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Biomedical subjects

P R Adams

Publications and source records attributed to P R Adams.

At least 37 records · Page 2Linked to original sources
PubMed1987

Factors affecting outcome of coronary reperfusion with intracoronary streptokinase in acute myocardial infarction.

Aggressive interventional therapy in acute myocardial infarction (AMI) is expensive, time-consuming and not without significant risk. To determine which patients are most likely to benefit from such therapy, the effects of patient age, reperfusion success, admission left ventricular (LV) function, infarct location, admission clinical class, time from onset of pain to reperfusion and admission electrocardiographic findings on the outcome of coronary reperfusion in AMI were assessed in 292 prospectively studied, sequential patients from August 1980 to January 1984. Two hundred ten patients received intracoronary streptokinase (SK) therapy on admission and 82 patients, who either refused the protocol or met exclusion criteria, served as control subjects. Patients older than 65 years showed little improvement in 1-year mortality risk and no significant improvement in LV function during hospitalization after treatment with intracoronary SK. The remaining patients, 178 treated with SK and 48 control, were well matched and served as the basis for further comparisons. In this subgroup of patients, reperfusion success was associated with improved survival and LV function (mortality rate 3%, vs 17% in control subjects; increase in ejection fraction [EF] 18% vs 4%). Patients with an EF of less than 45% on admission showed a 21 +/- 30% increase in EF, compared with an increase in control subjects of 8 +/- 19%, and a lower 1-year mortality rate than controls (6% vs 21%, p = 0.01). Patients with anterior AMI had a significant increase in EF in the SK group (22 +/- 31%) and lower mortality compared with control subjects (5% vs 25%, p = 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Spontaneous miniature outward currents in cultured bullfrog neurons.

Spontaneous miniature hyperpolarizations were observed in cultured bullfrog neurons. Depolarization increased the frequency and amplitude of the events. Under voltage-clamp, these events were manifested as spontaneous miniature outward currents of SMOCs which were usually less than 2 nA, had a rapid rising phase and a slower voltage-dependent exponential decay. Analysis of inter-event intervals suggested that SMOCs occurred randomly, while analysis of their amplitudes yielded exponential amplitude distributions. Mean SMOC amplitudes and SMOC frequency increased with depolarization, even with 100 microM CdCl2 present. Time constants of SMOC decay resembled time constants obtained from voltage-jump experiments on Ca2+-loaded cells, and together with the sensitivity of SMOCs to tetraethyl ammonium (TEA), suggested that SMOCs are due to activation of fast Ca2+-gated potassium channels. We propose that a SMOC occurs when 10-5000 of these channels are activated by punctate intracellular Ca2+ release.

Animals↗
PubMed1987

Effects of phorbol dibutyrate on M currents and M current inhibition in bullfrog sympathetic neurons.

1. Effects of bath-applied phorbol dibutyrate (PDBu) on M currents (IM) and on the inhibition of IM by muscarine and luteinizing hormone-releasing hormone (LHRH) were recorded in voltage-clamped bullfrog lumbar sympathetic ganglion cells. 2. PDBu (0.1-30 microM) produced a slowly developing, irreversible and partial (less than or equal to 60%) inhibition of IM. This effect was not replicated by 4-alpha-phorbol or by vehicle. 3. After treatment with PDBu, residual IM showed a reduced sensitivity to inhibition by muscarine or LHRH but not by Ba2+. The reduced response to muscarine appeared to result from a 10-fold shift in the concentration dependence for inhibition. 4. PDBu did not clearly reproduce the ability of muscarine to inhibit the slow, Ca-activated K current IAHP or to increase the leak conductance at hyperpolarized potentials. The latter effect of muscarine was enhanced, rather than inhibited, by PDBu. 5. IM and IAHP were not inhibited by 1 mM dibutyryl cyclic AMP or by 20 microM forskolin. 6. It is concluded that activation of protein kinase C, but not protein kinase A, partly replicates the effect of muscarine on frog sympathetic neurons.

Animals↗
PubMed1987

Peripheral pulmonary artery aneurysm in a patient with limited respiratory reserve: controlled resection using cardiopulmonary bypass.

