To quantify and determine the time course of hyperaemia adjacent to acutely ischaemic myocardium, 19 dogs underwent open-chest coronary-artery occlusion and 4 had sham-occlusion. At 15 min (19 animals) and 45 min (9 animals) post-occlusion regional myocardial blood flow (RMBF) was measured by the radionuclide-labelled microsphere technique. The dogs were sacrificed after 24 hours, the hearts were excised, sectioned into four segments from apex to base, and stained with triphenyl tetrazolium chloride (TTC). Transmural samples were taken from necrotic areas, normal areas, and the zone bordering the infarct. Each sample was divided into an endocardial and epicardial layer. At 15 min post-occlusion RMBF in the border zone was 16% greater than in the normal myocardium (116+/-16 vs 100+/-12 cm3xmin(-1)x100g(-1);P<0.05). In addition, the ratio of endocardial to epicardial flow was lower in the border zone (0.87+/-0.05) compared with normal myocardium (1.01+/-0.02; P<0.05) indicating that the hyperaemia observed was predominantly epicardial. From 15 to 45 min hyperaemic endocardial flow tended to decline: 126 to 108 cm3xmin(-1)x100g(-1) (P<0.05). In four sham-occlusion dogs there were no differences (P>0.05) in RMBF between sites equivalent to those sampled in occluded animals. These studies document a hyperaemic border zone persisting at least 45 min post-occlusion. Hyperaemia appears to be more prominent and of longer duration in the epicardium than endocardium.

Animals↗

PubMed1980

Comparative effects of verapamil and nifedipine on reactive hyperemia and ventricular arrhythmias during coronary artery reperfusion.

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Animals↗

PubMed1979

Cardiac lymph flow in conscious dogs.

The cardiac lymphatic duct was cannulated in dogs and the exteriorized cannula allowed chronic collection of lymph during the awake state for as long as 3 wk. The surgical methodology and inherent difficulties in the technique are describ:d. Cardiac lymph flow ranged from 0.45--5.6 ml/h in the control state in 14 dogs. An occluding device and flow probe were placed on the circumflex coronary artery (CFX); ultrasonic segment length crystals were placed in the left ventricular free wall in 4 dogs. Occlusion of the CFX in these conscious dogs caused lymph flow to fall as great as 46% below control during the 1st half-hour. Reperfusion of the occluded vessel caused an increase in lymph flow as great as 67% above control. The effect on cardiac lymph flow was demonstrated for a few select drugs that have known effects on the cardiovascular system. Cardiac lymph flow was altered from control as follows: isoproterenol, 42 +/- 11% increase; RO 2-2985, 118 +/- 8% increase; verapamil, 101 +/- 10% increase; propranolol caused no significant change. The conscious dog with cardiac lymph vessel cannulated should provide a model to further study the complexities of cardiac metabolism and physiology without interference of anesthesia and surgical stress.

Animals↗

PubMedDate not supplied

Total pericardial replacement. Design and preliminary evaluation in greyhounds.

Existing pericardial substitutes, used for the prevention of pericardial and pleural adhesions to the epicardium, are in the form of a patch. To improve on this concept, an elastic, anatomically correct, implantable sac has been developed for total pericardial replacement. Total pericardial substitutes fabricated from Silastic silicone rubber and Mitrathane polyetherurethane urea were implanted in greyhound dogs and harvested at 8 weeks. Pericardial adhesions were prevented by the substitutes that remained intact. Fibrous tissue formation had occurred on the epicardium underlying the substitutes, the extent being more severe in response to the Silastic compared with the Mitrathane. However, the Silastic was superior to the Mitrathane in retention of its tensile strength and elastic modulus over the implant period (p less than 0.05). Further development of total pericardial substitutes from different materials shows promise.

Animals↗

PubMedDate not supplied

Performance of a hydrogel composite pericardial substitute after long-term implant studies.

