Channel arrest

In a first attempt at a synthesis of information in this research (Hochachka, 1986), a channel arrest component of a hypoxia tolerance theory postulated (i) that hypoxia tolerant cells would have an inherent low permeability (either low channel densities or low channel activities) and (ii) that they would sustain a further suppression of membrane permeability to ions when exposed to oxygen lack (further channel arrest by either suppression of channel densities or channel activities). Turtle liver cells display both of these characteristics (especially when compared to mammalian homologs) thus they clearly fit the classical definition of metabolic and channel arrest as two telling signatures of hypoxia tolerance. 

Buck, L.T., and P.W. Hochachka (1993). Anoxic suppression of Na+ K+ ATPase and constant membrane potential in hcpatocytcs support for channel arrest. Am. J. Physiol. 265 R1020-R1025. 

Doll, C.J., P.W. Hochachka, and P.B. Reiner (1991). Channel arrest implications from membrane resistance in turtle neurons. Am. J. Physiol. 261 R1321-R1324. 

It is clear that the closure of voltage-gated K" " charmels by hypoxic exposure has implications for neuroprotection as demonstrated by K+ channel arrest in hypoxia-tolerant turtles (Pek and Lutz, 1997 Bidder and Buck, 1998 Hochachka and Lutz, 2001 Bidder and Donohoe, 2002), which reduces Ca" influx (Bidder and Buck, 1998). In some anoxia-tolerant spedes, neuronal energy is not only conserved by ion channel arrest but also by ATP-sensitive mitochondrial K+ channel arrest (reviewed by Buck and Pamenter, 2006). This may have implications for chnical interventions. 

Peers C. 2004. Interactions of chemostimuli at the single cell level Studies in a model system. Exp Physiol 89 60-65. Pek M, Lutz PL. 1997. Role for adenosine in channel arrest in... 

Endurance Burn Under certain cou(itious, a successfully arrested flame may stabilize on the unprotected side of an arrester element. Should this condition not be corrected, the flame will eventually penetrate the arrester as the channels become hot. An endurance burn time can be determined by testing, which specifies that the arrester has withstood a stabilized flame without penetration for a given period. The test should address either the actual or worst-case geometry, since heat transfer to the element will depend on whether the flame stabilizes on the top, bottom, or horizontal face. In general, the endurance burn time identified by test should not be regarded as an accurate measure of the time available to take remedial action, since test conditions will not necessarily approximate the worst possible practical case. Temperature sensors may be incorporated at the arrester to indicate a stabilized flame condition and either alarm or initiate appropriate action, such as valve closure. 

Pressure Drop Flow resistance depends on flame arrester channel arrangement and on a time-dependent fouling fac tor due to cor-... 

Pertussis toxin is produced by the bacterium Bordetella pertussis. It covalently modifies G-proteins of the G/Go family (transfer of a ADP-ribose moiety of NAD onto G-protein a-subunits). ADP-ribosylated G-proteins are arrested in their inactive state and, as a consequence, functionally uncoupled from their respective effectors. Examples for pertussis toxin-sensitive cellular responses include the hormonal inhibition of adenylyl cyclases, stimulation ofK+ channels, inhibition of Ca2+ channels and stimulation ofthe cGMP-phosphodiesterase in retinal rods. 

Three main routes exist for the spread of cancer cells throughout the body. These involve the lymphatic system, the blood system, and direct extension into body cavities. Spread by the lymphatic system is thought to be important for carcinomas. The walls of these channels offer little mechanical resistance to penetration by tumor cells. Malignant cells readily invade the walls of these vessels and are carried to regional lymph nodes. In the lymph node, the cancer cells can arrest, proliferate and produce a metastatic tumor. Malignant cells may later detach from the lymph node and be carried in the bloodstream to other sites throughout the body. 

The most important toxic effects reported for calcium channel blockers are direct extensions of their therapeutic action. Excessive inhibition of calcium influx can cause serious cardiac depression, including cardiac arrest, bradycardia, atrioventricular block, and heart failure. These effects have been rare in clinical use. 

Lidocaine is one of the least cardiotoxic of the currently used sodium channel blockers. Proarrhythmic effects, including sinoatrial node arrest, worsening of impaired conduction, and ventricular arrhythmias, are uncommon with lidocaine use. In large doses, especially in patients with preexisting heart failure, lidocaine may cause hypotension—partly by depressing myocardial contractility. 

Some of the tricyclic antidepressants also have the ability to block serotonin 2A receptors, which may contribute to the therapeutic actions of those agents with this property. Blockade of serotonin 2A receptors is discussed in Chapter 7. Tricyclic antidepressants also block sodium channels in the heart and brain, which can cause cardiac arrhythmias and cardiac arrest in overdose, as well as seizures. 

---