Biomedical subjects
Publications and source records attributed to R J Capone.
Prehospital coronary care is becoming a common feature of community emergency medical systems. To date, results have been reported in a variety of formats, making meaningful comparison and aggregate analysis impossible. A flexible patient encounter form and data analysis scheme are proposed for universal adoption in future published accounts.
The arrhythmogenic potential of elevated serum free fatty acids (FFA) was investigated in closed-chest pigs following acute coronary artery occlusion. Animals both with and without ventricular irritability before the FFA rise were studied. No significant increase in PVC frequency occurred and only 1 out of 17 animals developed ventricular fibrillation in the 60 min following acute FFA elevation. In this situation, FFA did not significantly influence the appearance of arrhythmias.
The effect of hyaluronidase on the early course of acute myocardial infarction was evaluated in closed chest anesthetized pigs. One hour after balloon catheter occlusion of the left anterior descending coronary artery, hyaluronidase (500 units/kg body weight) was rapidly infused in 10 animals while 9 received no treatment. The animals were than observed over the next 4 hours. Cardiac output, heart rate, mean arterial pressure and left atrial pressure were not significantly affected by treatment. Heart rate increased and arterial pressure decreased in each group to a comparable degree of 5 hours, but left atrial pressure and cardiac output were unaffected. Precordial S-T segment mapping revealed no significant difference between the two groups. S-T segments rose to a comparable degree in each group and peaked before 1 hour. Hyaluronidase had no acute effects on the S-T segment map in the first 30 minutes after infusion or during the subsequent return of the map toward control level. Slightly lower S-T segments in the hyaluronidase-treated group at 5 hours was of borderline significance but was attributed to factors other than the drug intervention. Changes in ventricular wall motion were assessed angiographically, and all animals manifested akinetic or dyskinetic segments. A significant reduction in shortening fraction of involved segments was seen after occlusion, but no difference was observed between the two groups at 5 hours. Shortening fraction of the combined anterior and anteropical segments decreased from 66 +/- 10 to 20 +/- 6 percent at 5 hours in the hyaluronidase group (no. = 7) whereas in the control group (no. = 6) it decreased from 68 +/- 6 to 28 +/- 9 percent. Comparable increases in end-diastolic volume were also present at 5 hours in each group. Volumes increased from 80.6 +/- 5.1 to 97.5 +/- 6.4 ml3 at 5 hours (P less than 0.05) in the hyaluronidase-treated group (no. = 10) compared with 86.9 +/- 8.9 to 104.8 +/- 11.0 ml3 (P less than 0.05) in the control group (no. = 8). Hyaluronidase did not alter the early course of acute myocardial infarction in pigs. Species differences may contribute to different results reported to date.
Although it has been demonstrated that during isotonic grip exercise patients with chronic congestive heart failure have an abnormally reduced forearm oxygen consumption resulting from a depressed forearm flood flow, there may be additional etiologies of this abnormality. To explore this possibility biopsies of the pronator teres muscle were taken in eight control subjects with normal cardiac hemodynamics and in seven severely decompensated chronic congestive heart failure subjects. Each sample was fixed, stained, and photomicrographs of the sections were obtained and the capillary basement membrane thickness determined. The control capillary basement membrane thickness was 3028 plus or minus 187 A (mean plus or minus SEM) compared to the congestive heart failure thickness of 4924 plus or minus 538 A (pless than .01). It is possible that the increased basement membrane thickness in congestive heart failure may result from or actually cause the depressed oxygen consumption by altering diffusion.
Myocardial ischemic injury was created acutely in pigs by a closed-chest technique utilizing an intracoronary balloon occluder for the interruption of flow in the left anterior descending coronary artery and ST-segment elevation was followed over a two hour period using an 18 lead precordial map. In an experimental group of 10 animals, occlusion was carried out within the left anterior descending coronary artery 8.3 plus or minus 0.5 cm distal to the origin of the main left coronary. Mean ST segment elevation (ST) showed a peak rise of 0.16 mV 10 minutes after occlusion. The balloon was moved proximally 1.6 plus or minus 0.2 cm giving a significant secondary rise of 0.16 mV within 5 minutes, despite indications of a generally small area of additional myocardial involvement, as judged from anatomic distribution of additional vessels occluded as well as a lack of significant change in hemodynamic parameters. In a control group of 5 additional pigs, a single distal occlusion at 6.4 plus or minus 0.9 cm from the origin of the main left coronary was produced by an identical technique. The ST rose to a peak of 0.20 mV at 15 minutes and was followed by a steady decline. Unlike the experimental group, no additonal rise in ST was seen. The technique of precordial mapping thus appears to be a sensitive index of myocardial injury. In addition, it appears from this study that the magnitude of ST elevation is a direct reflection of the extent of myocardial injury.
