Malignant hyperthermia syndrome.

Malignant hyperthermia is a pharmacogenetic disease involving uninhibited flow of calcium ion into the muscle substance. This leads to a combined metabolic and respiratory acidosis and the liberation of heat. If not immediately controlled, cellular death results. We treated a 4-year-old girl who suffered a malignant hyperthermia crisis during strabismus surgery. Hyperventilation with 100% oxygen and intravenously administered dantrolene sodium, furosemide, and fluids controlled the attack and the child recovered completely.

Anaesthesia for liver transplantation--a model for the anaesthetic management of end-stage hepatic failure.

Advances in the medical and surgical management of cirrhosis have brought an increasing number of such patients to the operating theatre. Although most anaesthesiologists will not directly participate in the care of patients during hepatic transplantation, the considerations involved in their anaesthetic management pertain to all patients with severe hepatic disease. Using orthotopic hepatic homo-transplantation as a model the physiologic changes and anaesthetic implications have been discussed.

Rapid-sequence induction technique in patients with severe ventricular dysfunction.

The hemodynamic effects of a rapid-sequence induction and intubation technique using etomidate, fentanyl, and succinylcholine for emergency surgery in patients with severe ventricular dysfunction were studied. Ten patients undergoing orthotopic heart transplantation received fentanyl, 10 microg/kg, etomidate, 0.3 mg/kg, and succinylcholine, 1.5 mg/kg, intravenously (IV) in rapid-sequence fashion for induction. Intubation was performed 60 seconds later. Heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), mean pulmonary arterial pressure (MPAP), pulmonary arterial occlusion pressure (PAo), and cardiac index (CI) were measured preinduction, postinduction, and 1 minute after intubation. Systemic vascular resistance index (SVRI) and pulmonary vascular resistance index (PVRI) were calculated from the measured data. No statistically significant changes in hemodynamics occurred with induction or intubation. These results indicate that etomidate, fentanyl, and succinylcholine given in a rapid-sequence technique produce a hemodynamically stable induction with minimal response to intubation in patients with end-stage cardiac disease.

Tobramycin-curare interaction.

A 59-year-old patient had urologic surgery under d-tubocurarine-fentanyl-N2O anesthesia. The muscle relaxant was reversed with prostigmine at the end of the 5-hour procedure. Reparalysis occurred after the administration of IV tobramycin and was successfully reversed with prostigmine.

Acute effects of pathogenic simian-human immunodeficiency virus challenge on vaccine-induced cellular and humoral immune responses to Gag in rhesus macaques.

Simian-human immunodeficiency virus (SHIV) infection in macaques provides a convenient model for testing vaccine efficacy and for understanding viral pathogenesis in AIDS. We immunized macaques with recombinant, Salmonella typhimurium (expressing Gag) or soluble Gag in adjuvant to generate T-cell-dependent lymphoproliferative or serum antibody responses. Immunized animals were challenged by intrarectal inoculation with SHIV89.6PD. Virus infection was accompanied by rapid losses of lymphoproliferative responses to Gag or phytohemagglutinin. By 8 weeks, mitogen responses recovered to near normal levels but antigen-specific immunity remained at low or undetectable levels. Serum antibody levels were elevated initially by virus exposure but soon dropped well below levels achieved by immunization. Our studies show a rapid depletion of preexisting Gag-specific CD4(+) T cells that prevent or limit subsequent antiviral cellular and humoral immune responses during acute SHIV infection.

Lymphocyte activation during acute simian/human immunodeficiency virus SHIV(89.6PD) infection in macaques.

Host-virus interactions control disease progression in human immunodeficiency virus-infected human beings and in nonhuman primates infected with simian or simian/human immunodeficiency viruses (SHIV). These interactions evolve rapidly during acute infection and are key to the mechanisms of viral persistence and AIDS. SHIV(89.6PD) infection in rhesus macaques can deplete CD4(+) T cells from the peripheral blood, spleen, and lymph nodes within 2 weeks after exposure and is a model for virulent, acute infection. Lymphocytes isolated from blood and tissues during the interval of acute SHIV(89.6PD) infection have lost the capacity to proliferate in response to phytohemagglutinin (PHA). T-cell unresponsiveness to mitogen occurred within 1 week after mucosal inoculation yet prior to massive CD4(+) T-cell depletion and extensive virus dissemination. The lack of mitogen response was due to apoptosis in vitro, and increased activation marker expression on circulating T cells in vivo coincided with the appearance of PHA-induced apoptosis in vitro. Inappropriately high immune stimulation associated with rapid loss of mature CD4(+) T cells suggested that activation-induced cell death is a mechanism for helper T-cell depletion in the brief period before widespread virus dissemination. Elevated levels of lymphocyte activation likely enhance SHIV(89.6PD) replication, thus increasing the loss of CD4(+) T cells and diminishing the levels of virus-specific immunity that remain after acute infection. The level of surviving immunity may dictate the capacity to control virus replication and disease progression. We describe this level of immune competence as the host set point to show its pivotal role in AIDS pathogenesis.