How does anesthesia work?

Bill Perkins, associate professor of anesthesiology at the Mayo Clinic College of Medicine, explains:

Local and general anesthetics work by blocking nerve transmission to pain centers in the central nervous system, although the exact mechanisms for general anesthetics are not well understood, despite use of such pharmacological agents for more than 150 years.

Local anesthetics, such as Novocain, bind to and inhibit the function of the sodium channel in the nerve cell membrane, a type of ion channel required for the propagation of nerve impulses. This action obstructs the movement of nerve impulses from tissue innervated by nerves at the site of local anesthetic injection but causes no changes in awareness and sense perception elsewhere in the body.

In contrast, general anesthetics provide overall insensibility to pain. The most commonly used such agents are inhaled, and they are structurally related to ether. Their primary site of action is in the central nervous system. Unlike local anesthetics, the general anesthetics reduce nerve transmission at the synapses, the sites at which neurotransmitters are released by neurons and adjacent nerve cells respond. General anesthetics affect the response of receptors and ion channels to neurotransmitters, thereby decreasing nerve cell activity.

General anesthetics bind only very weakly to their sites of action and interact with proteins in a lipid environment, factors that together make it difficult to determine their exact binding structure. Despite such limitations, researchers are taking advantage of various methods to better discern how anesthetics work at the molecular level.

Genetic tools, for example, enable researchers to alter specific protein function and then determine whether this protein can be linked to sensitivity or resistance to anesthetic action in lower organisms. Other approaches, including sophisticated structural modeling of anesthetic binding to protein targets, are also showing promise. The targets for different agents do not appear to be the same, so there is probably no single molecular mechanism of action for all anesthetics.

Are one's fingerprints similar to those of his or her parents?

—ERIC C., LAKELAND, FLA.

Glenn Langenburg, a certified latent print examiner at the Minnesota Bureau of Criminal Apprehension, offers this answer:

Yes, we inherit the overall size, shape and spacing of so-called friction ridge skin (FRS)—fingerprints. The individual details that make a fingerprint unique are not genetically determined, however. Made up of a series of ridges and furrows that aid in grasping, FRS is unique and permanent. No two individuals—including identical twins—have the same arrangement, which also does not change throughout life (except in the case of significant damage that creates a permanent scar).

Why are the general patterns but not the identifying ridge features inherited? The reason is in the timing of aspects in fetal development. Fetuses acquire smooth volar pads—raised pads on the fingers, palms and feet—because of swelling mesenchymal tissue, which is a precursor of blood vessels and connective tissues. Around week 10, the fetus's volar pads stop growing, but the hand continues to enlarge. Over the next few weeks, the volar pads are absorbed back into the hand. During this stage, the first signs of ridges appear on the skin of the pads. The shape of the volar pads at the time the first ridges appear will dictate the general pattern that develops.

Once the overall pattern has begun to take shape within its confines, the exact arrangement of the identifying ridge features is dictated by random, localized stresses on the skin. The timing of these two events—volar pad regression and primary ridge appearance—is genetically linked. The precise locations of the ridges and other features, however, are random.

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