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PubMed2001

The pathophysiology of varicocele-associated male infertility.

Varicocele is the most commonly identifiable, surgically correctable lesion associated with male-factor infertility. Surgical correction of a varicocele, whether unilateral or bilateral, results in improvement not only in semen parameters but also in spontaneous and assisted pregnancy rates. Varicoceles seem to induce a number of changes in the testicular microenvironment. These alterations in temperature, hemodynamics, and reactive oxidative species and antioxidant concentrations have been demonstrated to produce deleterious effects on spermatogenesis. However, despite current knowledge in the pathophysiology of varicocele-associated male infertility, the exact mechanism--or mechanisms--by which varicoceles impair fertility remains elusive. This review examines scientific evidence regarding the pathophysiology of varicocele-associated male infertility.

Humans↗

PubMed1994

Malaria and pregnancy: epidemiology, pathophysiology and control options.

Extensive research on the epidemiology, pathophysiology, and control of malaria during pregnancy has led to new developments and some controversies. Meanwhile, malaria remains a major environmental factor causing serious pregnancy complications, whose incidence and severity depend on gestational age, parity, and the level of malaria endemicity. There is no cohesive explanation for pregnancy-related immunosuppression, though several pathophysiological hypotheses have been proposed. Furthermore, the emergence and rapid spread of chloroquine resistance has complicated the epidemiology, and the policy on alternative chemoprophylaxis. Chemoprophylaxis is probably the only available option for the control of malaria during pregnancy in Africa. However, the best delivery strategy still has to be established. Daily proguanil is the best chemoprophylactic drug at hand. Its deployment should include constant monitoring for the emergence of proguanil resistance, as well as controlled supervision of the distribution of the drug. New control options, such as the use of insecticide-impregnated bed nets, and intermittent targeted mass chemotherapy, require more operational research before they can be broadly recommended.

Africa↗

PubMed1978

Myocardial infarction in young vs old male rats: pathophysiologic changes.

Young (90 days) and old (15 months) male, Sprague-Dawley rats were subjected to an acute and massive myocardial infarct by giving them two injections of a large dose of isoproterenol. The animals were autopsied at sequential time intervals to ascertain the similarities or dissimilarities in the pathophysiologic events which attend acute myocardial infarction and repair in young vs old rats. Although the signs and severity of hypotensive shock appeared to be equal, mortality was higher in the old rats, especially during the acute necrosis phase. The older rats also manifested more severe and persistent congestive heart failure, i.e., hydrothorax. Serum enzymes (CPK, SGOT, SGPT, and LDH), lipids (triglycerides, free fatty acids, and cholesterol), glucose, and BUN levels manifested a dynamic rise and fall concomitant with the induced myocardial necrosis and repair phases with distinct differences in these metabolic changes between young and old rats. Despite initially higher circulating levels of corticosterone in the old vs young rats, the older animals manifested little or no increase in circulating corticosterone levels during the acute stress of myocardial infarction. This apparent lack of adrenocortical responsiveness was accentuated by the concomitant finding of greatly hypertrophied, hemorrhagic, and lipid-depleted adrenal glands in the old rats vs a dynamic increase in circulating corticosterone levels and alterations in the weight of adrenal and thymus glands of the young rats. During the myocardial repair phase, the young rats manifested extensive endocardial fibrosis whereas the old rats displayed little or no endocardial fibrosis but copous and persistent myocardial edema and ground substance in keeping with their higher concentration of cardiac hexosamine. The pathophysiologic course of events which attends myocardial necrosis and repair is quite different in young vs old rats and may be related to the degree of responsiveness of the pituitary-adrenal axis which changes with age.

Adrenal Glands↗

PubMed1989

Changing concepts in the pathophysiology of myocardial ischemia.

