Adequacy of ascending aorta-descending aorta shunt during cross-clamping of the thoracic aorta for prevention of spinal cord injury.

The effectiveness of various sized shunts placed between the ascending and the descending aorta to prevent paraplegia in dogs with the thoracic aorta cross-clamped for 1 hour was tested. Three tapered shunts sizes were used with tip dimensions of 3.8, 5.2, and 6.3 mm inner diameter, with cross-sectional areas of 11.34, 21.23, and 33.18 mm2, respectively, and with an equal midportion diameter of 10 mm (3/8 inch). These shunts carried 40%, 60%, and 72% respectively, of baseline descending aortic flow during the cross-clamping period. Flow distribution was measured with radioactive microspheres in the spinal cord (gray and white matter) and kidneys. All dogs without shunts (Group I) developed paraplegia, severe proximal circulatory embarrassment, and severe ischemia of the spinal cord (mainly gray matter) that was followed by marked hyperemia persisting up to 24 hours following the experiment. Mortality was 33%. Only animals treated with large shunts (Groups III and IV) avoided paraplegia and postischemic injury. An effective shunt was characterized as carrying 60% or more of baseline descending aortic flow, having a cross-sectional area at its tip equal to or larger than 29% of the descending aorta, and equaling at least 54% of its diameter. Porportionately, the size of the tridodecylmethylamonium-heparin shunts being used in human beings (even the largest 9 mm inner diameter) is significantly inadequate to maintain distal flows and pressures for the prevention of spinal cord injury. Four clinical options are discussed.

Brain damage in profound hypothermia. Perfusion versus circulatory arrest.

To investigate brain changes in induced deep core hypothermia (18 degrees C) with or without circulatory arrest, four groups of dogs were subjected to cardiopulmonary bypass (CPB) under the following conditions: (1) differential head perfusion with pulsatile flow and simultaneous circulatory arrest to the rest of the body; (2) differential perfusion to the head with a nonpulsatile flow; (3) total circulatory arrest; and (4) continuous hypothermic perfusion. Parameters analyzed were: (1) blood flow distribution; (2) creatine kinase isoenzyme (CK-BB) elevation in the cerebrospinal fluid (CSF) and in the brain venous return; and (3) microscopy of the brain in animals killed at 30 minutes, 24 and 48 hours, 1 and 2 weeks, and 1 month. Although minor brain tissue flow differences were found at 37 degrees C among the groups, flows equalized at 18 degrees C. A significant seven-fold brain flow increase followed the period of circulatory arrest in Group III. Rise of CK-BB levels occurred in brain venous return but not in CSF in all groups. Microscopic cellular damage appeared in all groups with an equal degree of severity, regardless of the method of hypothermia and perfusion implemented.

Measurement of ATP synthesis rates by 31P-NMR spectroscopy in the intact myocardium in vivo.

The ability to measure ATP synthesis rates using 31P-NMR spectroscopy is demonstrated in the normal, ischemic, and postischemic myocardium in vivo. Cardiopulmonary bypass (CBP) was employed to induce 20 min of global myocardial ischemia, and to conduct magnetization transfer measurements during the ischemic episode and following reperfusion and return to normal circulation. For the first few minutes of ischemia, transfer of magnetization from ATP gamma to Pi was extensive and the resultant fractional reduction (delta M/M0) in the Pi resonance intensity reached approximately 100%. Subsequent to reperfusion and stabilization off CPB and on normal circulation, both the fractional reduction and the spin-lattice relaxation time, T1*, of the Pi resonance were determined when ATP gamma spins were saturated. Under these conditions, the unidirectional ATP synthesis rate was 0.41 +/- 0.09 (SEM, N = 4) mumol/s/g wet wt. The data suggest that in the canine myocardium in vivo, glycolytic enzymes mediate a very rapid exchange between Pi and ATP gamma-phosphates during early phases of ischemia; in the postischemic reperfused myocardium, however, the glycolytic contribution to the unidirectional Pi----ATP rate measured by NMR in vivo is relatively small compared to that observed in glucose-perfused, postischemic rat hearts.

Canine model for long-term evaluation of prosthetic mitral valves.

The evaluation of mechanical prosthetic heart valves would be aided by a more satisfactory animal model. For acute assessment, a variety of animals have been used, but for chronic studies, only larger animals (pigs, calves, baboons) have been employed, creating an expensive model with laboratory management difficulties. Previously, the use of dogs for chronic evaluation has been unsatisfactory because of the frequent occurrence of early sepsis and valve-related thrombotic deaths. We have modified our existing acute dog protocol to produce a successful chronic model. Our model employs perioperative systemic antibiotics, short cardiopulmonary bypass period (range 35-60 min), a minimum of perioperative intravenous lines, postoperative anticoagulation therapy, and strict postoperative antiseptic technique for blood sampling. To evaluate this model, 11 consecutive mongrel dogs underwent mitral valve replacement with either a standard Dacron sewing skirt or a newly devised carbon-coated Teflon sewing skirt No. 23 mm Bjork-Shiley Convexo Concave (CC) prosthetic valve. Nine animals (82%) survived and were evaluated after a predetermined observation interval of either 3 or 6 months for valve function, pannus formation, and possible carbon particle migration. At sacrifice, all animals had good hemodynamics and valve function, minimal pannus formation and no carbon washout. Consequently, this model provides a relatively inexpensive, reproducible method of chronic in vivo evaluation of prosthetic valve modifications.