Pulmonary artery aneurysms are rare lesions for which operative management is not frequently undertaken. When operation is indicated, central lesions involving the pulmonary trunk, right main pulmonary artery, or left main pulmonary artery are repaired using cardiopulmonary bypass. Peripheral aneurysms in segmental intrapulmonary arteries have been managed most frequently by lobectomy, but occasionally by aneurysmectomy and pulmonary arterial repair. We used cardiopulmonary bypass for peripheral pulmonary aneurysmectomy in a patient with limited respiratory reserve because he had undergone prior contralateral bilobectomy; this allowed controlled resection while preserving a maximal amount of pulmonary parenchyma.

Adult↗
PubMed1986

Durability and low thrombogenicity of the St. Jude Medical valve at 5-year follow-up.

Between November, 1978, and December, 1983, 736 patients had valve replacement with the St. Jude Medical valve prosthesis. There were 478 patients with aortic valve replacement (AVR), 188 with mitral valve replacement (MVR), 63 with double valve replacement, and 7 with tricuspid valve replacement (they were not included in this study). The mean age at the time of operation was 46.7 years for patients having AVR and 48.6 years for those having MVR and AVR + MVR. Follow-up totaled 1,116 patient-years (range, 4 to 82 months). Early (30-day) mortality was lowest for isolated MVR (2.3%) and AVR (3.7%), and increased with reoperation or when associated procedures were combined with valve replacement. Patients undergoing reoperation or having associated procedures made up 49% of the AVR and 54% of the MVR groups. All patients were advised of the need for long-term anticoagulation with warfarin sodium. Nine patients (7 with AVR, 1 with MVR, 1 with AVR + MVR) had suspected or confirmed episodes of systemic thromboembolism, a linearized incidence of 0.99% per patient-year for AVR, 0.36% per patient-year for MVR, and 0.98% per patient-year for AVR + MVR. Eight patients with AVR underwent reoperation for prosthetic valve endocarditis (5 of the 8 patients had endocarditis prior to initial valve replacement). There were no instances of structural valve failure. There were 37 late deaths. Actuarial survival at 5 years (excluding early mortality, 95% confidence limits) was 89.8% for AVR, 84.8% for MVR, and 95.2% for AVR + MVR.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1986

A method for the rapid exchange of solutions bathing excised membrane patches.

In this communication we describe a technique for rapidly exchanging solutions bathing excised membrane patches, and present examples of its implementation using both outside-out and inside-out patches. The ability to make step changes in the concentration of channel-activating ligands (e.g., acetylcholine, calcium) offers a novel and direct means of measuring kinetic processes in the 10-100-ms range. The responses to step ligand concentration changes are well suited to ensemble variance analysis, yielding estimates of the number of channels in a patch, and testing assumptions of channel independence and homogeneity. Kinetic analysis of the pseudomacroscopic currents obtained by averaging large numbers of responses can be compared and correlated with analysis of the microscopic behavior of single channels, using the same membrane patch for both approaches. Practical and theoretical limitations associated with the method are briefly discussed.

Animals↗
PubMed1986

Calcium-dependent current generating the afterhyperpolarization of hippocampal neurons.

A single-electrode voltage-clamp technique was employed on in vitro hippocampal slices to examine the membrane current responsible for the slow afterhyperpolarization (AHP) in CA1 pyramidal cells. This was achieved by using conventional procedures to evoke an AHP in current clamp, followed rapidly by a switch into voltage clamp (hybrid clamp). The AHP current showed a dependence on extracellular K+, which was close to that predicted for a K+ current by the Nernst equation. The AHP current could be blocked by Cd2+ or norepinephrine. Although the AHP current showed a requirement for voltage-dependent Ca2+ entry, the current did not show any clear intrinsic voltage dependence. Once activated, AHP current is not turned off by hyperpolarizing the membrane potential. The effects of norepinephrine, Cd2+, and tetraethylammonium (TEA) were used to identify an AHP current component to the outward current evoked by depolarizing voltage commands from holding potentials that approximate to the resting potential for these cells. The AHP current can contribute significantly to the outward current during the depolarizing command. Upon repolarization it is evident as a slow outward tail current. This slow tail current had the same time constant as AHP currents evoked by hybrid clamp. Fast components to the tail currents were also observed. These were sensitive to Cd2+ and TEA. They probably represent a voltage-sensitive gKCa, sometimes termed C-current. The strong sensitivity to voltage and TEA displayed by the conventionally described gKCa (IC) are properties inconsistent with the AHP. It seems likely that the AHP current (IAHP) represents a Ca2+-activated K+ current separate from IC and that these two currents coexist in the same cell.