The principal common pathway for myocardial ischemia is an oxygen supply-demand imbalance; more recently, greater emphasis has been placed on limitations of myocardial blood supply, as well as excessive myocardial oxygen demand. Myocardial ischemia is a metabolic event resulting from inadequate oxygen delivery to local tissues. The physiologic effects of ischemia are observed through abnormalities in left ventricular function, electrocardiographic changes, and often, by angina pectoris. Prognostic and therapeutic outcomes are significantly related to the pathophysiology of the underlying coronary lesion. Because myocardial ischemia often occurs without symptoms, clinical distinctions based on angina stability may more appropriately be represented by stable or unstable ischemic syndromes that incorporate silent ischemia. Stable ischemic syndromes occur secondary to coronary plaques, whereas unstable syndromes are the result of active lesions caused by plaque rupture with local thrombus and vasoreactivity that produce intermittent critical decreases in coronary supply. The prognosis of patients with stable ischemia is related to the extent of myocardium at jeopardy and overall left ventricular function. In contrast, unstable syndromes are associated with a worse short-term prognosis, which may be predictable by the presence of silent ischemia or left ventricular dysfunction or both. Therapeutic decisions based on an improved pathophysiologic understanding of ischemic mechanisms as well as the physiologic impact of therapy on cardiac function can enhance efficacy while avoiding adverse effects. Calcium channel blockers appear to afford certain advantages in the treatment of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Potential role of the tissue renin-angiotensin system in the pathophysiology of congestive heart failure.

The circulating renin-angiotensin system (RAS) plays an important role in the maintenance of cardiovascular homeostasis. It has recently been demonstrated that endogenous RAS exist in target tissues that are important in cardiovascular regulation. This article reviews the multiple effects of angiotensin II in target tissues, the evidence for the presence of functional tissue RAS and the data that suggest a role for these tissue RAS in the pathophysiology of heart failure. Activation of circulating neurohormones is predictive of worsened survival in heart failure; however, cardiac and renal tissue RAS activities are also increased in the compensated stage of heart failure, when plasma renin-angiotensin activity is normal. It is hypothesized that the plasma RAS maintains circulatory homeostasis during acute cardiac decompensation, while changes in tissue RAS contribute to homeostatic responses during chronic sustained cardiac impairment. This concept of different functions of circulating and tissue RAS in the pathophysiology of heart failure may have important pharmacologic implications.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1983

Hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome: a common endocrinopathy with distinct pathophysiologic features.

The HAIR-AN syndrome that consists of hyperandrogenism (HA), insulin resistance (IR), and acanthosis nigricans (AN) is an underdiagnosed endocrinopathy, because hyperandrogenic women are not commonly screened for insulin resistance or acanthosis nigricans. The distinct pathophysiologic features of the HAIR-AN syndrome are discussed in detail. In this syndrome, the primary pathophysiologic derangements are the insulin resistance and the hyperandrogenism. The acanthosis nigricans is an epiphenomenon of these primary processes. In patients with the HAIR-AN syndrome, the degree of severity of the insulin resistance is positively correlated with the degree of severity of the hyperandrogenism. In patients with adequate pancreatic beta-islet cell reserve, insulin resistance results in a long-term increase in circulating insulin levels. The hyperinsulinemia probably directly stimulates ovarian androgen production. In turn, hyperandrogenism itself produces insulin resistance. This positive feedback loop between insulin resistance and hyperandrogenism propagates the disease, and increases its severity over time. The relationship between insulin resistance and hyperandrogenism may explain the hyperandrogenemia seen in the following disease processes: obesity, acromegaly, lipoatrophic diabetes, leprechaunism, and Kahn types A and B insulin resistance.

Acanthosis Nigricans↗

PubMed1989

Does vasoactive intestinal polypeptide mediate the pathophysiology of bowel obstruction?

We hypothesized that bioactive peptides might be released into the portal circulation and mediate pathophysiologic alterations accompanying small bowel obstruction. We studied this question in a subacute canine small bowel obstruction model using 50 percent diameter occlusion. Control animals underwent sham laparotomy. Vasoactive intestinal peptide (VIP), peptide YY, and gastrin were measured in portal and systemic plasma by specific radioimmunoassays at 24-hour intervals as the obstruction progressed to completion over 5 days. All peptides in both groups demonstrated portal and peripheral gradients. In control dogs, peptide concentrations did not change postoperatively but VIP increased markedly in obstructed dogs, demonstrating a median portal level of 95 pmol/liter at 96 hours compared with 31.5 pmol/liter in control animals. These portal VIP levels are known to cause hypersecretion and splanchnic vasodilation in experimental models. The release of vasoactive compounds such as VIP may mediate local pathophysiology in human small bowel obstruction. A similar explanation of the systemic effects is consistent with the known cardiopulmonary bioactivity of VIP.

Animals↗

PubMed1994

Lower serum prolyl endopeptidase enzyme activity in major depression: further evidence that peptidases play a role in the pathophysiology of depression.