A novel composite patch has been tested as a pericardial substitute to reduce adhesion formation after cardiac surgery. The patch consists of poly 2-hydroxyethyl methacrylate (pHEMA) hydrogel reinforced with a polyethylene terephthalate (PET) mesh. The hydrogel-PET composite pericardial patches were implanted in canines for 6, 9, and 12 months. Upon termination, adhesion formation and epicardial reaction to the implant were rated. No adhesions formed between the patch and the native pericardium or epicardium. A thin fibrous layer on the epicardium progressively developed where the patch contacted the heart. The coronary anatomy remained visible. Histologically, the response to the implant was fibrous in nature. No significant signs of cellular inflammation were found. The gross appearance of the retrieved patches was nearly identical to that of preimplant patches. Mechanical tests showed no significant changes (alpha = 0.05) in patch strength or stiffness. Hydrogel water content initially increased during implantation. The thickness of the patch did not change significantly (alpha = 0.05) throughout the study. Scanning electron microscopy (SEM) revealed unequal layers of hydrogel on either side of the PET mesh and cracks in the hydrogel surfaces of retrieved patches. Both SEM and light microscopic observation of the patches showed traces of calcification in patches in the 9 and 12 month studies.

Animals↗

PubMedDate not supplied

Progressive pressure expansion in skeletal muscle ventricle conditioning.

Skeletal muscle ventricle (SMV) conditioning typically results in reduced muscle performance. This study investigated the effects of progressive SMV resting pressure expansion and dynamic muscle training on SMV pumping capability. SMVs were formed from latissimus dorsi muscle in five goats. Three experimental SMVs were conditioned against a compliant pneumatic implant system. SMV resting pressure was progressively increased as the SMV adapted to each increment. Resting pressure rose from 40 to 100-120 mmHg over an 8 week period of time. Two control SMVs were conditioned against a non expanded incompressible implant. Both experimental and control SMVs were electrically burst stimulated for at least 6 weeks after an initial 2 week vascular delay interval. Results demonstrate that 1) experimental SMVs increased in volume; 2) SMV passive and active (evoked isovolumetric pressure) pressure-volume curves adapted to the increasing or static resting volume; and 3) two of three experimental SMVs generated greater stroke volumes than control SMVs across a range of counterpulsation pressures and electrical stimulation parameters. Progressive pressure expansion using a compliant implant system improved final SMV pumping performance and merits further investigation.

Adaptation, Physiological↗

PubMedDate not supplied

Inhibition of platelet aggregation by verapamil: quantification by in vivo and in vitro techniques.

Platelet aggregation appears to play a prominent role in myocardial ischemia. Verapamil, a slow-channel blocking agent with important antiarrhythmic and vasodilating actions, has been shown to inhibit in vitro platelet aggregation. We used an electronic particle size analyzer to evaluate the effects of verapamil on platelet aggregation in vitro and in vivo in 88 rats. The intravenous injection of verapamil (0.4 mg/kg) did not change the platelet count compared to control animals receiving an equal volume of normal saline (verapamil, 1.1 +/- 0.04 x 10(6)/mm3, vs. control, 1.2 +/- 0.09 x 10(6)/mm3, (p greater than 0.05). The mean size of platelet aggregates induced by adenosine diphosphate (0.2 microM), was reduced by verapamil (verapamil, 15.3 +/- 1.2 x 10(3) micron3 vs. control 24.4 +/- 2.7 x 10(3) micron; p less than 0.01). Platelet aggregates induced in vivo, following a standardized technique of extravasation of right iliac artery blood into the peritoneal cavity, were also smaller following verapamil infusion (verapamil, 12.6 +/- 1.1 x 10(3)micron3, vs control, 17.3 +/- 0.9 x 10(3) micron3 p less than 0.001). We conclude that verapamil exerts and inhibitory effect on platelet aggregation both in vitro and in vivo. This property may add an important new dimension to its potential therapeutic usefulness in ischemic heart disease.

Adenosine Diphosphate↗

PubMedDate not supplied

Effects of ethanol and hemolysis on in vivo and in vitro platelet aggregation.

