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Biomedical subjects

E Khan

Publications and source records attributed to E Khan.

26 records · Page 2Linked to original sources
PubMed1987

Propranolol increases oxygen utilization during hypoxia.

The effects of propranolol on whole body oxygen consumption and blood oxygen content were measured in the dog during extreme hypoxic conditions. At 9% inspired oxygen four of eight control animals died within 40 min. An identical second group was pretreated with propranolol and none died during the same hypoxic stress. Hypoxia decreased oxygen consumption in both groups, but the decrease was less in the propranolol-pretreated dogs. A second set of 16 dogs was ventilated with 10% oxygen and all animals survived. A similar, although less pronounced, effect on oxygen consumption was noted and propranolol once again lessened the hypoxia-induced decrease in oxygen consumption. With hypoxaemia, metabolic acidosis developed in all animals and the arterio-venous oxygen content difference decreased; however, propranolol lessened the acidosis and the decrease in arterio-venous oxygen content difference. We conclude that, during hypoxia, propranolol increases oxygen utilization by the tissues and this might account for better survival.

Animals↗
PubMed1984

Propranolol premedication blunts stress response to nitroprusside hypotension.

Hypotension was induced in sixteen patients with nitroprusside during anesthesia for surgical correction of cerebral aneurysms. Eight patients were premedicated with propranolol (180 mg orally) for one day and the other eight were not. Before the start of anesthesia, the untreated patients had a mean arterial pressure of 102 +/- 3 mm Hg, a heart rate of 76 +/- 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 114 +/- 21 and 258 +/- 34 pg/ml, respectively. The propranolol-premedicated patients came to the operating room in a significantly different clinical state with a mean arterial pressure of 92 +/- 3 mm Hg, a heart rate of 71 +/- 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 76 +/- 28 and 144 +/- 28 pg/ml. During induced hypotension, plasma epinephrine and norepinephrine concentrations increased significantly in both groups (454 +/- 42 and 730 +/- 58 pg/ml in the untreated patients, 160 +/- 48 and 419 +/- 67 pg/ml in the propranolol premedicated patients), but the increase in catecholamines was significantly greater in the untreated patients. Thirty minutes after nitroprusside was discontinued, epinephrine and norepinephrine concentrations were higher than in the awake state in untreated patients and were associated with rebound hypertension and tachycardia. In contrast, in propranolol-premedicated patients, plasma epinephrine and norepinephrine concentrations decreased towards the preanesthesia values, mean arterial pressure gradually returned to the prehypotension level, and heart rate remained unchanged. This study thus demonstrates that propranolol premedication attenuates the release of catecholamines in response to nitroprusside-induced hypotension.

Adult↗
PubMed1981

Propranolol alters renin release during nitroprusside-induced hypotension and prevents hypertension on discontinuation of nitroprusside.

Ten patients who received hypotensive anesthesia for surgical correction of a cerebral aneurysm were pretreated for 1 day with propranolol. In the awake state, before start of anesthesia, mean arterial pressure was 91 +/- 3 torr and plasma renin activity 3.0 +/- 0.1 ng/ml/hr. Thirty minutes after the induction of anesthesia mean arterial pressure decreased to 79 +/- 2 torr and plasma renin activity increased to 3.5 +/- 0.1 ng/ml/hr. There was no further significant change in either measurement with surgical stimulation. During sodium nitroprusside-induced hypotension (the dose used was 0.35 +/- 0.02 mg/kg) mean arterial pressure was reduced to 53 +/- 2 torr, and plasma renin activity increased to 8.8 +/- 0.9 ng/ml/hr. Heart rate did not change. Discontinuation of sodium nitroprusside resulted in a gradual reduction of plasma renin activity to the awake level and concurrent gradual increase in mean arterial pressure to its basal anesthetic value. When compared with previous work, these results indicate that propranolol attenuates nitroprusside-induced renin release, reduces the dosage of nitroprusside required to induce hypotension, suppresses reflex tachycardia, and prevents overshoot hypertension on discontinuation of nitroprusside.