Prolyl endopeptidase (PEP) is a serine proteinase, which may cleave peptides that are involved in the pathophysiology of major depression, such as arginine vasopressin, beta-endorphin, luteinizing hormone-releasing hormone, thyrotropin-releasing hormone, and maybe corticotropin-releasing hormone. PEP may be involved in activation of cell-mediated immunity, autoimmune and inflammatory responses, which repeatedly occur in severe depression. The present study investigates serum PEP activity in 33 normal controls, 16 minor, 14 simple major, and 18 melancholic depressed subjects. Pre-dexamethasone and post-dexamethasone (DST) intact adrenocorticotropic hormone (ACTH) and cortisol values were determined in 33 depressed subjects. Serum PEP activity was significantly lower in depressed subjects compared to normal controls and in melancholic depressed subjects compared to minor and simple major depressed subjects. Up to 61.1% of the melancholic patients had serum PEP activities below the mean PEP values of normal controls minus two SDs. In the depressed study group, significant negative correlations between serum PEP activity and severity of illness, post-DST cortisol, and ACTH values were observed. There was a trend toward higher serum PEP activity with increasing age. It is hypothesized that lower serum PEP activity, and lower serum activity of other peptidases, may play a role in the neuroendocrine and immune pathophysiology of major depression.

Adrenocorticotropic Hormone↗

PubMed1993

Acute mesenteric ischemia: pathophysiology, diagnosis, and treatment.

Ischemia has traditionally been viewed as arising only from abnormalities of oxygen dynamics, namely the cellular hypoxia resulting from the imbalances between oxygen supply, consumption, and demand. Recently, it has become clear that such a view is too restrictive. Hypoperfusion may be caused by both anatomic and functional impediments to either inflow or to outflow from an organ. Furthermore, the pathophysiologic consequences are likely to involve not only cellular hypoxia, but also a restricted supply of nutrients and other important molecules and an abnormal elimination of physiologic wastes such as carbon dioxide. Hence the recommendation that ischemia be defined as a dual defect of oxygen deficit and carbon dioxide excess. AMI is, therefore, a severe anatomic or functional impediment to the splanchnic circulation, resulting in a dual defect of intestinal hypoxia and cellular hypercarbia. Although the functional and structural consequences of cellular hypoxia are well known, the pathophysiology of cellular hypercarbia has only begun to be explored. AMI syndromes include three related processes: occlusive mesenteric ischemia, nonocclusive ischemia, and sepsis-induced SI. Leakage of bacteria or bacterial toxins into the circulation during mesenteric ischemia forms the basis of the systemic components of this syndrome. Striving for an earlier diagnosis, treating the systemic (septic) consequences, and taking measures to promptly restore mucosal oxygen balance through aggressive pharmacologic and appropriate surgical intervention have significantly improved the prognosis. About 80% of patients with acute arterial embolism, 60% of those with nonocclusive ischemia, and only 20% of patients with arterial thrombosis are expected to live without significant residual nutritional deficits. The cause of death is usually sepsis and multisystem organ failure, and therefore, further reductions in mortality are likely to occur with the improved prevention and treatment of sepsis.

Acute Disease↗

PubMed1992

Gastrointestinal food hypersensitivity: basic mechanisms of pathophysiology.

Gastrointestinal symptoms occur in a large number of patients with food allergies. Immediate hypersensitivity mechanisms may give rise to the nausea, vomiting, abdominal pain, and diarrhea experienced by these patients. However, there are limited human data about the pathophysiological basis for these symptoms. Most of the available information comes from a variety of animal models. This article reviews the literature using models of intestinal food hypersensitivity, as well as human studies, that have contributed to our understanding of the pathophysiological mechanisms in gastrointestinal food hypersensitivity.

Animals↗

PubMed1992

Pathophysiology of congenital diaphragmatic hernia II: the fetal lamb CDH model is surfactant deficient.