In vivo and in vitro platelet function were measured in male rats after intravenous injection of ethanol or water. There was a dose-related ethanol suppression of platelet aggregation induced by extravasation. Increased volumes of preformed microaggregates were seen in samples taken directly from the vena cava after injection of ethanol in doses that caused hemolysis. Lower doses of ethanol produced no demonstrable microaggregates or hemolysis: however, extravasation-induced aggregation was inhibited. Hemolysis was noted after intravenous injection of water, which also reduced the total volume and mean aggregate size of platelet aggregates induced by extravasation. Blood drawn from the inferior vena cava after induction of hemolysis had an increased volume of microaggregates, regardless of the agent producing hemolysis. In vitro studies revealed changes in spontaneous and ADP-induced aggregation only at very high concentrations of ethanol (greater than 3,000 mg/dl) and no effects at ethanol levels that altered in vivo aggregation. Ethanol, in doses that do not hemolyze erythrocytes, decreases platelet aggregation.

Animals↗

PubMedDate not supplied

Activation of peripheral dopamine presynaptic receptors lowers blood pressure and heart rate in dogs.

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Animals↗

PubMedDate not supplied

In vivo results of hydrogel composite pericardial substitutes.

In this study, two improved pericardial patches were developed and evaluated for their efficacy as pericardial substitutes. The patches are composites consisting of a hydrogel (PHEMA) that coats an underlying mesh (either ETFE or PET). Studies were conducted using subcutaneous implants in rats and pericardial patch implants in greyhound dogs. Adhesions between the substitute and pericardium and the epicardium were minimal. The ETFE composite patch caused an unacceptable epicardial reaction. The PET patch results were encouraging; the epicardium was largely unaffected by the patch.

Animals↗

PubMedDate not supplied

A hydrogel pericardial patch.

Patients undergoing repeat cardiac operations are higher operative risks than those undergoing an initial cardiac procedure because adhesion formation can occur if the native pericardium is not closed. A unique composite patch that may be used to augment the pericardial tissue when primary closure is not possible has been developed. The patch is made of a hydrogel, poly (2-hydroxyethyl methacrylate), reinforced with an ethylene tetrafluoroethylene (ETFE) mesh. The mesh provides the needed mechanical properties, whereas the patch's surface properties are comparable to the hydrogel. Two types of patches were fabricated: one with the mesh weave at a perpendicular orientation and one at 45 degrees to the principle loading direction. The patches were mechanically tested and compared with canine pericardium. Ultimate tensile strength of the patches is not significantly different from canine pericardium (p less than 0.05), are the patch suture strength is nearly twice that of canine pericardium. The perpendicular patch is stiffer than canine pericardium, whereas the 45 degree patch is not (p less than 0.05). The 45 degree patch shows considerable promise as a pericardial substitute because it closely matches the properties native canine pericardium.

Animals↗

PubMedDate not supplied

An efficient method for removing bilirubin.

Bilirubin is tightly bound to albumin, making hemoperfusion an ineffective treatment for hyperbilirubinemia. By adding a safe unbinding agent to the blood (solutizer), which itself is adsorbed, hemoperfusion can become efficient and practical. Canines were made hyperbilirubinemic with an intravenous infusion of a 5 mg/ml solution (with Na2CO3) for 1 hour. Peak concentrations of 14-22 mg/dl were reached in adult dogs (25-35 kg). Hemoperfusion was then initiated with or without (control) the solutizer (sodium benzoate). The bilirubin unbinding effect of sodium benzoate was rapid and effective. Because of the simultaneous adsorption of sodium benzoate, a small activated carbon section that was presaturated with the solutizer was located proximal to the main hemoperfusion column, in addition to continuous infusion to reach 20 mM in the blood. Comparison of the normalized bilirubin concentration for benzoate augmented hemoperfusion with the average for control dogs, shows that benzoate results in a threefold decrease in the normalized bilirubin concentration after 1.5 hr of hemoperfusion. Sodium benzoate may also have the advantage of protecting platelets during hemoperfusion.

Animals↗