Biomedical subjects

David R Jones

Publications and source records attributed to David R Jones.

93 records · Page 6Linked to original sources

PubMed2002

Pharmacological blockade of the dive response: effects on heart rate and diving behaviour in the harbour seal (Phoca vitulina).

While diving, harbour seals (Phoca vitulina) manage their oxygen stores through cardiovascular adjustments, including bradycardia, a concurrent reduction in cardiac output, and peripheral vasoconstriction. At the surface, post-dive tachycardia facilitates rapid reloading of oxygen stores. Although harbour seals can tolerate >20 min of submergence, the majority of their natural dives are only 2-6 min and are usually followed by surface intervals that are <1 min, so they spend approximately 80% of their time submerged. Given that harbour seals meet their ecological needs through repetitive short aerobic dives, we were interested in the functional role, if any, of the dive response during these short dives. During voluntary diving in an 11 m deep tank, the cardiovascular responses to submergence of five harbour seals were manipulated using specific pharmacological antagonists, and the effects on diving behaviour were observed. Effects of pharmacological blockade on heart rate were also examined to assess the autonomic control of heart rate during voluntary diving. Heart rate was recorded using subcutaneous electrodes and data loggers, while diving behaviour was monitored using a video camera. The muscarinic blocker methoctramine blocked diving bradycardia, the alpha-adrenergic blocker prazosin blocked diving vasoconstriction, and the beta-adrenergic blocker metoprolol blocked post-dive tachycardia. Heart-rate analysis indicated that diving bradycardia is primarily modulated by the vagus, while post-dive tachycardia results from parasympathetic withdrawal as well as increased sympathetic stimulation of the heart. None of the pharmacological blockers had any effect on average dive or surface interval duration. Seals maintained a high percentage of time spent diving in all treatments. Thus, harbour seals do not appear to need the dive response during short dives in order to maintain an efficient dive strategy.

Adrenergic alpha-Antagonists↗

PubMedDate not supplied

A comparative study of the effects of molsidomine and 3-morpholinosydnonimine on the redox status of rat erythrocytes and reticulocytes.

After enzymic biotransformation, molsidomine (MO) acts via the metabolite 3-morpholinosydnonimine (SIN-1) through spontaneous liberation of nitric oxide (NO) and superoxide (O(2)(.-)). The aim of this study was to compare the effects of MO and its active metabolite SIN-1 on the redox status of rat erythrocytes and reticulocytes. Rat erythrocyte as well as reticulocyte-rich red blood cell (RBC) suspensions were aerobically incubated (2 h, 37 degrees C) without (control) or in the presence of different concentrations of MO or SIN-1. In rat erythrocytes, biotransformation of MO resulted in the production of NO and nitroxyl (NO(-)). Endogenous superoxide anion (O(2)(.-)) participated in peroxynitrite generation. SIN-1 simultaneously liberated NO and O(2)(.-), which formed peroxynitrite (at least in part), but the liberated NO predominantly reacted with haemoglobin, forming methaemoglobin in erythrocytes. In reticulocytes, MO and SIN-1 caused an increase in the levels of both nitrite and 3-nitrotyrosine (an indicator of peroxynitrite), whereas they decreased the level of O(2)(.-). In reticulocytes, MO was metabolized into SIN-1 which led to the generation of NO, which reacted with O(2)(.-) (endogenous or exogenous) forming reactive nitrogen species. In conclusion, there are two metabolic pathways for MO biotransformation: one causing NO and NO(-) generation predominantly in erythrocytes and the other, via SIN-1 metabolism, in reticulocytes. The main difference between the action of MO and SIN-1 was that the latter caused oxidative damage in RBCs.

Animals↗

PubMedDate not supplied

Laparoscopic gastric bypass complicated by gastric pouch necrosis: considerations in gastroesophageal reconstruction.

Gastric pouch necrosis and intraabdominal sepsis is an uncommon complication following laparoscopic gastric bypass. The intraoperative management of this complication centers on resection of the necrotic pouch, esophageal diversion, drainage, and enteral access for nutrition. Reestablishing gastrointestinal continuity at a later surgery following this complication can be challenging. We present a case in which the colon was found to be unacceptable for use in reconstruction; the remaining stomach was used as the conduit for a transhiatal reconstruction of gastrointestinal continuity instead.

Adult↗