The high mortality for congenital diaphragmatic hernia (CDH) has been attributed to a combination of pulmonary hypoplasia and pulmonary hypertension. We hypothesize that a surfactant deficiency may in part be contributing to the pathophysiology of CDH. This study documents the functional, quantitative, and qualitative aspects of the surfactant status of the alveolar air-liquid interface and the type II pneumocyte in the fetal lamb CDH model. Ten lamb fetuses (gestational age, 80 days) had a CDH created via a left thoracotomy and then were allowed to continue in utero development until term. Three litter mates and three nonoperated time-dated fetuses served as controls. At term, pressure-volume curves were performed to measure pulmonary compliance and total lung capacity. Alveolar lavage was then performed to measure the quantitative and the qualitative aspects of pulmonary surfactant. Finally, isolation of type II pneumocytes allowed quantification of phospholipid synthesis. When compared with controls (N = 6), the CDH lambs (N = 5) had significantly smaller lungs (P = .009), decreased total lung capacity (P less than .001) and compliance (P less than .001), reduced total lavaged phospholipids (P = .006), and decreased percent phosphatidylcholine (P = .02). CDH lambs also had increased total lavaged proteins (P = .05) and higher minimum dynamic surface tension (P less than .001). A surfactant deficiency may be contributing to the pathophysiology of CDH. Surfactant replacement therapy in premature infants has been shown to improve lung compliance, decrease morbidity, and improve survival. Exogenous surfactant may also benefit infants with CDH.

Animals↗

PubMed1993

Is phantom tooth pain a deafferentation (neuropathic) syndrome? Part I: Evidence derived from pathophysiology and treatment.

Phantom tooth pain is a syndrome of persistent pain or paresthesia in teeth and other oral tissues that may follow dental or surgical procedures such as pulp extirpation, apicoectomy, tooth extractions, or exenteration of the contents of the maxillary antrum. It can also occur when nerves are injured after trauma to the face or even after routine inferior alveolar nerve blocks if the needle pierces the nerve sheath. In the case of tooth extraction, the pain is found in the edentate area. After periodontal surgery, pain or paresthesia is located in the gingiva. The incidence of phantom tooth pain after extirpation may be as high as 3% of cases. Clinically, phantom tooth pain is similar in many essential characteristics to deafferentation pain syndromes also known as phantom pain syndromes. A limitation to this taxonomy is the lack of definitive information with respect to the pathophysiology of deafferentation pain in the trigeminal nerve. This article amplifies previous clinical descriptions of phantom tooth pain. Current concepts in the pathophysiology of neuropathic pain are reviewed as they pertain to phantom tooth pain. Treatments are described that use three routes of drug administration: oral, nerve blocks by injections, and intranasal applications. Reasons are discussed for the high rates of morbidity after dental and neurosurgery in attempts to treat phantom tooth pain.

Afferent Pathways↗

PubMed1985

Pathophysiological interrelations of obesity, impaired glucose tolerance, and arterial hypertension.

There is a large amount of epidemiological and clinical evidence for associations among obesity, impaired glucose tolerance, and arterial hypertension; nevertheless, the pathophysiological mechanisms underlying these associations have not yet been elucidated. In this article, some working hypotheses are discussed, and original data are presented from two studies focusing on these pathophysiological interrelations. A case-control study of obese normotensive and hypertensive patients, matched for sex, age, and degree of overweight, has shown that obese patients with associated arterial hypertension have higher fasting serum insulin levels and reduced glucose tolerance compared with their normotensive peers. A second study compared subjects with impaired glucose tolerance with a control group of clinically healthy individuals of comparable sex, age, and body mass index, and it revealed that impaired glucose tolerance is associated with significantly higher blood pressure levels, independent of body weight. The results of the two studies together suggest that the association between hypertension and impaired glucose tolerance is independent of overweight; they also give some support to the hypothesis that hyperinsulinemia may contribute to the development of high blood pressure in obese patients.

Adult↗

PubMedDate not supplied

Physiological and pathophysiological roles of excitatory amino acids during central nervous system development.

Recent studies suggest that excitatory amino acids (EAAs) have a wide variety of physiological and pathophysiological roles during central nervous system (CNS) development. In addition to participating in neuronal signal transduction, EAAs also exert trophic influences affecting neuronal survival, growth and differentiation during restricted developmental periods. EAAs also participate in the development and maintenance of neuronal circuitry and regulate several forms of activity-dependent synaptic plasticity such as LTP and segregation of converging retinal inputs to tectum and visual cortex. Pre- and post-synaptic markers of EAA pathways in brain undergo marked ontogenic changes. These markers are commonly overexpressed during development; periods of overproduction often coincide with times when synaptic plasticity is great and when appropriate neuronal connections are consolidated. The electrophysiological and biochemical properties of EAA receptors also undergo marked ontogenic changes. In addition to these physiological roles of EAAs, overactivation of EAA receptors may initiate a cascade of cellular events which produce neuronal injury and death. There is a unique developmental profile of susceptibility of the brain to excitotoxic injury mediated by activation of each of the EAA receptor subtypes. Overactivation of EAA receptors is implicated in the pathophysiology of brain injury in several clinical disorders to which the developing brain is susceptible, including hypoxia-ischemia, epilepsy, physical trauma and some rare genetic abnormalities of amino acid metabolism. Potential therapeutic approaches may be rationally devised based on recent information about the developmental regulation of EAA receptors and their involvement in the pathogenesis of these disorders.

