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Biomedical subjects

N Iwatsuki

Publications and source records attributed to N Iwatsuki.

At least 37 records · Page 2Linked to original sources
PubMed1989

[Anesthesia for a patient with HELLP syndrome].

A case of 30 year-old female with HELLP syndrome, who had undergone emergency caesarean section under general anesthesia, was reported. HELLP syndrome is characterized by hemolysis, liver dysfunction and thrombocytopenia, besides symptoms of severe toxemia of pregnancy. After an awake orotracheal intubation, anesthesia was maintained with nitrous oxide, oxygen and muscle relaxant. Blood pressure was controlled with intravenous administration of nitroglycerin. Though the eclampsia was recognized several times during and after the operation, the patient and her baby had no complication nor sequela on their discharge. The key in the anesthetic management of caesarean section in a patient with HELLP syndrome is to control hypertension and eclampsia, to consider the presence of liver and kidney dysfunctions, and to improve anemia and bleeding tendency.

Adult↗
PubMed1989

[A case of anaphylactoid reactions to lactated Ringer's solution with 5% maltose].

A 27-years-old man was admitted for correction of nasal fracture. He presented with circulatory collapse and generalised erythema on induction of general anesthesia and during preparation of intradermal test for identifying the offending agent. As both of these responses occurred during intravenous infusion of lactated Ringer's solution with 5% maltose, anaphylactoid responses to this intravenous solution were strongly suspected.

Adult↗
PubMed1988

Cardiovascular interaction between sevoflurane and nicardipine in open chest dogs.

Cardiovascular interaction between nicardipine and sevoflurane was examined in dogs and compared with nicardipine-thiopental interaction and nicardipine-halothane interaction. The bolus intravenous injection of nicardipine at dosages of 15 micro g/kg and 30 micro g/kg under sevoflurane anesthesia produced transient decreases in blood pressure, systemic vascular resistance, left ventricular pressure, left ventricular (dp)/(dt) and -(dp)/(dt), and a slight increase in cardiac output. The degrees of these changes were almost identical to those under thiopental or halothane anesthesia. Left and right atrial pressure, pulmonary arterial pressure, pulmonary vascular resistance were not changed by nicardipine under any of the three anesthetics. These results suggest that the cardiovascular interaction of nicardipine and sevoflurane is additive and similar to that of nicardipine and halothane and that the cardiovascular changes induced by nicardipine are not modified by the presence of anesthetics.

Journal Article↗
PubMed1987

Direct effects of H2-receptor antagonists on airway smooth muscle and on responses mediated by H1- and H2-receptors.

Because it has been suggested that histamine H2-receptor antagonists may worsen airway constriction in asthmatic patients, we investigated the comparative effects of three histamine H2-receptor antagonists on guinea pig tracheal smooth muscle in vitro. When tested against resting tone, cimetidine, ranitidine and famotidine produced dose-related relaxation with pD2 values (negative log of ED50 for relaxation) (+/- SE, n; eq 5) of 3.20 +/- 0.04, 2.95 +/- 0.16 and 2.97 +/- 0.14, respectively. Concentrations that were below threshold for relaxation, did not elicit contraction. However, when the preparations were precontracted with histamine (10(-5)M), dose-response curves for relaxation were shifted to the right, and low-concentrations of all three histamine H2-antagonists augmented histamine-induced tone. When preparations were pretreated with cimetidine (10(-6) to 10(-4) M) and then tested for sensitivity to histamine, dose-response curves for histamine-induced contraction were shifted to the left (potentiated). These results provide further evidence for a modulatory effect of airway H2-receptors on the contractile response to histamine. In addition, since the concentrations associated with potentiation of histamine-induced contraction were about the same for all three H2-receptor antagonists (greater than or equal to 10(-5) M), our studies suggest a greater likelihood of airway constriction for the less potent H2-receptor antagonists that must be administered in higher clinical doses.

Animals↗
PubMed1987

Prevention of postischemic hypoperfusion after canine cardiac arrest by nicardipine.

We studied the effect of nicardipine (NC) on canine cerebral blood flow (CBF) after cerebral ischemia induced by cardiac arrest. Cerebral ischemia was produced by 10 min of electrically mediated ventricular fibrillation. An iv injection of NC (10 micrograms/kg) bolus was followed by continuous NC infusion (0.33 micrograms/kg X min) immediately after the circulation re-established itself. Local CBF was measured using the hydrogen-gas clearance method. The administration of NC maintained CBF at the pre-arrest level during postischemia, thus preventing the hypoperfusion observed in the control group with no NC. However, in the controls, CBF, reduced at 180 min after re-circulation, was not improved by NC infusion. Consequently, administering NC immediately after re-establishment of circulation may help maintain CBF during the postresuscitation period.

Animals↗
PubMed1985

Inhibition of Ca2+-activated K+ channels in pig pancreatic acinar cells by Ba2+, Ca2+, quinine and quinidine.

