Biomedical subjects

J W Esther

Publications and source records attributed to J W Esther.

3 recordsLinked to original sources

PubMed1992

Differential effects of general anesthesia on cGMP-mediated pulmonary vasodilation.

We investigated the effects of an intravenous (pentobarbital sodium) and an inhalational (halothane) general anesthetic on guanosine 3',5'-cyclic monophosphate- (cGMP) mediated pulmonary vasodilation compared with responses measured in the conscious state. Multipoint pulmonary vascular pressure-flow plots were generated in the same nine dogs in the fully conscious state, during pentobarbital sodium anesthesia (30 mg/kg iv), and during halothane anesthesia (approximately 1.2% end tidal). Continuous intravenous infusions of bradykinin (2 micrograms.kg-1.min-1) and sodium nitroprusside (5 micrograms.kg-1.min-1) were utilized to stimulate endothelium-dependent and -independent cGMP-mediated pulmonary vasodilation, respectively. In the conscious state, both bradykinin and nitroprusside decreased (P less than 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary arterial wedge pressure) over the entire range of flows studied; i.e., bradykinin and nitroprusside caused active flow-independent pulmonary vasodilation. Pulmonary vasodilator responses to bradykinin (P less than 0.01) and nitroprusside (P less than 0.05) were also observed during pentobarbital anesthesia. In contrast, during halothane anesthesia, the pulmonary vasodilator responses to both bradykinin and nitroprusside were abolished. These results indicate that, compared with the conscious state, cGMP-mediated pulmonary vasodilation is preserved during pentobarbital anesthesia but is abolished during halothane anesthesia.

Anesthesia, General↗

PubMed1990

Time-dependent effects of theophylline on myocardial reactive hyperaemias in the anaesthetized dog.

1. The effects of a loading dose of theophylline (5 mg kg-1 i.v.) on the hyperaemias resulting from short-term (15 and 30 s) interruptions in coronary blood flow and intracoronary adenosine were studied at given intervals over a 2 h period in the anaesthetized dog. 2. These hyperaemic responses were affected differently by theophylline and each effect was time-dependent. The reactive hyperaemic response progressively decreased after drug delivery, reaching 46% of control at 2 h. In contrast, after a maximal attenuation to 23% of control 5 min after theophylline, the hyperaemia resulting from intracoronary adenosine progressively increased over the same period, reaching 64% of control 2 h after the loading dose. 3. Two-compartment model results based on plasma theophylline measurements and the time course of theophylline accumulation in pericardial infusates, suggested that complete drug distribution throughout the heart may require at least 20 min following a single intravenous dose. 4. If it is assumed that theophylline blocks coronary vascular adenosine receptors, these pharmacokinetics are consistent with the time-dependent pattern of response attenuation we observed for the adenosine-induced hyperaemias, but they cannot entirely explain the pattern of response attenuation observed for the occlusion-induced hyperaemias. The continued increase in attenuation of this response after complete drug distribution suggests an additional pharmacodynamic action of theophylline. 5. We conclude that a single therapeutic dose of theophylline results in distinct time-dependent pharmacological effects with respect to the ability of the coronary vasculature to dilate in response to temporary interruptions in oxygen supply and in response to exogenously administered adenosine. These effects deserve consideration in both experimental studies in which adenosine antagonists are used to assess adenosine action in vivo, and in clinical practice where theophylline pharmacotherapy for pulmonary disorders is commonplace.

Adenosine↗

PubMed1988

Posttraumatic Pasteurella multocida meningitis.

The patient described was immunologically compromised by multisystem trauma. Pasteurella multocida was isolated from the respiratory tract and subsequently from the cerebrospinal fluid; direct spread apparently occurred by way of a basilar skull fracture. Sepsis was absent. He was successfully treated but subsequently had hydrocephalus, which has not previously been reported to occur after P multocida meningitis. Because of the opportunistic nature of this infrequent human commensal and the significant morbidity and mortality associated with it, we believe that isolation of Pasteurella multocida from the respiratory tract justifies treatment, especially in the compromised host.

Adult↗