Action Potentials↗
PubMed1986

Slow synaptic transmission in frog sympathetic ganglia.

Bullfrog ganglia contain two classes of neurone, B and C cells, which receive different inputs and exhibit different slow synaptic potentials. B cells, to which most effort has been directed, possess slow and late slow EPSPs. The sEPSP reflects a muscarinic action of acetylcholine released from boutons on B cells, whereas the late sEPSP is caused by a peptide (similar to teleost LHRH) released from boutons on C cells. During either sEPSP there is a selective reduction in two slow potassium conductances, designated 'M' and 'AHP'. The M conductance is voltage dependent and the AHP conductance is calcium dependent. Normally they act synergistically to prevent repetitive firing of action potentials during maintained stimuli. Computer stimulation of the interactions of these conductances with the other five voltage-dependent conductances present in the membrane allows a complete reconstruction of the effects of slow synaptic transmission on electrical behaviour.

Animals↗
PubMed1986

Management of traumatic sinus of valsalva-right ventricular fistulae.

Residual intracardiac defects following penetrating injuries to the heart require thorough invasive evaluation and strong consideration for operative repair based upon the degree of hemodynamic compromise. Traumatic aortico-right ventricular fistulae result in high flow left-to-right shunts, and are associated with early onset of congestive failure. Operative repair requires utilization of total cardiopulmonary bypass, ventriculotomy and aortotomy to allow for thorough inspection of the ventricular septum, aortic valve cusps, and coronary ostia. Obliteration of both ends of the fistula (septal and sinus of Valsalva repair) minimizes the risk of recurrence.

Journal Article↗
PubMed1986

Voltage-dependent currents of vertebrate neurons and their role in membrane excitability.

This chapter reviews what is known of the voltage-dependent conductances of three classes of vertebrate nerve cell, as assessed by somatic voltage clamping. These classes are: (1) bullfrog paravertebral sympathetic ganglion cells; (2) rodent superior cervical sympathetic ganglion cells; and (3) rodent hippocampal pyramidal cells. Of these, bullfrog neurons are the most thoroughly characterized. They possess at least seven distinct voltage-activated conductances. Two of these, called GNa and GCa, carry inward, depolarizing current. They both activate rapidly, and can, under appropriate conditions, generate action potentials. The remaining five conductances are all potassium-mediated, and can thus in principle produce hyperpolarizations or repolarize the action potential. However, because each of these potassium conductances have different sizes, speeds, and voltage thresholds, they play a variety of hyperpolarizing, stabilizing, or braking roles. IC is large, fast, and voltage dependent. Action potentials trigger calcium influx, which rapidly turns on IC. This repolarizes the action potential and turns off IC. However another Ca-dependent current, IAHP, remains active even at negative potentials and leads to a prolonged hyperpolarization. If IC is blocked, spike repolarization slows somewhat, allowing the Hodgkin-Huxley delayed rectifier current IK to develop. This is also large enough to repolarize the spike rapidly, although it is normally preempted by IC. IA and IM are other small potassium currents that activate at more negative potentials than do IC, IK, and IAHP. IA is a transient outward current that mainly influences voltage trajectories following hyperpolarizing current pulses. IM activates progressively during prolonged depolarizing current pulses, and, together with IAHP, explains most of the adaptation seen in these cells. The harmonious counterpoint of this septet of currents explains most of the electrical excitability properties of these cells. However, several of the currents are also synaptically regulated, as a result of transmitters acting on muscarinic or peptide receptors. These slow synaptic actions can lead to dramatic changes in the electrical behavior of the cells. These currents all appear to be present in rat sympathetic ganglion cells also, although detailed analysis here has been hampered by the more complex geometry of these neurons. Furthermore, the roles of the various currents have not been completely defined. It seems possible that IA can contribute to spike repolarization, and clean separation of IC and IAHP has not yet been achieved.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Amylase and growth characteristics of Papulaspora thermophilia.

