial pressure (MAP) of 40 mm Hg with BP maintained at that level for 30 min. Six animals were resuscitated with lactated Ringer's solution, 60 ml/kg iv, and six with 6% hetastarch, 20 ml/kg iv. Both solutions effectively restored systemic hemodynamic stability, increasing cardiac output and MAP. Intracranial pressure was significantly (p less than .05) lower after resuscitation in the hetastarch group, but CBF, which had decreased during shock, was not normalized by either fluid, and cerebral oxygen transport fell further with resuscitation secondary to a hemodilutional reduction of hemoglobin. Although 6% hetastarch may improve systemic hemodynamics and maintain a low intracranial pressure during resuscitation, it fails, as does lactated Ringer's solution, to restore cerebral oxygen transport to prehemorrhagic shock levels.

Animals↗
PubMed1986

Effects of hypertonic saline versus lactated Ringer's solution on cerebral oxygen transport during resuscitation from hemorrhagic shock.

Hypertonic saline successfully restores systemic hemodynamics in dogs and humans with severe hemorrhagic shock and, in contrast to lactated Ringer's solution, does not increase intracranial pressure (ICP). This study compares cerebral oxygen delivery in 12 dogs subjected to hemorrhagic shock by the rapid removal of blood (mean arterial pressure of 40 mm Hg maintained for 30 minutes), and then resuscitated with lactated Ringer's solution (six dogs) or 7.5% saline solution (six dogs) to restore systolic arterial pressure. Both solutions effectively restored systemic hemodynamic stability, increasing cardiac output and systolic blood pressure while decreasing mean and diastolic arterial pressure and systemic vascular resistance. The ICP was significantly lower after resuscitation in the hypertonic saline group (p less than 0.05), but cerebral blood flow, which had decreased during shock, was not restored by either fluid, and cerebral oxygen transport fell further secondary to a hemodilutional reduction of hemoglobin. Although hypertonic saline may improve systemic hemodynamics and maintain a low ICP during resuscitation, it fails, as does Ringer's solution, to restore cerebral oxygen transport to prehemorrhagic shock levels.

Animals↗
PubMed1986

Nosocomial pulmonary infection: possible etiologic significance of bacterial adhesion to endotracheal tubes.

Biomaterials are essential for life support and monitoring of critically ill patients, but their use increases the risk of nosocomial infection. Of the various plastics used for life support and monitoring devices, polyvinylchloride is one to which bacteria most readily adhere. Through the use of qualitative culture techniques and scanning and transmission electron microscopy, we studied the surfaces of polyvinylchloride endotracheal tubes removed from 25 ICU patients, to determine if bacterial adhesion to those tubes was sufficient to provide a possible source for repeated contamination of the tracheobronchial tree. Of the surfaces studied, 16% were partially covered and 84% were completely covered by an amorphous bacteria-containing matrix. Some biofilm-enclosed bacterial aggregates projected from the matrix into the lumen of the tube. The mechanism by which endotracheal tubes repeatedly inoculate the lungs of intubated patients may prove to be dislodgment of such aggregates by suction apparatus.

Adult↗
PubMed1985

Adult respiratory distress syndrome secondary to ethylene glycol ingestion.

Presented is a case of ethylene glycol poisoning in a 24-year-old man who subsequently developed adult respiratory distress syndrome. The noncardiogenic nature of the patient's pulmonary edema was documented with hemodynamic monitoring, and a successful outcome was achieved with hemodialysis, ethanol, and intermittent mechanical ventilation with positive end-expiratory pressure.

Adult↗