The Dahl strain of genetically salt-resistant (DR) and salt-sensitive (DS) rats affords an opportunity to explore mechanisms responsible for salt resistance and sensitivity. Dahl sensitive rats exhibit abnormalities in sympathetic neural control of the circulation and in renal sodium handling. Since cardiac baroreflexes participate in regulation of sympathetic nerve activity and sodium excretion, we have evaluated cardiac baroreflex function in DR and DS rats. This article briefly reviews evidence that cardiac sensory endings with vagal afferents are reset to a higher threshold in DS rats before elevation of arterial or cardiac filling pressures, as a result of this resetting, cardiac baroreflex inhibition of sympathetic nerve activity during volume expansion is impaired in prehypertensive DS rats, a high-sodium diet enhances the gain of cardiac baroreflex inhibition of sympathetic nerve activity in DR but not DS rats, and atrial natriuretic factor stimulates cardiac sensory receptors with vagal afferents. Taken together, these studies prompt speculation that humoral factors released during intake of a high-sodium diet may sensitize cardiac baroreflexes and thereby protect against sodium retention and hypertension. An absence of this compensatory adjustment or plasticity in cardiac baroreflex function in DS rats may predispose to salt-induced hypertension.

The endogenous opioid system includes three major families of peptides: dynorphins (derived from pre-proenkephalin B), endorphins (derived from pre-proopiomelanocortin), and enkephalins (derived from pre-proenkephalin A). Multiple species of opioid peptides are derived from these major precursors and many of them possess potent cardiovascular properties. Opioid peptides and opioid receptors, of which multiple forms have been defined, are present in the central nervous system and peripheral neural elements. In the central nervous system, opioid peptides and receptors are found in forebrain and hindbrain nuclei involved in baroregulation, sympathoadrenal activation, and several other vital autonomic functions. In the periphery, opioid peptides are found in autonomic ganglia, adrenal gland, heart, and other organs; multiple opioid receptors are also found in vascular tissue, heart, and kidneys. Although little is known to date on the regulatory mechanisms of the opioid system in normal cardiovascular states, it became clear that cardiovascular stress situations substantially modify the activity of the endogenous opioid system. The purpose of this review is to clarify the sites of interaction of the opioid system with all major components of the cardiovascular system and indicate the potential role of this system in the ontogenesis of cardiac malfunction, vascular diseases, and hypertension.

The extracellular structural protein, collagen, is responsible for the functional integrity of the myocardium permitting reversible interdigitation and transmission of force between contracting myocytes. In the pressure-overloaded, hypertrophied myocardium, clinical and experimental evidence indicates that the proportion of collagen relative to muscle is increased. Factors that appear to influence collagen growth during the hypertrophic process include age, species, the rapidity with which the overload occurs, the nature of the lesion leading to the pressure-overload, and the severity and duration of the overload. Morphologically, the heart's collagen matrix consists of a complex weave with tendinous insertions that surrounds myocytes grouping them into myofibers, strands of collagen that connect adjoining myofibers, and collagenous struts that join myocytes to other myocytes and capillaries. In a primate preparation of perinephritis with systemic hypertension, it was observed that the tendinous elements of the weave and the strands of collagen lying between myofibers were increased in number and physical dimension. The functional consequences of a remodeling of the collagen matrix that accompanied myocardial hypertrophy remain to be elucidated. A better understanding of the dynamic behavior of the collagen matrix may offer new insights into the pathogenesis of ventricular dysfunction that accompanies the chronic pressure-overloaded state.

During the past decade our understanding of the complex interaction between cardiac muscle and coronary vascular growth has increased substantially. Some types of cardiac hypertrophy, for example, left ventricular hypertrophy secondary to hyperthyroidism, are associated with increased coronary vascular growth. However, in most animal preparations of hypertrophy and in several clinical types of hypertrophy of the left and/or right ventricles, pathologic cardiac enlargement impairs the ability of the coronary circulation to allow normal increases and perfusion in response to intense dilator stimuli. In general, clinical studies have demonstrated far more profound abnormalities than studies in experimental animals. These observations provide a plausible explanation of why patients with hypertrophied ventricles often exhibit signs and symptoms of myocardial ischemia in the absence of coronary obstructive disease. The recent observation that experimentally produced left ventricular hypertrophy secondary to renal hypertension augments infarct size and the incidence of sudden lethal arrhythmias has additional implications relevant to the interaction between cardiac hypertrophy and myocardial perfusion. Although coronary reserve is impaired in many types of pathologic hypertrophy, the anatomic or biochemical basis for these observations remains elusive.