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Elevation of circulating free fatty acids (FFA) has been implicated as a deleterious influence during conditions of myocardial ischemia. To further explore this question, acute coronary artery occlusion was produced in closed-chest, anesthetized pigs. FFA levels were elevated by injecting heparin and then infusing a lipid emulsion at 1 or 2 h following occlusion. Precordial ECG mapping was used to assess the degree of myocardial injury. At both 1 and 2 h following occlusion the lipid infusion elevated the mean FFA level to over 2,500 muM. ST segment levels failed to indicate any concomitant increase in degree of myocardial injury. By contrast, an isoproterenol infusion (30 min, 4-8 mug/min) under similar conditions did result in ST segment changes suggestive of extended myocardial injury. Augmented arterial FFA levels do not influence the degree of myocardial injury following acute coronary artery occlusion.
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To evaluate the effects of morphine on the peripheral venous and arterial beds, 69 normal subjects were evaluated before and after the intravenous administration of 15 mg morphine. Venous tone was determined by three independent techniques in 22 subjects. The venous pressure measured in a hand vein during temporary circulatory arrest (isolated hand vein technique) fell from 20.2+/-1.4 to 13.4+/-0.9 mm Hg (P < 0.01) 10 min after morphine, indicating that a significant venodilation had occurred. With the acute occlusion technique, morphine induced a reduction in forearm venous tone from 12.8+/-1.1 to 7.9+/-2.3 mm Hg/ml/100 ml (P < 0.01). Although forearm venous volume at a pressure of 30 mm Hg (VV[30]) was increased from 2.26+/-0.17 to 2.55+/-0.26 ml/100 ml, measured by the equilibration technique, the change was not significant (P > 0.1). Of note is that the initial reaction to morphine was a pronounced venoconstriction, demonstrated during the first 1-2 min after the drug. (Isolated hand vein pressure increased to 37.2+/-5.4 mm Hg, P < 0.01). This rapidly subsided, and by 5 min a venodilation was evident. Morphine did not attenuate the venoconstrictor response to a single deep breath, mental arithmetic, or the application of ice to the forehead when measured by either the isolated hand vein technique or the equilibration technique. To evaluate the effects of morphine on the peripheral resistance vessels in 47 normal subjects, forearm blood flow was measured plethysmographically before and 10-15 min after the intravenous administration of 15 mg of morphine. Although mean systemic arterial pressure was unchanged, forearm blood flow increased from 2.92+/-0.28 to 3.96+/-0.46 ml/min/100 ml (P < 0.01), and calculated vascular resistance fell from 42.4+/-5.2 to 31.6+/-3.2 mm Hg/ml/min/100 ml (P < 0.01). When subjects were tilted to the 45 degrees head-up position, morphine did not block the increase in total peripheral vascular resistance that occurs; however, it did significantly attenuate the forearm arteriolar constrictor response (before morphine, + 25.7+/-5.4; after morphine, + 13.7+/-5.3 mm Hg/ml/min/100 ml, P < 0.05). However, morphine did not block the post-Valsalva overshoot of blood pressure, nor did it block the increase in forearm vascular resistance produced by the application of ice to the forehead. Similarly, morphine did not block the arteriolar or venoconstrictor effects of intra-arterially administered norepinephrine. Morphine infused into the brachial artery in doses up to 200 mug/min produced no changes in ipsilateral forearm VV[30], forearm blood flow, or calculated forearm resistance. Intra-arterial promethazine, atropine, and propranolol did not block the forearm arteriolar dilator response to intravenous morphine; however, intra-arterial phentolamine abolished the response. These data suggest that in human subjects, morphine induces a peripheral venous and arteriolar dilation by a reflex reduction in sympathetic alpha adrenergic tone. Morphine does not appear to act as a peripheral alpha adrenergic blocking agent but seems to attenuate the sympathetic efferent discharge at a central nervous system level.
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