Patch-clamp whole-cell and single-channel current recordings were made from pig pancreatic acinar cells to test the effects of quinine, quinidine, Ba2+ and Ca2+. Voltage-clamp current recordings from single isolated cells showed that high external concentrations of Ba2+ or Ca2+ (88 mM) abolished the outward K+ currents normally associated with depolarizing voltage steps. Lower concentrations of Ca2+ only had small inhibitory effects whereas 11 mM Ba2+ almost blocked the K+ current. 5.5 mM Ba2+ reduced the outward K+ current to less than 30% of the control value. Both external quinine and quinidine (200-500 microM) markedly reduced whole-cell outward K+ currents. In single-channel current studies it was shown that external Ba2+ (1-5 mM) markedly reduced the probability of opening of high-conductance Ca2+ and voltage-activated K+ channels whereas internal Ba2+ (6 X 10(-6) to 3 X 10(-5) M) caused activation at negative membrane potentials and inhibition at positive potentials. Quinidine (200-400 microM) evoked rapid chopping of single K+ channel openings acting both from the outside and inside of the membrane and in this way markedly reduced the total current passing through the channels.

Animals↗
PubMed1985

Action of tetraethylammonium on calcium-activated potassium channels in pig pancreatic acinar cells studied by patch-clamp single-channel and whole-cell current recording.

The effects of tetraethylammonium ions on currents through high-conductance voltage- and Ca2+-activated K+ channels have been studied with the help of patch-clamp single-channel and whole-cell current recording on pig pancreatic acinar cells. In excised outside-out membrane patches TEA (1 to 2 mM) added to the bath solution virtually abolishes unitary current activity except at very positive membrane potentials when unitary currents corresponding to a markedly reduced conductance are observed. TEA in a lower concentration (0.2 mM) markedly reduces the open-state probability and causes some reduction of the single-channel conductance. In inside-out membrane patches bath application of TEA in concentrations up to 2 mM has no effect on single-channel currents. At a higher concentration (10 mM) slight reductions in single-channel conductance occur. In whole-cell current recording experiments TEA (1 to 2 mM) added to the bath solution completely suppresses the outward currents associated with depolarizing voltage jumps to membrane potentials of 0 mV and blocks the major part (70 to 90%) of the outward currents even at very positive membrane potentials (30 to 40 mV). In contrast TEA (2 mM) added to the cell interior (pipette solution) has no effect on the outward K+ current. Our results demonstrate that TEA in low concentrations (1 to 2 mM) acts specifically on the outside of the plasma membrane to block current through the high-conductance Ca2+- and voltage-activated K+ channels.

Animals↗
PubMed1985

Human pancreatic acinar cells: studies of stimulus-secretion coupling.

Elements of stimulus-secretion coupling were studied in human pancreatic acinar cells by using tissue samples obtained from cadaver organ donors. In pancreatic fragments, acetylcholine evoked amylase secretion as well as potassium release and increased the outflux of 45Ca and 86Rb from the prelabeled tissue. In patches of basolateral plasma membrane excised from acinar cell clusters, single-channel potassium currents were recorded. The inside of the plasma membrane faced the bath solution, allowing the effects of changes in the free ionized calcium concentration in contact with the membrane interior to be tested. Two types of calcium-activated potassium-selective channels were found with unit conductances of about 250 and 50 picosiemens (pS), respectively. In both cases channel opening was determined by the electrical potential difference across the plasma membrane and the free ionized calcium concentration in the bath solution. The probability of channel opening was markedly increased by elevation of the free ionized calcium concentration in contact with the membrane inside. The results suggest that the acetylcholine-evoked cellular potassium release occurs via selective membrane potassium channels opened by calcium released intracellularly after the action of the secretagogue.

Acetylcholine↗
PubMed1985

Activation of Ca2+-dependent Cl- and K+ conductances in rat and mouse parotid acinar cells.

Isolated acinar cells from rat and mouse parotid glands were studied with patch-clamp whole-cell current recordings. Acetylcholine (ACh) stimulation caused a transient inward current at a membrane potential of -70 mV, and a sustained outward current at a membrane potential of 0 mV, in quasi physiological Na+, K+ ion gradients, except the zero-Cl- ion gradient condition across the membrane. The reversal potential obtained from the ACh-evoked steady current was about -75 mV, in this ionic condition. When major Cl- ions of both the pipette and the bath solution were replaced, either by glutamate or by sulphate, only a large outward current was observed, at a membrane potential of -60 mV, in the presence of ACh. The addition of Ca2+-ionophore A23187 caused responses similar to those evoked by ACh. The reversal potential of A23187-induced current was close to the K+ equilibrium potential of -90 mV, in a Cl- -free condition. When K+-free NaCl solution was used in the pipette and the bath, A23187 caused only a large inward current, at a membrane potential of -60 mV. The reversal potential of A23187-evoked current was about -15 mV, in a symmetrical K+-free, NaCl condition. These results suggest that the ACh and A23187 activate Cl- as well as K+ conducting pathways via an increase in [Ca2+]i in the parotid acinar cells. The A23187-evoked large K+ current could not be explained solely by a rise in open probability of the channels.

Acetylcholine↗