Adult↗
PubMed1979

Hypertension during anesthesia on discontinuation of sodium nitroprusside-induced hypotension.

The authors had observed that on intraoperative discontinuation of sodium nitroprusside being administered to induce hypotension, mean arterial pressure increased to above the pre-hypotension level. Twelve patients who recieved hypotensive anesthesia for surgical correction of cerebral aneurysms were studied to evaluate the role of the renin-angiotensin system in this phenomenon. In the awake state, mean arterial pressure was 100 +/- 2 torr and plasma renin activity 3.0 +/- 0.1 ng/ml/hr. Thirty minutes after the establishment of stable halothane-nitrous oxide anesthesia, mean arterial pressure decreased to 85 +/- 1 torr and plasma renin activity increased to 4.4 +/- 0.1 ng/ml/hr. No appreciable change in either occurred over the next two hours of operation. During sodium nitroprusside-induced hypotension, mean arterial pressure decreased to 49 +/- 2 torr and plasma renin activity increased to 15.2 +/- 0.2 ng/ml/hr. Thirty minutes after discontinuation of sodium nitroprusside administration, mean arterial pressure increased to 112 +/- 2 torr, which was not only higher than the prehypotension level, but also significantly higher than that recorded in the awake state. Plasma renin activity at that time was 10.9 +/- 0.1 ng/ml/hr. As the half-life of plasma renin is 15 min, the data suggest that the persistently increased plasma renin activity is probably responsible for the increase of arterial pressure following sodium nitroprusside-induced hypotension.

Adolescent↗
PubMedDate not supplied

Use of biodegradable dissolved organic carbon to assess treatment process performance in relation to solids retention time.

A biodegradable dissolved organic carbon (BDOC) method has been developed and used to analyze secondary- and advanced-treated wastewater effluents and to investigate correlations between residual organic content and the solids retention time (SRT). Conventional biochemical oxygen demand (BOD) bottles and a 28-day incubation period were used. Secondary wastewater effluents from Hawaii were found to contain between 9.0 and 14.0 mg/L of dissolved organic carbon (DOC), of which 23 to 35% was biodegradable in the 28-day BDOC test (from a survey of nine treatment plants). Bench-scale, continuous-flow activated-sludge biological reactors treating synthetic wastewater were operated at SRTs between 2 and 15 days, and effluent BDOCs were determined. A good BDOC prediction equation was developed that incorporates the initial DOC, the DOC remaining after 5 days, and the SRT of the system from which the sample originated. This equation can be used to determine the BDOC value using data that can be obtained during a conventional 5-day BOD test. The determined equation was found to be appropriate for some of the full-scale wastewater effluent survey data.

Biodegradation, Environmental↗
PubMedDate not supplied

Monitoring of bacterial morphology for controlling filamentous overgrowth in an ultracompact biofilm reactor.

This research was part of a study of filamentous growth and control in an ultracompact biofilm reactor (UCBR). Morphologies of biofilm and filamentous bacteria in the UCBR were investigated. Ethanol was used as a substrate and sodium hypochlorite was applied as a toxicant to control filamentous growth. The results indicated that factors such as chemical oxygen demand, surface loading rate, pH, and dissolved oxygen could initiate filamentous overgrowth in the UCBR. Different biofilm and filamentous morphologies in the UCBR were observed under different operational conditions. Chlorination was an effective approach to control filamentous growth during and after biofilm formation. Proper chlorine dosing had no effect on biofilm, but killed filaments. Overdose of chlorine damaged biofilm and caused adverse effects such as low treatment efficiency, media clogging and washout, and biofilm color change in the reactor. Frequent monitoring of the morphologies of filaments and biofilm was needed during chlorination to prevent chlorine overdose.

Bacteria↗