Amino Acids↗

PubMed1987

The 5-hydroxytryptamine system of blood platelets: physiology and pathophysiology.

The 5-hydroxytryptamine (5HT)-system of human blood platelets consists of a relatively specific uptake mechanism for 5HT at the plasma membrane, intracellular storage organelles (dense bodies), a metabolizing enzyme (monoaminoxidase B) and a 5HT2-receptor whose stimulation leads to activation of the phosphatidylinositide turnover, a rise in free cytoplasmic Ca2+, phosphorylation of proteins and a shape change reaction. There is neither a relevant 5HT-biosynthesis nor a marked physiological 5HT-turnover in platelets. Under physiological conditions the platelet 5HT-system may have a role as a scavenger for free extracellular 5HT and in hemostasis. Disturbances which have been described in pathophysiological states include impairment of 5HT-uptake (hypertension, migraine), impairment of 5HT-storage (storage pool deficiencies, thromboembolic disorders, hypertension) and increased sensitivity to activating agents like 5HT (cardiovascular disorders, diabetes). Besides their role in physiology and pathophysiology platelets may be useful partial models for vascular smooth muscle cells.

Blood Platelets↗

PubMed1986

The pathophysiology of severe falciparum malaria.

By the end of the 1940s, the clinical and pathological features of severe falciparum malaria had been well described by military physicians and pathologists working in theatres of war where the disease was endemic. From that time serious efforts were made to discover the pathophysiology of the severe manifestations of malaria because an understanding of these mechanisms forms an important basis for the clinical management of affected patients. Recently, after a period of neglect, there has been a revival of interest in malaria as a subject for clinical and laboratory research. In this article, Rodney Phillips and David Warrell review aspects of that work and attempt to unravel the mysteries of the pathophysiology of severe malaria in man.

Journal Article↗

PubMed1990

High permeability pulmonary oedema: pathophysiology and mechanisms of injury.

Many critically ill patients are at risk for developing HPPE. Since 60% of patients develop HPPE within 24 hours of the pulmonary insult with 11% developing respiratory failure within 72 hours, it is imperative that the critical care nurse understand the pathophysiological responses (Bernard & Bradley, 1986). While the pathophysiological responses are specific, injury to the alveolar-capillary membrane, the mechanisms of injury are diffuse. Knowing the mechanisms can alert health care providers to those patients who are at risk for developing HPPE and more quickly mobilize interventions to alleviate or lessen its occurrence.

Cell Membrane Permeability↗

PubMed1986

Alcoholic organic brain disease: nosology and pathophysiologic mechanisms.

Study of alcoholic chronic organic brain syndrome may have applicability to the large population of alcoholics with less severe cerebral dysfunction. Brain impairment in alcoholics may be conceptualized as two clinically and neuropathologically distinguishable organic brain syndromes: alcohol amnestic disorder or Korsakoff's psychosis (KP) and alcoholic dementia. Alcoholic organic brain disease may result from two interacting pathophysiological processes: nutritional (thiamine) deficiency and ethanol neurotoxicity. Subcortical periventricular lesions associated with KP result primarily from thiamine deficiency, whereas ethanol neurotoxicity and various secondary effects of alcoholism may contribute to the cortical neuropathological changes associated with alcoholic dementia. These two patterns of brain damage may be differentiable in individual alcoholics using cognitive tests and other measures of CNS function and, therefore, allow selection of a treatment strategy based on pathophysiological considerations. Studies in animals and humans suggest that a genetic predisposition to thiamine deficiency may contribute to alcoholism-associated dysfunction of brain and other organ systems and possibly have a causative role in the development of alcoholism.

Alcohol Amnestic Disorder↗