A short and up-to-date review on the great advances made in the field of the atrial natriuretic factor (ANF) is presented. All the short active peptides (up to 33 AA) isolated after purification of atrial homogenates have the same core of 23 amino acids (Ser 103-ARG 125). The ANF liberated in the medium of cultures of rat atrial cardiocytes is the 26 amino acid Arg 101-Tyr 126. Cloning of the cDNA encoding for ANF and of the rat, mouse, and human ANF gene has been accomplished. ANF has a most potent and short-lasting diuretic and natriuretic effect that appears to be predominantly due to a significant increase in glomerular filtration rate. ANF inhibits the release of aldosterone both in vitro and in vivo. It produces a profound inhibition of vascular contraction induced by norepinephrine and angiotensin II. This vasorelaxation is followed by a prolonged refractory period. ANF administration corrects the hypertension in 2K-1C hypertensive rats and in spontaneously hypertensive rats. Specific high-density binding sites have been found in the brain, especially in the hypothalamus, subfornical organ, median eminence, area postrema, and nucleus tractus solitarius, all areas involved in the brain control of hypertension and in the regulation of salt and water. ANF has no effect on the known sodium transport mechanisms across cell membrane. It has a major effect on the stimulation of guanylate cyclase activity, especially in renal glomeruli. Specific radioimmunoassay procedures have been established and results of preliminary studies that establish clearly that ANF is a circulating hormone are presented.

The finding that blood flow during external chest compression may be due to increased intrathoracic pressure, and the subsequent reporting of increased carotid blood flow with simultaneous ventilation and chest compression or with abdominal binding during CPR ignited a flurry of investigations into alternative approaches to CPR. A number of alterations of the conventional CPR technique were proposed, many resulting in improved hemodynamics when compared with standard CPR techniques in the same subject. However, some of the proposed methods increased cerebral blood flow but decreased myocardial perfusion. Others improved systolic pressures but decreased vital organ blood flow. More importantly, most studies with survival as an end point failed to show a benefit when alternative approaches to CPR were used. Therefore, it is unlikely that there will be significant changes in the recommendations for the use of adjuncts during CPR. Not all studies support the conclusion that blood flow during closed-chest compression is secondary to increased intrathoracic pressure. It is probable that in man there is a spectrum. In some individuals the predominant mechanism of blood flow during CPR may be cardiac and/or vascular compression, and in others flow may be secondary to an increased intrathoracic pressure.

Calcium channel-blocking drugs have potent antiarrhythmic and antianginal effects and in addition may reduce the extent of cellular injury after anoxia/ischemia. Verapamil is the treatment of choice (90% effective) for uncomplicated episodes of paroxysmal supraventricular tachycardia. All three calcium-channel blockers available, diltiazem, nifedipine, and verapamil, can reduce the frequency of angina occurring both at rest and with exertion. Calcium may mediate several cytotoxic events during the reperfusion period after prolonged ischemia that lead to irreversible cell injury. There is experimental evidence that calcium-channel blockers may reduce the cellular influx of calcium after ischemia and reperfusion, and thereby attenuate cerebral and myocardial injury, although most studies have failed to show benefit of treatment unless the drug is administered before the onset of ischemia. Most trials using calcium-channel blockers in the setting of acute myocardial infarction have failed to show a benefit of treatment. The safety and efficacy of calcium-channel blockers have yet to be shown in controlled studies of human resuscitation, although the potential for such treatment, if it is effective in attenuating myocardial cerebral cellular injury, could be enormous.

Calcium chloride has been advocated since the 1920s for the resuscitation of asystole, electromechanical dissociation (EMD), and ventricular fibrillation. Reports of side effects and complications have been numerous. Studies of calcium assays following American Heart Association recommended dosages have shown dangerously elevated serum levels. Large retrospective clinical studies in Milwaukee and Tampa have found no evidence of improved survival with calcium chloride in asystole and EMD. A prospective randomized double-blind study comparing calcium chloride and saline controls in the Milwaukee Paramedic system for asystole and EMD using standard AHA protocols showed no statistically significant difference in resuscitation rates or long-term survival between the calcium and no-calcium groups for the rhythm of asystole. Although patients with EMD had statistically improved resuscitation rates when calcium chloride was given, only one of the patients survived to hospital discharge. Because of the low rates of resuscitation and long-term survival in patients presenting in asystole and EMD, proving that calcium chloride does not enhance survival would require large multicenter trials. However, since no controlled study has ever documented significant benefit, its routine use in asystole and EMD cannot be supported. Calcium has long been used in medical treatment of hypocalcemic and hyperkalemic states and should be administered in moribund patients who have the proper clinical history and clinical signs of hypocalcemia.

More than 30 million Americans are disabled. Wide experience has shown that these conditions do not prevent these individuals from becoming proficient in the knowledge and skills of CPR. Instructional materials and methods can be modified to help this special population learn CPR despite handicaps. The American Heart Association has supported these special efforts since 1978, but no comprehensive resource exists for CPR instructors interested in helping the "physically challenged" individual learn CPR. This article addresses general and specific suggestions for teaching selected handicapped populations. They are: hearing impaired, visually impaired, other physical impairment such as obesity, chronic obstructive pulmonary disease, arthritis, angina, and other medical conditions that may limit one's ability to learn the psychomotor skill of CPR.