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Biomedical subjects

A Waters

Publications and source records attributed to A Waters.

At least 55 records · Page 3Linked to original sources
PubMed1983

Electromechanical coupling in feline basilar artery in response to serotonin.

This study was undertaken to define some of the cellular mechanisms of action of serotonin on cerebral vascular muscle. Application of serotonin to cat basilar artery resulted in a dose dependent depolarization and contraction beginning at 10(-8) M. The correlation coefficient relating the degree of force development with the change in membrane potential (Em) was 0.98. Excess K+ depolarized these vascular muscle cells with a slope (between 10 and 100 mM [K]0) of 54 mV/decade. When the muscle cells within this artery were depolarized by only 7 mV by addition of excess K+ there was a significant reduction in force development in response to serotonin. When the membrane was depolarized from -63 to -40 mV the mechanical response to serotonin was reduced by around 50%. Steady state current/voltage curves demonstrated a reduction in input resistance suggesting that serotonin's mechanism of depolarization is not due to a reduction in gk. These data demonstrate that serotonin contracts cat basilar artery through mechanisms involving vascular muscle cell depolarization and that factors which influence the level of Em will markedly effect the contractile response to serotonin.

Animals↗
PubMed1983

Electromechanical coupling in rat basilar artery in response to morphine.

Force development, intracellular membrane potential (Em), and voltage vs. current curves were measured in rat basilar artery to help elucidate the mechanism of action of morphine sulfate and a synthetic narcotic, meperidine hydrochloride, on this preparation. Morphine sulfate caused a dose-dependent contraction of these vessels, which was reversible with naloxone. Electrical studies show that morphine may act upon this vascular smooth muscle preparation by decreasing potassium conductance (gk). This hypothesis is supported by the findings that morphine sulfate depolarized these cells and increased the input resistance (rin) determined by the application of rectangular hyperpolarizing and depolarizing current pulses through the microelectrode during impalement and recording of the associated voltage changes (delta V). Meperidine hydrochloride had significantly less effect on this preparation than morphine sulfate. Further studies show that the vehicular medium used for the commercially available preparation of naloxone (viz. the methyl and propyl esters of p-hydroxybenzoic acid in a ratio of 9:1) is, in vitro, a vasodilator of cerebral vascular smooth muscle.

Animals↗
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Altered membrane properties of cerebral vascular smooth muscle following subarachnoid hemorrhage: an electrophysiological study. I. Changes in resting membrane potential (Em) and effect on the electrogenic pump potential contribution to Em.

Subarachnoid hemorrhage was produced experimentally in cats by intracisternal injection of non-heparinized autologous arterial blood obtained by cardiac puncture under ketamine and xylazine anesthesia. Cats were sacrificed at varying time intervals between 30 min and 7 days post ictus. Measurements of resting membrane potential were recorded from smooth muscle cells of the basilar artery. These measurements were obtained by impalement from the adventitial surface of isolated but otherwise intact segments of the artery using glass microelectrodes with tip sizes less than 0.1 micron. The resting membrane potential recorded in vitro from animals previously subjected to subarachnoid hemorrhage in vivo was consistently and significantly depolarized when compared to normal controls. This depolarization was present as early as 30 min post ictus. Addition of the cardiac glycoside, ouabain, in a concentration of 10(-5)M depolarized cells from both control and experimental animals. There is a significant electrogenic pump potential contribution to the resting membrane potential of vascular smooth muscle cells. Ouabain is a potent blocker of Na+, K+-ATPase, the enzyme responsible for maintaining the cation electrochemical gradients. The depolarization recorded in these cells following subarachnoid hemorrhage is not, therefore, due to impairment of the electrogenic pump. The significance and implications of these findings are discussed.

Animals↗
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The big issue.

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Persons with Disabilities↗
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Ward leadership.

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Attitude of Health Personnel↗
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Capital crisis.

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Financial Management, Hospital↗
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Creative recruitment.

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