Mycelial dry weight of Papulaspora thermophilia reached a maximum of about 96 mg after six days of growth in a starch-yeast medium. Extracellular amylase activity was not measurable during this growth period and remained thereafter only about 0.1 unit per ml for 30 days, yet starch concentration reduced rapidly, and reducing sugar appeared in the extracellular medium within the first few days of incubation.

Amylases↗
PubMed1985

Two distinct Ca-dependent K currents in bullfrog sympathetic ganglion cells.

Healthy bullfrog sympathetic ganglion cells often show a two-component afterhyperpolarization (AHP). Both components can be reduced or abolished by adding Ca-channel blockers or by removing external Ca. Application of a single electrode "hybrid clamp"--i.e., switching from current- to voltage-clamp at the peak of the AHP, reveals that the slow AHP component is generated by a small, slow, monotonically decaying outward current, which we call IAHP. IAHP is blocked by Ca-removal or by apamin and is a pure K current. It is slightly sensitive to muscarine and to tetraethylammonium ion but is much less so than muscarine-sensitive (IM) and fast Ca-dependent (IC) K currents. It also can be recorded in dual-electrode voltage-clamp experiments, where it is seen as a slow, small component of the outward tail current that follows brief depolarizations to 0 mV or beyond. IC is seen as an early, fast, large component of the same tail current. Both components are blocked by Ca removal, but only the IC component is blocked by low doses of tetraethylammonium ion. Thus, bullfrog ganglion cells exhibit two quite distinct Ca-dependent K currents, which differ in size, voltage-sensitivity, kinetics, and pharmacology. These two currents also play quite separate roles in shaping the action potential.

Action Potentials↗
PubMed1985

Hemopericardium and tamponade following intracoronary thrombolysis with streptokinase.

Two patients underwent surgery for hemopericardium and pericardial tamponade after intracoronary thrombolysis by streptokinase for acute myocardial infarction. In both instances, the artery had reopened, but left ventricular function had not improved. A subxiphoid pericardial window relieved the tamponade, and both patients made good recovery. Hemopericardium is rare in myocardial infarction without cardiac rupture or anticoagulant therapy, and may constitute a specific complication of reperfusion with streptokinase. Pericardial window may be preferable to pericardiocentesis because of the possibility of cardiac rupture.

Journal Article↗
PubMed1984

Teleost luteinizing hormone-releasing hormone: action on bullfrog sympathetic ganglia is consistent with role as neurotransmitter.

Bullfrog sympathetic ganglion neurons have a "late, slow" excitatory postsynaptic potential (EPSP) that is mediated by a peptide similar to mammalian luteinizing hormone-releasing hormone (M-LHRH) (Jan, Y. N., L. Y. Jan, and S. W. Kuffler (1979) Proc. Natl. Acad. Sci. U. S. A. 76: 1501-1505). On biochemical evidence (Eiden, L. E., E. Loumaye, N. Sherwood, and R. L. Eskay (1982) Peptides 3:323-327) the endogenous LHRH-like peptide in the ganglion may be identical to teleost LHRH (T-LHRH; [Trp7,Leu8]M-LHRH) (Sherwood, N., L. Eiden, M. Brownstein, J. Speiss, J. Rivier, and W. Vale (1983) Proc. Natl. Acad. Sci. U. S. A. 80: 2794-2798). We have found that T-LHRH acts qualitatively like M-LHRH on bullfrog ganglion cells, but it is quantitatively more potent. As for M-LHRH, the primary action of T-LHRH under single-electrode voltage clamp is to inhibit the M-current, a voltage-dependent potassium current that is active in the region between rest and threshold in these cells. The M-current is also inhibited during the late, slow EPSP. Both T-LHRH and the late, slow EPSP can also induce an additional inward current, associated with an increased conductance, in some cells. An LHRH antagonist is effective against both T-LHRH and the late, slow EPSP. These results are consistent with a role for T-LHRH as the natural transmitter for the late, slow EPSP in bullfrog sympathetic ganglia.

Animals↗